Sunday, January 21, 2018

Are We Raising Our Children to Be Slaves?

You can’t make it without an education!" "Go to college!" "Graduate from high school, go to college, get a good job." How many of us heard these mantras while growing up? How many of us have said these mantras to our children? Other people's children? Despite the fact that getting a  college degree today paves the road to debt slavery  where the chains and fetters are invisible and the wealthy, powerful owners, anonymous.

Slavery is likely to be abolished by the war power and chattel slavery destroyed. This, I and my European friends are glad of, for slavery is but the owning of labor and carries with it the care of the laborers, while the European plan, led by England, is that capital shall control labor by controlling wages." -- Chas. Hazzard, The Hazzard Circular, 1862
As we start 2018, student loan debt is close to $1.5 trillion, where an estimated 44.2 million Americans have one or more student loans on file.  Student loan debt surpasses total U.S. credit card debt by approximately $659 billion. It is the second largest financial asset on the federal government's balance sheet, making up 51.8% of total assets. Only mortgage debt is higher. Not to mention, according to the Federal Reserve is the only form of consumer debt that continued to grow in the wake of the Great Recession.

Parents and students have little understanding of how this loan program operates.   They don't understand that there is an entire "ecosystem feeding on federal student loans."
The companies making those calls are just one part of an ecosystem feeding on federal student loans. There are also debt servicers, refinance lenders, firms that help former students stay out of default and for-profit schools that make money as borrowers try to repay more than $1.2 trillion in government-backed education debt.
They don't understand that the cost of living is rising faster than income that make it increasingly difficult for people to keep up with the everyday expenses of life. They don't understand that a four-year degree is no longer the golden ticket to full time job with benefits and job security. They don't understand that the "four-year" degree actually takes five, six or even more years, which, of course, costs even more money.

When will we catch up with reality?  What was true 40 years ago doesn't make it true today.  What was true for baby boomers is not true for millennials and/or generations x,y,z, etc. 
It’s not unusual for me to talk to a couple that between them has $200,000 in student loan debt now. It’s not unusual at all. I talk to them almost every day on this show. And they’re 32 years old, they’ve been out of school for four, five or six years and they’re just treading water. They’re stuck because no one in their life—no supposed high school counselor, no parent, no financial-aid officer—smack you silly. Financial aid is $200,000 in student loan debt. Give me a break. Nobody looked at you and said, “You know, when you bring that baby home from the hospital, there’s a possibility you may want to use your education to raise your children.” -- Dave Ramsey


Student Debt Crisis

Hazard Chronicle Documentary Evidence

Student Debt Relief

Student Debt Slavery: Bankrolling Financiers on the Backs of the Young

Narrow bankruptcy laws make it nearly impossible to discharge student debt: From the The Cost of Opportunity: A series chronicling the student loan debt crisis in Wisconsin series

Rising Tuition Costs and the History of Student Loans


Tuesday, October 24, 2017

War on Health: Profits Before Patient Safety

Keep in mind, according to CDC statistics, no one has died from the use of food or dietary supplements, yet now, thanks to the FDA, you’ve got 3x as much regulation for food and dietary supplements as you have for pharmaceutical drugs, despite the fact that pharmaceutical drugs have proved to be one of the top killers of American citizens.

The relationship between physicians and the drug industry doesn’t begin once you have your MD or once you own your private practice; it begins the day you hit medical school. Big Pharma often give medical students gifts on their very first day. These gifts are always “Big Pharma” propaganda disguised as education, or something medical industry related that leaves the hard pressed medical student feeling like, at least someone cares, because we all know how tough medical school is.

But why is it so tough? Why are there intern boot camps?  Why must medical students and residents go through Why is "the private group that oversees physician training in the United States proposed rolling back rules so that young doctors just out of medical school can work shifts as long as 28 hours"? I mean, who wants an exhausted medical student/intern/resident practicing their craft on you when you are at your most vulnerable? Well one answer is that "medical school functions as a highly efficient system of inDOCtrination to ensure that physicians are less likely to question or confront the systems of power."
Professors who have already been indoctrinated to think a particular way ensure discussions are kept "on topic," or within the traditional bounds of acceptable debate that do not challenge power. I personally have lost track of the number of times I have heard a professor say, "That is interesting, but it is just outside of the scope of the discussion we are trying to have." This is a highly efficient and subtle way of controlling thought.

It makes more sense when you consider modern medicine was founded by a robber barons and an oil tycoon in particular, John D. Rockefeller. The conspiracy to limit and eliminate competition from non-drug therapies began with the Abraham Flexner Rockefeller Report on Medical Education of 1910. Abraham Flexner was engaged by John D. Rockefeller to  “evaluate” the effectiveness of therapies taught in medical schools and other institutions of the healing arts. The Flexner report unequivocally recommended the closure of all the homeopathic and naturopathic medical schools, in other words, anyone or any institution who use natural medicines to heal.

Subsequently, federal alphabet agencies--FDA, CDC, etc.-- were created to enforce the allopathic model under the guise of "protecting" the American food and drug supply.   In actuality, these agencies serve the medical industrial complex, not American citizens as you will see in the following documentaries.  The reason is obvious: alternative, mostly inexpensive non-toxic therapies represent a potential loss of billions, if not trillions of dollars to allopathic (drug) medicine and drug companies, not to mention, there is nothing more threatening to elite power than a healthy, robust public.


Overdosed America: The Broken Promise of American Medicine by John Abramson, M.D.

AIDS, Opium, Diamonds, and Empire: The Deadly Virus of International Greed. by Nancy Turner Banks, M.D.

Treaties and International Agreements


Wednesday, October 04, 2017

Las Vegas Shooting: Cui Bono?

I don't claim to know the truth about the Las Vegas incident, but I do know that like most lone gunman mass shooting events that turn into giant 24/7 media circuses, the official story just doesn't make sense even before you scratch the surface.

I mean, the guy carried 23 guns to his room and none of the security cameras caught it? Where is the camera footage of him prior to the shooting, carrying all of his weapons? Casinos literally hire former Marines with sharpshooter training in addition to the incredible surveillance of every public area, not to mention 22,000 people with smart phones. We should be awash with CCTV and cell phone footage of the chaos an event like this would create. 22,000 people with smart phones and so little , didn't smart-phone video this. Dig even deeper and the story gets even more ludicrous, preposterous, and should be downright offensive to anyone who spends five minutes on the official narrative.

High Incident Project?

Cui Bono? It certainly wasn't the alleged patsy shooter. Who benefits? An insidious industry that reaps maximum profit and influence for all the institutions that live off fear: the police, the justice system, the media, the weapons and security trade and most importantly, government, who create the "Big Brother" laws that increases their power over the masses. In other words, government and private contractors who have a stake in an exponentially growing national security state from which they stand to make a fortune and further limit our freedom of movement.

Collateral damage to push hidden agendas? Seems that way.


Sunday, September 24, 2017

Organ Harvesting: Dissected Alive for Profit?

Most of us sign up to become organ donors, literally, out of the goodness of our hearts, but I've always been a little skeptical (fear of my death being hastened by an eagerness to procure my organs) even before I knew the truth: that our vital organs, in order to be viable for transplant, must be harvested from human beings with a pulse, in other words, alive.

You say, how can that be? What part of after-I'm-dead don't they understand?  Well, you must ask yourself: "What is the legal definition of death?" "What was the legal definition of death?" "Why did the legal definition of death change?" "If a determination of death must be made in accordance with "accepted medical standards", how are "accepted medical standards" created and what are they based on?" "What happened to the great principle, both medical and moral, that governs the medical profession: Primum, non nocere (First, do no harm)?"

In a nutshell, in order for organ transplantation to occur, the need for "dead patients with live organs" became paramount.Below, is an attempt to answer some of those questions, while exposing the truth about organ donation; however, I implore you to do your own research.

The common law standard of death used to be total cessation of cardiac and respiratory function; that is, observable signs that life has ended.  Unfortunately, that  clear definition of death renders organ transplantation, impossible. Yet, human organ transplantation is a multi-billion dollar industry. What gives?  What gives is the legal definition of death. The medical industrial complex, specifically the 1968 Ad Hoc Harvard Committee on Irreversible Coma, created in response to the development of organ transplantation redefined the end of life in such a way that made the transplantation of organs possible.  So, the legal definition of death became subjective, a matter of opinion.

From the book, Death Investigation in America: Coroners, Medical Examiners, and the Pursuit of Medical Certainty By Jeffrey M Jentzen

The proponents of organ donation--transplant surgeons and bioethicists--represented two powerful new specialties. A decades long conflict began between these specialists and medical examiners, coroners, and prosecutors over the major basis of the latter's professional status--the possession of the body. Now, a lucrative business of organ procurement and a sentimental public relations campaign pressing for organ transplantation began to criticize medical examiners. Created in part in response to the development of organ transplantation, the 1968 Ad Hoc Harvard Committee on Irreversible Coma established that an individual could be legally pronounced dead by the physician based on the constellation of clinical findings that did not include the heart ceasing to beat.  Against aggressive organ procurement agencies, for profit, tissue recovery teams, and transplant surgeons entered the fight for desperate patients in a battle over possession of the body. Coe and his colleagues faced new challenges in having to wrestle with the sometimes conflicting goals of their obligation to investigate death and their responsibility to supply the public's increasing demand for organs and tissues to support life.

The definition of what constituted death changed from the absence of observable sign of breathing, movement and heartbeat to more subtle definitions based on lack of blood flow to the brain."
Now that the legal determination of death, since the advent of "cadaver" organ transplantation, has eliminated the total cessation of cardiac and respiratory function, death is now defined as the cessation of brain function--brain death--but, what is brain death? How can you be completely dead if your heart is still pumping, if your lungs are still working? Keep in mind, ventilators do not breathe for the patient, they only force air into the lungs; the patient must breathe out on his or her own.  And the diagnosis of Persistent Vegetative State (PVS) is incorrect almost half the time.  In other words, there is no true standard, and the diagnosis of brain death is completely subjective, a matter of opinion based on hospital  policy that is often influenced by profit margin.

But how do they determine "brain death"? Well, there is no legal or even statewide standard State law varies greatly and hospitals dictate what tests (if any) are used for the diagnosis. Many states allow nurses or nurse practitioners to declare brain death. However, there is one test that stands out above the rest and that is the Apnea Test.

Doctors and hospitals proclaim that an Apnea test can be used to confirm brain death. It does no such thing. In fact, it only makes things worse for the patient, your loved one. During the Apnea test, they take the ventilator away for up to ten minutes, at a time when the patient needs oxygen the most, to see how the patient responds. Without that crucial oxygen, the carbon dioxide level goes up which makes the brain swell, making it much more likely the patient will experience true brain death. Once again, keep in mind that a ventilator will not work on a dead person. The only thing a ventilator does is push air in. It does not push air out. Despite what they tell you, the ventilator only works when the lungs, heart, kidneys, liver are functioning. In other words, the patient is not dead!

Now, if you choose to opt out, it's not simply a matter of unchecking the little box on your driver's license or informing family members that should something happen to you, you do not want to donate your organs. Thanks to the Uniform Anatomical Gift Act, adopted in 48 states, you must have a document of refusal to opt out.
donor cards are legally binding in 48 states and health professionals who act on them are immune from liability in every state."
The revised UAGA (2006) reaffirms that if a donor has a document of gift, there is no reason to seek consent from the donor family as they have no right to give it legally.  If an individual has not made a document of gift during life, the Revised UAGA (2006) presumes the intent to donate organs, therefore has expanded the list of person (in section 9a  who can consent on behalf of the individual...Finally, if an individual prefers not to donate, this must be documented in a signed, explicit refusal."

It's a good idea to do your homework and research the evolution of major laws that make organ transplantation possible. The major ones are Uniform Determination of Death Act (UDDA) created in 1981, and the Uniform Anatomical Gift Act (UAGA), not to mention the Dead Donor Rule, which isn't exactly a law, but a general ethical assumption, enshrined in the UDDA.
The 1998 DHHS Referral and Request Regulation.

In light of the current problems regarding the lack of supply of suitable cadaveric organs, on December 15, 1997, Vice President Al Gore along with the DHHS launched a national initiatives to increase organ donation by 20%.

One element of the national initiative was to propose a rule ensuring that next-of-kin are asked to consent to the procurement of their loved ones organs. As a result, the DHHS passed a Referral and Request Regulation in August of 1998. 

The new regulation provides that hospitals wishing to receive Medicare payments must refer their patients who died along with their patient whose deaths are imminent to a local Organ Procurement Organization (OPO). Consequently, the OPO would provide personnel trained and experienced in obtaining consent to consult with the patient's next of kin and request consent to procure their loved ones organs.

At the same time that an increasing amount of research is finding the brain can heal itself, the use of aggressive tactics by organ procurement teams towards families to accept a diagnosis of "brain death" is increasing.  The result is that the diagnosis of "brain death" has been rapidly increasing over the past several years.  There is no doubt that lucrative financial outcomes factor in when determining brain death. 

To put it simply, the organ donor card gives doctors your permission (under contract law) to remove your organs from your warm, breathing and UN-anesthetized, doctor-declared “brain-dead” body. Keep in mind that young people with healthy organs  are the best candidates for organ harvesting.

As, Dr. Robert Truog, Professor of Medical Ethics, Anesthesiology and Pediatrics at Harvard Medical School asked,
Is our understanding of the facts driving our conclusion or is our desire for certain conclusions driving our interpretation of the facts? Are we gerrymandering the lines between life and death solely to meet social goals? In the long run, is this more likely to bolster or erode the confidence and trust of the people in the organ donation enterprise? "

P.S. I'm only advocating for fully informed organ donors--informed consent--not the end of organ transplantation. I'm only trying to encourage due diligence and the education of oneself and others on the organ donation program. The bottom line is: Challenge the "brain death" diagnosis. Don't sign off on the hospital's advanced directives.   And above all, do not consent to an Apnea test for loved ones!

Think about it, why do they administer paralyzing drugs and sometimes even anti anxiety drugs--however, no anesthesia-- to the organ donor while operating on them?  Because they're not brain dead! Or any kind of dead!    I woke up in the middle of an operation...all I can tell you is that I've never experienced so much pain.  Thank God I could move and scream to alert the doctors.  My worst nightmare is being operated on, feeling every little move of the surgeon, without the ability to move, scream, alert anyone that I'm being tortured. I imagine I'm not the only one.


Controversies in the Determination of Death: A White Paper by the President's Council on Bioethics

How to revoke organ donation consent by state

Horror as patient wakes up in NY hospital with doctors trying to harvest her organs for transplant profits

An 8-year-old was taken off life support, his organs donated. Now, police are investigating

Full Court Document filed regarding lawsuit regarding coroner's office and 8-year old taken off life support to get his organs

Surgeon Accused of Speeding a Death to Get Organs

Ruben Navarro Civil Case Filing:

Doctor Cleared of Harming Man to Obtain Organs

Can Brain Dead Patients Respond?

"Brain Dead" Patient Begins Breathing During Surgery After Liver Removed and Other Horrific Accounts:
There's a big difference between mostly dead and all dead. Now, mostly dead … is slightly alive."


Friday, September 15, 2017

Immersed In an Ocean of Electromagnetic Radiation

We can't turn on the TV/radio, open a newspaper/magazine/book without being bombarded by warnings about anthropomorphic global warming/climate change (by the way, a multi-billion dollar industry based on psuedoscience), yet we hear nothing about the very real danger of anthropomorphic electrosmog. The earth is completely smothered in man-made electromagnetic radiation.

The pulse of the earth 7.83 Hz. The human alpha waves of the human brain is 7.83 Hz. That's not a coincidence, but the power grid, crisscrossing the country, radio, TV, satellite, pagers, cell phone,wireless networking, etc., surrounding us have almost totally permeated our environment with an invisible electromagnetic attack practically impossible to escape.
In the mid eighties fewer than 3% of all people in most of the countries were using cell phones, but if you fast forward to today almost 100% of the people are using cell phones so the question we should all be asking, "is there anyone protecting the public from the invisible ocean of microwave radiation generated from the trillion dollar telecommunications industry?" The answer is a resounding NO!

Brushing aside smart meters, Wifi, and other forms of electromagnetic radiation, the most popular gadget of our age--the cell phone-- has now been shown to damage DNA, break down the brain's defenses, reduce sperm count, increase memory loss, and dramatically increase the risk of Alzheimer's disease and cancer. The growing brains of children make them especially vulnerable, yet half of the world's four billion cell phone users are under twenty.

So, with the constant smog of man-made frequencies surrounding our daily lives and no testing as to its safety, is it any wonder people's bodies have started to react?"

Measuring Schumann resonance in or around a city has become impossible. Electromagnetic pollution from cell phones has forced us to make our measurements at sea. – Dr. Wolfgang Ludwig, physicist


Disconnect: The Truth About Cell Phone Radiation, What the Industry Has Done to Hide It, and How to Protect Your Family by Devra Davis
Davis, the founding director of the toxicology and environmental studies board at the U.S. National Academy of Sciences, takes listeners through the dark side of this trillion-dollar industry. Health experts have long been frozen out of policy-making decisions about cell phones; federal regulatory standards are set by the cell phone industry itself. Cell phone manufacturers have borrowed the playbook of the tobacco industry. One secret memo reveals their war plan against reports of cell phone dangers. Among a host of fascinating characters, Davis introduces Om P. Gandhi, a world expert on how cell phone radiation penetrates the human brain. Once a consultant to major cell phone companies, Gandhi now refuses to work with them. We also meet Franz Adlkofer, who led the multi-lab study that showed once and for all that brain cell DNA is unraveled by cell phone microwave radiation-and, as Davis dramatically portrays, it nearly cost him his career. As this eye-opening call to action shows, we can make safer cell phones now. Why would we put our children at risk of a devastating epidemic of brain illness in the years to come?


Monday, August 21, 2017

Meet the Should Be Exonerated: Crosley Green

Crosley Green
Update: (August 19, 2017):

Despite a mountain of evidence that proves Crosley Green's innocence, in January 2016, due to a trivial procedural technicality (one day late), Green's petition for a new trial was denied. So, in other words, 59-year old Crosley Green could stay in prison for the rest of his life even though there is very clear evidence of his innocence and very clear evidence that he should never have been convicted in the first place.
"People are alarmed to find out that courts have no problem at all saying you filed one day late… we're gonna use that as a basis to keep you in prison for the rest of your life not withstanding the fact that you can prove a clear miscarriage of justice," -- Seth Miller, runs the Innocence Project of Florida.

And then, in June 2017,the 11th Circuit Federal Court of Appeals will allow Green's attorneys to argue in person why his case should not have been dismissed. If the three-judge panel agrees, Crosley Green will finally get his case heard in federal court.

Please watch the the most recent 48 Hours episode which also features three similar cases of wrongful convictions from Brevard County Florida in the 1980s that were subsequently overturned.

Please sign this petition for clemency (or new trial) on


Something new and different, a Florida man convicted for murder and sentenced to death simply because he was black. As attorney, Keith Harrison said, "an example of race being a substitute for evidence,race substituted for evidence.

For more than 16 years, 48 Hours has investigated the case of the 1989 murder of 22-year old Charles "Chip" Flynn because they believed it involved prosecutorial misconduct, which resulted in the conviction of Crosley Green (left) who was later sentenced to death, an absolute travesty of justice not uncommon as I have documented repeatedly.

It all began on April 4, 1989 when Flynn's former girlfriend, Kimberly Hallock called 911 saying she thought her boyfriend had been shot by a a black man with a gun who had hijacked and drove them to a remote Florida citrus grove. Keep in mind, this black guy would've had to steer and shift gears all while he was holding the gun on them. Oh, and after her ex-boyfriend, with his hands tied behind his back, grabbed a gun and shot the assailant, she alone managed to get back into the truck and escape.

Despite a story that kept changing, littered with troubling inconsistencies:
  • Crosley didn't match the original description of the assailant;
  • ex-girlfriend waiting almost an hour to call for help;
  • a truck that was hard to handle because it had a custom gear shift;
  • shoe prints that did not match...that tracked in different direction than testimony indicated;
  • no gun powder residue on Flynn's hands; no shell casings from Flynn's testified to gunshots;
  • no bare footprints or knee prints of either Flynn and Hallock at scene
  • witnesses who later said they were coerced into testifying recanted their testimony
  • a police dog, despite not having an item of Green's to scent upon, somehow connected him to the crime scene
  • no fingerprints or any physical evidence that linked Green to the crime
  • ten alibi witnesses who place Green miles away from the murder,
Crosley Green was arrested and charged with kidnapping, robbery and murder. It took the all-white jury just three hours to convict Crosley Green; the judge sentenced him death.

Crosley Green, top row center, target with a bull's eye...the black spot you focus on.
That's a target with a bull's-eye for Crosley Green. ...His picture is smaller and darker than the other pictures," Harrison said of the photo lineup. "Anybody involved in police investigation and prosecution knows this. ...the position that your eyes are normally drawn to are right in the middle."

"It's a black spot," Green said of the photo. "That's what you focus on, that black spot." [...]
When I went to homicide school ... they told us that this spot is the most likely that someone will pick a picture from," Mark Rixey said of the photo lineup.

"And where exactly is Crosley Green in that--"

"That's Crosley Green right in that spot," Green said, pointing to the second of three images in the top row.

"Anything that strikes you about this lineup?" Moriarty asked Christopher White.

"You can't see the guy in the top middle very well at all," he replied. "Crosley Green's photo is the darkest."

"If you don't specifically know who you're looking for, then that's the spot you will pick nine times out of 10," said Rixey.
And why was Kim Hallock eliminated as a suspect when it's normal procedure to investigate the last people to see victim alive...everyone closest to the scene? No one knows.
That's homicide 101, anybody who is present at the scene of a shooting ... gets their hands tested for gunshot residue," Rixey explained. "That should have been the very first thing that was done. ...That was never done."
Moreover, the Brevard County State's Attorney's Office had a history of pressuring, coercing witnesses into lying. In the 1980s, Brevard County put away three men whose convictions have since been overturned.
They coerced witnesses ... to lie and it's really as though you see -- a deliberate pattern of the state creating evidence to achieve a result that they wanted to achieve and that's what they got," said Jeane Thomas.
In 2009, Green received a reduced sentence (life in prison)  due to an error in sentencing. In total, Crosley Green has spent almost 26 years incarcerated for a crime he did not commit.  Three witnesses recanted their testimony. 
Every witness recanted their story," Moura explained. "And every one of them had reason to be afraid of the police. ...They were squeezed. ...And they were squeezed hard."
As it stands now, undeterred by exculpatory evidence withheld by the prosecution, the recantations of four of the prosecution's star witnesses, not to mention, more inconsistencies than a government's official story, the Florida Attorney General's Office is fighting to uphold Crosley Green's conviction. It says Green failed to meet a filing deadline for his appeal.


Investigators say condemned man not guilty

Former Florida Death Row Inmate Crosley Green Asks Orlando Federal Court To Overturn His Conviction: Crowell & Moring Files Habeas Corpus


Sunday, April 23, 2017

World War III or Perpetual War?

A few years ago, I spoke to a former database administrator for a defense contractor to the CIA from the 1970s to the late 1990s who had to prepare reports for the Joint Chiefs every morning. He said, over the course of that time, there wasn't a day that went by that we weren't at war with someone, somewhere in the world. And this was before 9/11.

Take the philosophical thought experiment, "If a tree falls in a forest and no one is around to hear it, does it make a sound?" and replace it with, "If one nation makes war upon another, and no one reports on it, did that war really happen?" The modern science of mass manipulation through mainstream mesmerizing media and the distortions, lies and fabrications, incessantly pouring out of this media, has ensured that it hasn't, or if it has, it's not even close to what really occurred.  

WWIII is a loaded term. It assumes that these mass murders that humanity calls war are isolated events with distinct beginnings and ends. This simplification obscures the multi-generational chain reactions that lead up to that moment when swords are drawn or missiles fly.
Of course, there is another reason that the public is rarely conscious of these chain reactions. The ruling class has learned long ago that the best way to take a nation to war is to trick them into it."

Remember, proxy wars are still wars.


The Elite, the ‘Great Game’ and World War III
The control of the US, and of global politics, by the wealthiest families of the planet is exercised in a powerful, profound and clandestine manner. This control began in Europe and has a continuity that can be traced back to the time when the bankers discovered it was more profitable to give loans to governments than to needy individuals.

These banking families and their subservient beneficiaries have come to own most major businesses over the two centuries during which they have secretly and increasingly organized themselves as controllers of governments worldwide and as arbiters of war and peace.


Friday, April 14, 2017

Natural Cancer Bullets A - Z

There are many silver bullets that you can use to fight cancer. I will post some of these bullets (alphabetically) along with sources and brief explanations over the next several months.

Acai Berries

Source: Fruits from the Açaí Palm.

Brazilian berry destroys cancer cells in lab, UF study shows
Published today in the Journal of Agricultural and Food Chemistry, the study showed extracts from acai (ah-SAH’-ee) berries triggered a self-destruct response in up to 86 percent of leukemia cells tested, said Stephen Talcott, an assistant professor with UF’s Institute of Food and Agricultural Sciences. “Acai berries are already considered one of the richest fruit sources of antioxidants,” Talcott said. “This study was an important step toward learning what people may gain from using beverages, dietary supplements or other products made with the berries.”


Sources: Aloe Vera Plant, Aloe Vera Juice

Aloe-Emodin Induces Apoptosis in T24 Human Bladder Cancer Cells

AE inhibited cell viability, and induced G2/M arrest and apoptosis in T24 cells. AE increased the levels of Wee1 and cdc25c, and may have led to inhibition of the levels of cyclin-dependent kinase 1 and cyclin B1, which cause G2/M arrest. AE induced p53 expression and was accompanied by the induction of p21 and caspase-3 activation, which was associated with apoptosis. In addition, AE was associated with a marked increase in Fas/APO1 receptor and Bax expression but it inhibited Bcl-2 expression.

Anticancer effect of aloe-emodin on cervical cancer cells involves G2/M arrest and induction of differentiation.
Aloe-emodin inhibited the growth of HeLa cells in a dose-dependent manner at concentrations ranging between 2.5 and 40 micromol/L. The flow cytometric analysis showed that HeLa cells were arrested at the G2/M phase. This effect was associated with the decrease in cyclin A and CDK2, and the increase in cyclin B1 and CDK1. More importantly, the ALP activity was found to be increased by aloe-emodin treatment, and accompanied by the inhibition of PCNA expression. In addition, aloe-emodin suppressed the expression of PKCalpha and c-myc.

Aloe-emodin suppresses prostate cancer by targeting the mTOR complex 2
Our results herein are noteworthy in that prostate cancer cell growth is suppressed by aloe-emodin in vivo. Moreover, the low in vivo toxicity and tumor inhibitory activity of aloe-emodin observed in nude mice suggest that aloe-emodin is an effective chemopreventive agent against prostate cancer (Figure 6A and B). In conclusion, we showed here that mTORC2 is closely associated with prostate cancer cell growth. We also provided clear evidence showing that aloe-emodin effectively suppresses anchorage-independent cell growth and in vivo tumor growth in PC3 cancer cell-bearing nude mice by inhibiting Akt activity. Collectively, these findings support the anticancer efficacy of aloe-emodin through its targeting of mTORC2 for the inhibition of prostate cancer progression.
Protein kinase C involvement in aloe-emodin- and emodin-induced apoptosis in lung carcinoma cell
This study demonstrated aloe-emodin- and emodin-induced apoptosis in lung carcinoma cell lines CH27 (human lung squamous carcinoma cell) and H460 (human lung non-small cell carcinoma cell). Aloe-emodin- and emodin-induced apoptosis was characterized by nuclear morphological changes and DNA fragmentation.

The antiproliferative activity of aloe-emodin is through p53-dependent and p21-dependent apoptotic pathway in human hepatoma cell lines

The aim of this study is to investigate the anticancer effect of aloe-emodin in two human liver cancer cell lines, Hep G2 and Hep 3B. We observed that aloe-emodin inhibited cell proliferation and induced apoptosis in both examined cell lines, but with different the antiproliferative mechanisms.
Aloe-emodin Is a New Type of Anticancer Agent with Selective Activity against Neuroectodermal Tumors
Here we report that aloe-emodin (AE), a hydroxyanthraquinone present in Aloe vera leaves, has a specific in vitro and in vivo antineuroectodermal tumor activity. The growth of human neuroectodermal tumors is inhibited in mice with severe combined immunodeficiency without any appreciable toxic effects on the animals. The compound does not inhibit the proliferation of normal fibroblasts nor that of hemopoietic progenitor cells. The cytotoxicity mechanism consists of the induction of apoptosis, whereas the selectivity against neuroectodermal tumor cells is founded on a specific energy-dependent pathway of drug incorporation. Taking into account its unique cytotoxicity profile and mode of action, AE might represent a conceptually new lead antitumor drug.
Aloe-emodin induced in vitro G2/M arrest of cell cycle in human promyelocytic leukemia HL-60 cells.
Aloe-emodin inhibited cell proliferation and induced G2/M arrest and apoptosis in HL-60 cells. Investigation of the levels of cyclins B1, E and A by immunoblot analysis showed that cyclin E level was unaffected, whereas cyclin B1 and A levels increased with aloe-emodin in HL-60 cells. Investigation of the levels of cyclin-dependent kinases, Cdk1 and 2, showed increased levels of Cdk1 but the levels of Cdk2 were not effected with aloe-emodin in HL-60 cells. The levels of p27 were increased after HL-60 cells were cotreated with various concentrations of aloe-emodin.
Aloe-emodin-induced apoptosis in human gastric carcinoma cells
The purpose of this study was to investigate the anticancer effect of aloe-emodin, an anthraquinone compound present in the leaves of Aloe vera, on two distinct human gastric carcinoma cell lines, AGS and NCI-N87. We demonstrate that aloe-emodin induced cell death in a dose- and time-dependent manner. Noteworthy is that the AGS cells were generally more sensitive than the NCI-N87 cells. Aloe-emodin caused the release of apoptosis-inducing factor and cytochrome c from mitochondria, followed by the activation of caspase-3, leading to nuclear shrinkage and apoptosis.

Aloe-emodin induces in vitro G2/M arrest and alkaline phosphatase activation in human oral cancer KB cells
Aloe-emodin is a natural anthraquinone compound from the root and rhizome of Rheum palmatum. In this study, KB cells were treated with 2.5, 5, 10, 20, and 40 microM aloe-emodin for 1 to 5 days. The results showed that aloe-emodin inhibited cancer cells in a dose-dependent manner. Treatment with aloe-emodin at 10 to 40 microM resulted in cell cycle arrest at G2/M phase. The alkaline phosphatase (ALP) activity in KB cells increased upon treatment with aloe-emodin when compared to controls. This is one of the first studies to focus on the expression of ALP in human oral carcinomas cells treated with aloe-emodin. These results indicate that aloe-emodin has anti-cancer effect on oral cancer, which may lead to its use in chemotherapy and chemo preventment of oral cancer.


Source: Cannabis

Anandamide May Fight Aggressive Skin Cancer
According to the study’s results, anandamide may be involved in a complex mechanism that includes the CB1 receptor, and possibly GPR55 – a cannabinoid receptor in its own right. Although not much is known about GPR55, it is sometimes referred to as the CB3 receptor, because it responds to both endogenous and plant-derived cannabinoids.
The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation
Anandamide was the first brain metabolite shown to act as a ligand of “central” CB1 cannabinoid receptors. Here we report that the endogenous cannabinoid potently and selectively inhibits the proliferation of human breast cancer cells in vitro. Anandamide dose-dependently inhibited the proliferation of MCF-7 and EFM-19 cells with IC50 values between 0.5 and 1.5 μM and 83–92% maximal inhibition at 5–10 μM. The proliferation of several other nonmammary tumoral cell lines was not affected by 10 μM anandamide. The anti-proliferative effect of anandamide was not due to toxicity or to apoptosis of cells but was accompanied by a reduction of cells in the S phase of the cell cycle. ...These data suggest that anandamide blocks human breast cancer cell proliferation through CB1-like receptor-mediated inhibition of endogenous prolactin action at the level of prolactin receptor.

Anti-proliferative and apoptotic effects of anandamide in human prostatic cancer cell lines
ANA induced a decrease of EGFR levels on LNCaP, DU145, and PC3 prostatic cancer cells by acting through cannabinoid CB1 receptor subtype and this leaded to an inhibition of the EGF-stimulated growth of these cells. Moreover, the G1 arrest of metastatic DU145 and PC3 growth was accompanied by a massive cell death by apoptosis and/or necrosis while LNCaP cells were less sensitive to cytotoxic effects of ANA. The apoptotic/necrotic responses induced by ANA on these prostatic cancer cells were also potentiated by the acidic ceramidase inhibitor, N-oleoylethanolamine and partially inhibited by the specific ceramide synthetase inhibitor, fumonisin B1 indicating that these cytotoxic actions of ANA might be induced via the cellular ceramide production. The potent anti-proliferative and cytotoxic effects of ANA on metastatic prostatic cancer cells might provide basis for the design of new therapeutic agents for effective treatment of recurrent and invasive prostatic cancers.
Cannabinoids, Endocannabinoids and Cancer
Cannabinoids exert a number of interesting effects that are dependent on the cell line or tumor type. Synthetic cannabinoids and the endocannabinoid system are implicated in inhibiting cancer cell proliferation and angiogenesis, reducing tumor growth and metastases, and inducing apoptosis.
Anandamide is an endogenous inhibitor for the migration of tumor cells and T lymphocytes
Cell migration is of paramount importance in physiological processes such as immune surveillance, but also in the pathological processes of tumor cell migration and metastasis development. The factors that regulate this tumor cell migration, most prominently neurotransmitters, have thus been the focus of intense investigation. While the majority of neurotransmitters have a stimulatory effect on cell migration, we herein report the inhibitory effect of the endogenous substance anandamide on both tumor cell and lymphocyte migration. ...Using the specific agonist docosatetraenoylethanolamide (DEA), we have observed that the norepinephrine-induced migration of colon carcinoma cells is inhibited by the CB1-R. The SDF-1–induced migration of CD8+ T lymphocytes was, however, inhibited via the CB2-R, as shown by using the specific agonist JWH 133. Therefore, specific inhibition of tumor cell migration via CB1-R engagement might be a selective tool to prevent metastasis formation without depreciatory effects on the immune system of cancer patients.
The endogenous cannabinoid, anandamide, induces cell death in colorectal carcinoma cells
These findings suggest anandamide may be a useful chemopreventive/therapeutic agent for colorectal cancer as it targets cells that are high expressors of COX-2, and may also be used in the eradication of tumour cells that have become resistant to apoptosis.


Sources: Parsley, Celery, Coriander, Licorice, Majoram, Oregano, Rosemary, Tarragon, Citrus, Tea and Wheat.

Breast cancer effectively treated with chemical found in celery, parsley, mouse study suggests
Apigenin, a natural substance found in grocery store produce aisles, shows promise as a non-toxic treatment for an aggressive form of human breast cancer, following a new study. Researchers found apigenin shrank a type of breast cancer tumor that is stimulated by progestin, a synthetic hormone given to women to ease symptoms related to menopause.
Apigenin induces breast cancer cells
Apigenin is a low toxicity and non-mutagenic phytopolyphenol and protein kinase inhibitor. It exhibits anti-proliferating effects on human breast cancer cells. Here we examined several human breast cancer cell lines having different levels of HER2/neu expression and found that apigenin exhibited potent growth-inhibitory activity in HER2/neu-over expressing breast cancer cells but was much less effective for those cells expressing basal levels of HER2/neu
Selective growth-inhibitory, cell-cycle deregulatory and apoptotic response of apigenin in normal versus human prostate carcinoma cells
The growth-inhibitory and apoptotic potential of apigenin was also observed in a variety of prostate carcinoma cells representing different stage and androgen responsiveness. Apigenin may be developed as a promising chemopreventive and/or chemotherapeutic agent against prostate cancer.
Signal pathways involved in apigenin inhibition of growth and induction of apoptosis of human anaplastic thyroid cancer cells
Recently we demonstrated that several flavonoids can inhibit the proliferation of certain human thyroid cancer cell lines. Among the flavonoids tested, apigenin and luteolin are the most effective inhibitors of these tumor cell lines. In the present study, we investigated the signal transduction mechanism associated with the growth inhibitory effect of apigenin, using a human anaplastic thyroid carcinoma cell line, ARO.

5,6-Dichloro-ribifuranosylbenzimidazole- and apigenin-induced sensitization of colon cancer cells to TNF--mediated apoptosis

Here we report that inhibition of CK2 in HCT-116 and HT-29 cells with the use of two specific CK2 inhibitors, 5,6-dichloro-ribifuranosylbenzimidazole (DRB) and apigenin, effected a synergistic reduction in cell survival when used in conjunction with TNF-. Furthermore, there was a demonstrable synergistic reduction in colony formation in soft agar with the use of the same combinations.

Induction of apoptosis by apigenin in leukaemia HL-60 cells
The potency of these flavonoids on these features of apoptosis were in the order of: apigenin>quercetin>myricetin>kaempferol in HL-60 cells treated with 60μM flavonoids. These results suggest that flavonoid-induced apoptosis is stimulated by the release of cytochrome c to the cytosol, by procaspase-9 processing, and through a caspase-3-dependent mechanism. The induction of apoptosis by flavonoids may be attributed to their cancer chemopreventive activity. Furthermore, the potency of flavonoids for inducing apoptosis may be dependent on the numbers of hydroxyl groups in the 2-phenyl group and on the absence of the 3-hydroxyl group. This provides new information on the structure–activity relationship of flavonoids.
Arachidonyl Ethanolamide

Source: Cannabis

Arachidonyl ethanolamide induces apoptosis of uterine cervix cancer cells via aberrantly expressed vanilloid receptor-1
The major finding was that AEA induced apoptosis of CxCa cell lines via aberrantly expressed vanilloid receptor-1, whereas AEA binding to the classical CB1 and CB2 cannabinoid receptors mediated a protective effect. Furthermore, unexpectedly, a strong expression of the three forms of AEA receptors was observed in ex vivo CxCa biopsies.

Sources: wormwood plant

Artemisinin Induces Apoptosis in Human Cancer Cells
Artemisinin is a chemical compound extracted from the wormwood plant, Artemisia annua L. It has been shown to selectively kill cancer cells in vitro and retard the growth of implanted fibrosarcoma tumors in rats. In the present research, we investigated its mechanism of cytotoxicity to cancer cells. ...This rapid induction of apoptosis in cancer cells after treatment with DHA indicates that artemisinin and its analogs may be inexpensive and effective cancer agents.
Effects of artemisinin and its derivatives on growth inhibition and apoptosis of oral cancer cells
Artemisinin is of special biological interest because of its outstanding antimalarial activity. Recently, it was reported that artemisinin has antitumor activity. Its derivatives, artesunate, arteether, and artemeter, also have antitumor activity against melanoma, breast, ovarian, prostate, CNS, and renal cancer cell lines. Recently, monomer, dimer, and trimer derivatives were synthesized from deoxoartemisinin, and the dimers and the trimers were found to have much more potent antitumor activity than the monomers. ...The deoxoartemisinin trimer was found to have greater antitumor effect on tumor cells than other commonly used chemotherapeutic drugs, such as 5-FU, cisplatin, and paclitaxel. Furthermore, the ability of artemisinin and its derivatives to induce apoptosis highlights their potential as chemotherapeutic agents, for many anticancer drugs achieve their antitumor effects by inducing apoptosis in tumor cells.
Transferrin overcomes drug resistance to artemisinin in human small-cell lung carcinoma cells
Multiple drug resistance is a significant problem in small-cell lung cancer (SCLC). Artemisinin (ART) is a natural product used to treat drug-resistant malaria. The drug is effective because the Fe2+ present in infected erythrocytes acts non-enzymatically to convert ART to toxic products. We tested the effects of ART on drug-sensitive (H69) and multi-drug-resistant (H69VP) SCLC cells, pretreated with transferrin (TF) to increase the intracellular Fe2+ level. ...These data indicate the potential use of ART and TF in drug-resistant SCLC.
Dihydroartemisinin induces apoptosis and sensitizes human ovarian cancer cells to carboplatin therapy
The present study was designed to determine the effects of artemisinin (ARS) and its derivatives on human ovarian cancer cells, to evaluate their potential as novel chemotherapeutic agents used alone or in combination with a conventional cancer chemotherapeutic agent, and to investigate their underlying mechanisms of action. Human ovarian cancer cells (A2780 and OVCAR-3), and immortalized non-tumourigenic human ovarian surface epithelial cells (IOSE144), were exposed to four ARS compounds for cytotoxicity testing. The in vitro and in vivo antitumour effects and possible underlying mechanisms of action of dihydroartemisinin (DHA), the most effective compound, were further determined in ovarian cancer cells. ...These effects were also observed in in vivo ovarian A2780 and OVCAR-3 xenograft tumour models. In conclusion, ARS derivatives, particularly DHA, exhibit significant anticancer activity against ovarian cancer cells in vitro and in vivo, with minimal toxicity to non-tumourigenic human OSE cells, indicating that they may be promising therapeutic agents for ovarian cancer, either used alone or in combination with conventional chemotherapy.


Natural Cancer Bullets A - Z

Natural cancer bullets A - Z continued:


Source: Ginger Root

Antitumor effect of β-elemene in non-small-cell lung cancer cells is mediated via induction of cell cycle arrest and apoptotic cell death
Beta-elemene is a novel anticancer drug, which was extracted from the ginger plant. However, the mechanism of action of beta-elemene in non-small-cell lung cancer (NSCLC) remains unknown. Here we show that beta-elemene had differential inhibitory effects on cell growth between NSCLC cell lines and lung fibroblast and bronchial epithelial cell lines. ...These data indicate that the effect of beta-elemene on lung cancer cell death may be through a mitochondrial release of the cytochrome c-mediated apoptotic pathway.

Elemene displays anti-cancer ability on laryngeal cancer cells in vitro and in vivo
Elemene inhibited the growth of HEp-2 cells in vitro in a dose- and time-dependent manner with an IC50 of 346.5 μM (24 h incubation). Increased apoptosis was observed in elemene-administered cells. Elemene is suspected to enhance caspase-3 activity, and thus inhibit protein expression of eIFs (4E, 4G), bFGF, and VEGF. In vivo, the growth of HEp-2 cell-transplanted tumors in nude mice was inhibited by intraperitoneal injection of elemene. Compared with control groups, elemene significantly inhibited the protein expression of eIFs (4E and 4G), bFGF, and VEGF and decreased the MVD. Conclusions: Elemene inhibits the growth of HEp-2 cells in vitro and in vivo. These data provide useful information for further clinical study on the treatment of LSCC by elemene.

Antiproliferative effect of β-elemene in chemoresistant ovarian carcinoma cells

In this study, we show that beta-elemene inhibited the proliferation of cisplatin-resistant human ovarian cancer cells and their parental cells, but had only a marginal effect in human ovary cells, indicating differential inhibitory effects on cell growth between ovarian cancer cells and normal ovary cells.
Effect of Local Arterial Infusion of β_elemene on Breast Cancer Tissue Inhibition and Cell Apoptosis and Proliferation
The effect of local arterial infusion of β_elemene on breast cancer tissue inhibition and cell apoptosis and proliferation was observed.
N-(beta-Elemene-13-yl)tryptophan methyl ester induces apoptosis in human leukemia cells
Beta-elemene is an active component of herb medicine Curcuma Wenyujin and N-(beta-elemene-13-yl)tryptophan methyl ester (ETME) was synthesized for increasing its antitumor activity. ETME induced apoptosis in human leukemia HL-60 and NB4 cells at concentrations less than 40 microM. The apoptosis induction ability of ETME was associated with the production of hydrogen peroxide (H(2)O(2)), the decrease of mitochondrial membrane potential, and the activation of caspase-3 that was blocked by catalase. ETME in combination with arsenic trioxide (As(2)O(3)), an agent used to treat acute promyelocytic leukemia, synergistically induced apoptosis in both cell lines by enhanced production of H(2)O(2). These data suggest that ETME induces apoptosis and synergizes with As(2)O(3) in leukemia cells through a H(2)O(2)-dependent pathway.


Foods: Mushrooms, Grains & Yeast.
Mushrooms: Shiitake (Lentinula edodes), Reishi (Ganoderma lucidum & Ganoderma tsugae), Maitake (Grifola frondosa), Oyster Mushroom (Pleurotus ostreatus), Cauliflower Mushroom (Sparassis). Grains: Oats, Barley.

Fights cancer and eases the effects of radiation.

NOTE: Literally all of the listed mushrooms above have other important anti-cancer effects not necessarily specified here

ß-Glucan...Uses Antibodies to Target Tumors for Cytotoxic Recognition by Leukocyte Complement Receptor Type 3

ß-Glucans were identified 36 years ago as a biologic response modifier that stimulated tumor rejection. In vitro studies have shown that ß-glucans bind to a lectin domain within complement receptor type 3 (CR3; known also as Mac-1, CD11b/CD18, or Mß2-integrin, that functions as an adhesion molecule and a receptor for factor I-cleaved C3b, i.e., iC3b) resulting in the priming of this iC3b receptor for cytotoxicity of iC3b-opsonized target cells. This investigation explored mechanisms of tumor therapy with soluble ß-glucan in mice. Normal mouse sera were shown to contain low levels of Abs reactive with syngeneic or allogeneic tumor lines that activated complement, depositing C3 onto tumors. Implanted tumors became coated with IgM, IgG, and C3, and the absent C3 deposition on tumors in SCID mice was reconstituted with IgM or IgG isolated from normal sera. Therapy of mice with glucan- or mannan-rich soluble polysaccharides exhibiting high affinity for CR3 caused a 57–90% reduction in tumor weight. In young mice with lower levels of tumor-reactive Abs, the effectiveness of ß-glucan was enhanced by administration of a tumor-specific mAb, and in SCID mice, an absent response to ß-glucan was reconstituted with normal IgM or IgG. The requirement for C3 on tumors and CR3 on leukocytes was highlighted by therapy failures in C3- or CR3-deficient mice. Thus, the tumoricidal function of CR3-binding polysaccharides such as ß-glucan in vivo is defined by natural and elicited Abs that direct iC3b deposition onto neoplastic cells, making them targets for circulating leukocytes bearing polysaccharide-primed CR3. Therapy fails when tumors lack iC3b, but can be restored by tumor-specific Abs that deposit iC3b onto the tumors.

Yeast ß-Glucan Amplifies Phagocyte Killing of iC3b-Opsonized Tumor Cells

Anti-tumor mAbs hold promise for cancer therapy, but are relatively inefficient. Therefore, there is a need for agents that might amplify the effectiveness of these mAbs. One such agent is -glucan, a polysaccharide produced by fungi, yeast, and grains, but not mammalian cells. -Glucans are bound by C receptor 3 (CR3) and, in concert with target-associated complement fragment iC3b, elicit phagocytosis and killing of yeast. -Glucans may also promote killing of iC3b-opsonized tumor cells engendered by administration of anti-tumor mAbs. In this study, we report that tumor-bearing mice treated with a combination of -glucan and an anti-tumor mAb show almost complete cessation of tumor growth.

Chemosensitization of Carmustine with Maitake β-Glucan on Androgen-Independent Prostatic Cancer Cells
This study demonstrates a sensitized cytotoxic effect of BCNU with β-glucan in PC-3 cells, which was associated with a drastic (~80%) inactivation of Gly-I. Therefore, the BCNU/β-glucan combination may help to improve current treatment efficacy by targeting Gly-I, which appears to be critically involved in prostate cancer viability.

Beta glucan induces proliferation and activation of monocytes in peripheral blood of patients with advanced breast cancer

Glucans are glucose polymers that constitute a structural part of fungal cell wall. They can stimulate the innate immunity by activation of monocytes/macrophages. In human studies it has been shown that beta glucan has an immunomodulatory effect and can increase the efficacy of the biological therapies in cancer patients. In this prospective clinical trial we assessed in vivo effects of short term oral beta glucan administration on peripheral blood monocytes and their expression of activation markers in patients with advanced breast cancer. ...Oral beta glucan administration seems to stimulate proliferation and activation of peripheral blood monocytes in vivo in patients with advanced breast cancer.


Source: Lithospermum (herbs).

ß-Hydroxyisovalerylshikonin Inhibits the Cell Growth of Various Cancer Cell Lines and Induces Apoptosis in Leukemia HL–60 Cells
ß-Hydroxyisovalerylshikonin (ß-HIVS), which was isolated from the plant, Lithosper-mium radix, inhibited the growth of various lines of cancer cells derived from human solid, tumors at low concentrations between 10-8 and 10-6 M. When HL-60 cells were treated with 10-6 M ß-HIVS for 3 h, characteristic features of apoptosis, such as DNA fragmentation, nuclear fragmentation, and activation of caspase-3–like activity, were observed.

β-Hydroxyisovalerylshikonin and Cisplatin Act Synergistically to Inhibit Growth and to Induce Apoptosis of Human Lung Cancer DMS114 Cells

beta-Hydroxyisovalerylshikonin (beta-HIVS) and cisplatin (CDDP) had a synergistic growth-inhibitory effect on cultured human small-cell lung carcinoma DMS114 cells, as well as on human leukemia U937 and epidermoid carcinoma A431 cells, while beta-HIVS and CDDP alone at the same respective concentrations had little effect.


Source: The bark of Red Alder trees & White Birch trees, and the mushroom Chaga that grows on White Birch.

Anti-Cancer Effect of Betulin on a Human Lung Cancer Cell Line
Betulin is a representative compound of Betula platyphylla, a tree species belonging to the Betulaceae family. In this investigation, we revealed that betulin showed anticancer activity on human lung cancer A549 cells by inducing apoptosis and changes in protein expression profiles were observed.

Betulinic Acid Inhibits Prostate Cancer Growth

Betulinic acid is a pentacyclic triterpene natural product initially identified as a melanoma-specific cytotoxic agent that exhibits low toxicity in animal models. Subsequent studies show that betulinic acid induces apoptosis and antiangiogenic responses in tumors derived from multiple tissues;
Betulinic acid induces apoptosis in human neuroblastoma cell lines
Neuroblastoma has long been recognized to show spontaneous regression during fetal development and in the majority of stage 4s infants
Apoptotic activity of betulinic acid derivatives on murine melanoma B16 cell line
Exposure of B16 cells to betulinic acid, 23-hydroxybetulinic acid and 3-oxo-23-hydroxybetulinic acid caused a rapid increase in reactive oxidative species production and a concomitant dissipation of mitochondrial membrane potential in a dose- and time-dependent manner, which resulted in cell apoptosis, as demonstrated by fluorescence microscopy, gel electrophoresis and flow-cytometric analysis. Cell cycle analysis further demonstrated that both 3-oxo-23-hydroxybetulinic acid and 23-hydroxybetulinic acid dramatically increased DNA fragmentation at the expense of G1 cells at doses as low as 12.5 and 25 microg/ml, respectively, thereby showing their potent apoptotic properties. Our results showed that hydroxylation at the C3 position of betulinic acid is likely to enhance the apoptotic activity of betulinic acid derivatives (23-hydroxybetulinic acid and 3-oxo-23-hydroxybetulinic acid) on murine melanoma B16 cells.

Betulinic acid: A new cytotoxic compound against malignant head and neck cancer cells

In two HNSCC cell lines betulinic acid induced apoptosis, which was characterized by a dose-dependent reduction in cell numbers, emergence of apoptotic cells, and an increase in caspase activity. Western blot analysis of the expression of various Bcl-2 family members in betulinic acid–treated cells showed, surprisingly, a suppression of the expression of the proapoptotic protein Bax but no changes in Mcl-1 or Bcl-2 expression.


Evidence for anti-cancer properties of blueberries: a mini-review.
Blueberries are amongst the most commonly consumed berries in the United States. Berries in general are rich in phenolic compounds, which are known for their high antioxidant capacity. Specifically, evidence from in vitro, in vivo and a few clinical studies suggest that blueberries and their active constituents show promise as effective anti-cancer agents, both in the form of functional foods and as nutritional supplements. Some of the mechanisms by which blueberries have been shown to prevent carcinogenesis include inhibition of the production of pro-inflammatory molecules, oxidative stress and products of oxidative stress such as DNA damage, inhibition of cancer cell proliferation and increased apoptosis. This review will focus on the preclinical and clinical evidence that supports blueberries as an anti-cancer fruit, as well as expressing the need for more preclinical studies and the conduction of clinical studies with respect to the cancer preventive ability of blueberries.

Effect of Anthocyanin Fractions from Selected Cultivars of Georgia-Grown Blueberries on Apoptosis and Phase II Enzymes

The response correlated positively with dose. The QR activity was lower in all cells treated with an anthocyanin fraction from Tifblue, Powderblue, Brightblue, and Brightwell cultivars than in control cells (P < 0.05). The activity decreased gradually when treated with increased concentrations of anthocyanin fractions (50−150 μg/mL) in the Tifblue and Powderblue cultivars. The GST activity was lower (P < 0.05) in cells treated with anthocyanin fractions from all of the cultivars and at all concentrations. These results indicated that apoptosis was confirmed in HT-29 cells when treated with anthocyanins from blueberry cultivars at 50−150 μg/mL concentrations, but these same concentrations decrease QR and GST activities rather than induce them.
Availability of blueberry phenolics for microbial metabolism in the colon and the potential inflammatory implications
Blueberries are a rich source of phenylpropanoid-derived phytochemicals, widely studied for their potential health benefits. Of particular interest for colonic health are the lower molecular weight phenolic acids and their derivatives, as these are the predominant phenolic compounds detected in the colon. Blueberries contained a wide variety of phenolic acids, the majority of which (3371.14 ± 422.30 mg/kg compared to 205.06 ± 45.34 mg/kg for the free phenolic acids) were attached to other plant cell-wall components and therefore, likely to become available in the colon. Cytokine-induced stimulation of the inflammatory pathways in colon cells was four-fold up-regulated in the presence of the free phenolic acid fraction. Incubation of the bound phenolic acids with human faecal slurries resulted in qualitative and quantitative differences in the phenolic compounds recovered. The metabolites obtained by incubation with faecal slurries from one volunteer significantly decreased (1.67 ± 0.69 ng/cm3) prostanoid production, whereas an increase (10.78 ± 5.54 ng/cm3) was obtained with faecal slurries from another volunteer. These results suggest that any potential protective effect of blueberry phenolics as anti-inflammatory agents in the colon is a likely result of microbial metabolism. Studies addressing a wide-range of well-characterised human volunteers will be required before such health claims can be fully established.


Relatives: Romanesco, Broccoflower, Cauliflower, Kale, Raab, Brussel Sprouts, Cabbage, Collards and Kohl Rabi.

Natural Compound in Broccoli Slows Breast Cancer Stem Cells
In lab studies, when breast cancer cells were exposed to sulforaphane extract from broccoli, the growth of cancer stems cells slowed down and tumors shrank. The researchers speculate about the possible use of sulforaphane extract to prevent as well as treat breast cancer, someday.
Broccoli Sprouts contain 3X the amount of Sulforaphane Glucosinolate
Johns Hopkins University researchers found that young broccoli sprouts, in particular, contained high concentrations of SGS. The scientists believe that SGS boosts the body's own antioxidant defense system, including Phase 2 detoxification enzymes, which promote long-lasting antioxidant activity in the body.

Diindolylmethane (DIM)
At the University of California at Berkeley, the Chairman of the Nutritional Sciences Department and the Director of the National Institutes of Health Cancer Research Program were studying the biological properties of Diindolylmethane (DIM), a naturally occurring compound found in Brassica vegetables (broccoli, cauliflower, cabbage, kale, brussels sprouts), when they made a remarkable discovery: DIM is a potent activator of the immune response system. They patented their discovery and ActivaMune was launched as a first-in-class nutritional supplement to enhance the immune system and support multiple organs throughout the body: breast, prostate, cardiovascular, vision, skin and colon health. ActivaMune's unique and patented formula combines multiple nutrients for maximum effectiveness: Diindolylmethane (DIM), Sulforaphane, Selenium, Lycopene, Lutein, Zeaxanthin, Calcium and Vitamins C, D3 & E.

Surprising Discovery Reveals How Broccoli Fights Cancer

Broccoli — and to an even greater degree broccoli sprouts — has gained a reputation as a potent cancer-fighter, and recent research sheds new light on the actual mechanics behind its chemoprotective abilities.

One of the compounds in broccoli known to have anti-cancer activity is sulforaphane, a naturally occurring organic sulfur.

Studies have shown sulforaphane supports normal cell function and division while causing apoptosis (programmed cell death) in colon,1 prostate,2 breast3 and tobacco-induced lung cancer4 cells, and reducing the number of cancerous liver tumors in mice.5

Three servings of broccoli per week may reduce your risk of prostate cancer by more than 60 percent.6 Now, Oregon State University (OSU) researchers believe they've discovered yet another way sulforaphane works to protect you against cancer.


Natural Cancer Bullets A - Z

Caffeic Acid

Sources: Sweetpotato Leaves, Propolis, Apples, White Grapes, White Wine, Olives, Olive Oil, Spinach, Cabbage, Turnips, Radish, Cauliflower, Bok Choy, Arugula, Kale, Asparagus, and Coffee. 

Growth Suppression of Human Cancer Cells by Polyphenolics from Sweetpotato (Ipomoea batatas L.) Leaves
Sweetpotato leaves (Ipomoea batatas L.) contain a high content of polyphenolics that consist of caffeic acid, chlorogenic acid, 3,4-di-O-caffeoylquinic acid, 3,5-di-O-caffeoylquinic acid, 4,5-di-O-caffeoylquinic acid, and 3,4,5-tri-O-caffeoylquinic acid. We investigated the suppression of the proliferation of selected human cancer cells by phenolic compounds isolated from sweetpotato leaf. ...Growth suppression of HL-60 cells by 3,4,5-tri-O-caffeoylquinic acid was determined to be the result of apoptotic death of the cells. These results indicate that 3,4,5-tri-O-caffeoylquinic acid may have potential for cancer prevention.
Caffeic acid phenethyl ester induces mitochondria-mediated apoptosis in human myeloid leukemia U937 cells
Caffeic acid phenyl ester (CAPE), a biologically active ingredient of propolis, has several interesting biological properties including antioxidant, anti-inflammatory, antiviral, immunostimulatory, anti-angiogenic, anti-invasive, anti-metastatic and carcinostatic activities. Recently, several groups have reported that CAPE is cytotoxic to tumor cells but not to normal cells. In this study, we investigated the mechanism of CAPE-induced apoptosis in human myeloid leukemia U937 cells. Treatment of U937 cells with CAPE decreased cell viability in a dose-dependent and time-dependent manner.

Caffeic Acid Phenethyl Ester Induces Apoptosis by Inhibition of NFκB and Activation of Fas in Human Breast Cancer MCF-7 Cells

Our findings demonstrate that NFκB inhibition is sufficient to induce apoptosis and that Fas activation plays a role in NFκB inhibition-induced apoptosis in MCF-7 cells.

The antioxidant caffeic acid phenethyl ester induces apoptosis associated with selective scavenging of hydrogen peroxide in human leukemic HL-60 cells

These results suggest that apoptosis induced by CAPE is associated with mitochondrial dysfunction, GSH depletion and selective scavenging of H2O2 in human leukemic HL-60 cells.
Effect of caffeic acid phenethyl ester on proliferation and apoptosis of colorectal cancer cells in vitro
After HCT116 cells were exposed to CAPE (80, 40, 20, 10, 5, and 2.5 mg/L) for 24, 48, 72, 96 h, CAPE displayed a strong growth inhibitory effect in a dose- and time-dependent manner against HCT116 cells. FCM analysis showed that the ratio of G(0)/G(1) phase cells increased, S phase ratio decreased and apoptosis rate increased after HCT116 cells were exposed to CAPE (10, 5, and 2.5 mg/L) for 24 h. CAPE treatment was associated with decreased cytoplasmic beta-catenin, nuclear beta-catenin and a concurrent increase in beta-catenin protein expression at cell-cell junctions.


Foods: Hot Peppers.

Sources: Pepper Spray (It's probably a very bad idea to try and breath this stuff). Capsaicin (what makes peppers "hot") has been proven to trigger apoptosis in multiple lines of cancer.

Capsaicin Displays Anti-Proliferative Activity against Human Small Cell Lung Cancer in Cell Culture and Nude Mice Models via the E2F Pathway
BrdU assays and PCNA ELISAs showed that capsaicin displays robust anti-proliferative activity in four human SCLC cell lines. Furthermore, capsaicin potently suppressed the growth of H69 human SCLC tumors in vivo as ascertained by CAM assays and nude mice models. The second part of our study attempted to provide insight into molecular mechanisms underlying the anti-proliferative activity of capsaicin. We found that the anti-proliferative activity of capsaicin is correlated with a decrease in the expression of E2F-responsive proliferative genes like cyclin E, thymidylate synthase, cdc25A and cdc6, both at mRNA and protein levels.

Capsaicin-induced cell death in a human gastric adenocarcinoma cell line
Capsaicin, a pungent ingredient found in red pepper, has long been used in spices, food additives, and drugs. Cell death induced by the binding of capsaicin was examined in a human gastric adenocarcinoma cell line (AGS cells).
...Recently, a series of studies have demonstrated that capsaicin inhibits mutagenicity and DNA binding of some chemical carcinogens, possibly by suppressing their metabolic activation[16-18]. With cells in culture, capsaicin-inhibited proliferation of HeLa, ovarian carcinoma, and mammary adenocarcinoma by decreasing NADH oxidase activity[19]. Capsaicin can also alter the expression of tumor forming-related genes by mediating the overexpression of p53 and/or c-myc genes in a Korean stomach cancer cell line[20]. Capsaicin was found to induce apoptosis in T cells by increasing the reactive oxygen species and by a subsequent mitochondrial ransmembrane potential[21]. In this report, we examined the underlying mechanism by which capsaicin induces apoptotic cell death in a human gastric adenocarcinoma cell line (AGS).
Capsaicin-induced apoptosis and reduced release of reactive oxygen species in MBT-2 Murine Bladder Tumor cells
Capsaicin, the major pungent ingredient in genusCapsicum, has recently been tried as an intravesical drug for overactive bladder and it has also been shown to induce apoptotic cell death in many cancer cells. In this study, we investigated the apoptosis-inducing effect and alterations in the cellular redox state of capsaicin in MBT-2 murine bladder tumor cells. Capsaicin induced apoptotic MBT-2 cell death in a time- and dose-dependent manner. The capsaicin-induced apoptosis was blocked by the pretreatment with Z-VAD-fmk, a broad-range caspase inhibitor, or AcDEVD-CHO, a caspase-3 inhibitor.
Capsaicin-induced apoptosis in human breast cancer MCF-7 cells through caspase-independent pathway
Our results suggest that capsaicin induces cellular apoptosis through a caspase-independent pathway in MCF-7 cells, and that reactive oxygen species and intracellular calcium ion fluctuation has a minimal role in the process.
Capsaicin Shows Promise In Inhibiting Growth Of Pancreatic Cancer
In our study, we discovered that capsaicin fed orally to mice with human pancreatic tumors was an extremely effective inhibitor of the cancer process, inducing apoptosis in cancer cells,” said Sanjay K. Srivastava, Ph.D., lead investigator and assistant professor, department of pharmacology, University of Pittsburgh School of Medicine. “Capsaicin triggered the cancerous cells to die off and significantly reduced the size of the tumors.”
TRPV6 mediates capsaicin-induced apoptosis in gastric cancer cells
In this study, both gastric cancer and normal epithelial cells were treated with capsaicin and examined for apoptosis by Annexin V binding. Our results showed that capsaicin induces apoptosis in both cells, although cancer cells are more susceptible. This susceptibility is dependent on the availability of TRPV6, a calcium-selective channel protein, as overexpression of TRPV6 in normal cells increased capsaicin-induced apoptosis and knockdown of TRPV6 in cancer cells suppressed this action. Our results further demonstrated that capsaicin increases mitochondrial permeability through activation of Bax and p53 in a JNK-dependent manner.

Capsaicin Mediates Cell Death in Bladder Cancer T24 Cells Through Reactive Oxygen Species Production and Mitochondrial Depolarization
RESULTS: CAP decreased the viability of T24 cells in a dose-dependent manner without marked apoptosis. CAP induced ROS production and mitochondrial membrane depolarization, thereby inducing cell death, not apoptosis, in T24 cells at a concentration of 100 microM or higher. Furthermore, these effects of CAP could be reversed by capsazepine, the antagonist of transient receptor potential vanilloid type 1 channel. In vivo experiment showed that CAP significantly slowed the growth of T24 bladder cancer xenografts as measured by size (661.80 +/- 62.03 vs 567.02 +/- 43.94 mm(3); P

Chillies could help beat cancer as research finds capsaicin destroys diseased cells

Scientists say breast, colon, bone and pancreatic cancer cells could be caused to self destruct by the spicy ingredient


Food: Cinnamon 

Can Cinnamon be the Silver Bullet for Cancer?
Surprisingly, one of the potential agents for this role, cinnamon, is readily available at your local Café. Two of the main ingredients of cinnamon, cinnamaldehyde and procyanidins, have been previously shown to have health-beneficial activities, such as antioxidant, antimicrobial, anti-inflammatory, and anti-diabetic activity. Moreover, an extract from cinnamon (CE) was recently shown to have antitumor and anti-angiogenesis activity as well.

In a recent article published in Molecular Carcinogenesis, scientists from the US have showed that treatment with CE results in reduced migration of invasive breast and ovarian cancer cells, accompanied by reduced protein expression levels of both VEGF and HIF-1. In addition, a significant suppression of blood-vessel formation (see Figure below) and tumor growth was shown after CE treatment in a human ovarian tumor mouse model, which is the most deadly malignancy in women.
Cinnamon Compound Curtails Cancer
The second leading cause of cancer deaths in the US, colorectal cancer is a progressive disease generally with poor prognosis. Consequently, scientists are exploring approaches that may prevent the disease. Previously, Georg Wondrak, from the University of Arizona (Arizona, USA) identified the ground bark of Cinnamomum aromaticum (cassia cinnamon) and Cinnamomum verum (Ceylon cinnamon), as rich dietary sources of cinnamaldehyde – an inducer of Nrf2 (nuclear factor-E2-related factor 2), a master regulator of the cellular antioxidant defense that represents a promising molecular target for colorectal cancer chemoprevention.
Cinnamaldehyde induces apoptosis by ROS-mediated mitochondrial permeability transition in human promyelocytic leukemia HL-60 cells
Cinnamaldehyde is an active compound isolated from the stem bark of Cinnamomum cassia, a traditional oriental medicinal herb, which has been shown to inhibit tumor cell proliferation. In this study, we investigated the effects of cinnamaldehyde on the cytotoxicity, induction of apoptosis and the putative pathways of its actions in human promyelocytic leukemia cells. ...Taken together, our data indicate that cinnamaldehyde induces the ROS-mediated mitochondrial permeability transition and resultant cytochrome c release. This is the first report on the mechanism of the anticancer effect of cinnamaldehyde.
More Cinnamon, Less Cancer
It has been know for a few years that several types of spices contain large amounts of cancer-fighting compounds that could help in the prevention of the disease. In addition to the well-known health properties of tumeric and ginger, a recent study has suggested that cinnamon could be equally useful in reducing tumour growth by blocking the formation of new vessels using a process called angiogenesis.
Cinnamon extract induces tumor cell death through inhibition of NFκB and AP1
Cinnamon extract strongly inhibited tumor cell proliferation in vitro and induced active cell death of tumor cells by up-regulating pro-apoptotic molecules while inhibiting NFκB and AP1 activity and their target genes such as Bcl-2, BcL-xL and survivin. Oral administration of cinnamon extract in melanoma transplantation model significantly inhibited tumor growth with the same mechanism of action observed in vitro.


Food: Lemon Grass
Sources: Asian grocery's (lemon grass), Health food stores (extracts).

Fresh lemon grass fields in Israel become Mecca for cancer patients

A drink with as little as one gram of lemon grass contains enough citral to prompt cancer cells to commit suicide in the test tube. Israeli researchers find way to make cancer cells self-destruct - Ben Gurion University

Lemongrass Fights More than a Dozen Different Types of Cancers

A 2009 study published in the journal Chemico-Biological Interactions revealed that lemongrass essential oil is effective in targeting at least 12 different human cancer cell lines. Animal trials show that direct injection of lemongrass essential oil inhibits cancer tumors in a dose-dependent way, meaning the higher the dose of the oil, the better the outcome.

When administered at a dosage of 200 milligrams per kilogram (mg/kg) concentration, lemongrass essential oil was shown to inhibit both ascitic (in the fluid of the abdominal cavity) and solid tumors of Ehrlich Ascites (a type of tumor cell line) by 97.34 percent and 57.83 percent, respectively. For Sarcoma-180 tumor cells, the same dosage resulted in ascitic and solid tumor inhibition of 94.07 percent and 36.97 percent, respectively.

An essential oil and its major constituent isointermedeol induce apoptosis by increased expression of mitochondrial cytochrome c and apical death receptors in human leukaemia HL-60 cells.
An essential oil from a lemon grass variety of Cymbopogon flexuosus (CFO) and its major chemical constituent sesquiterpene isointermedeol (ISO) were investigated for their ability to induce apoptosis in human leukaemia HL-60 cells because dysregulation of apoptosis is the hallmark of cancer cells. ...The easy and abundant availability of the oil combined with its suggested mechanism of cytotoxicity make CFO highly useful in the development of anti-cancer therapeutics.
Citral is a New Inducer of Caspase-3 in Tumor Cell Lines

Citral, 3,7-dimethyl-2,6-octadien-1-al, a key component of the lemon-scented essential oils extracted from several herbal plants such as lemon grass (Cymbopogon citratus), melissa (Melissa officinalis), verbena (Verbena officinalis) is used as a food additive and as a fragrance in cosmetics. In this study, we investigated the anti-cancer potential of citral and its mode of action. Concentrations of 44.5 μM, comparable to the concentration of citral in a cup of tea prepared from 1 g of lemon grass, induced apoptosis in several hematopoietic cancer cell lines. Apoptosis was accompanied by DNA fragmentation and caspase-3 catalytic activity induction. Citral activity (22.25 μM) was compared to a reference compound like staurosporine (0.7 μM), in respect to DNA fragmentation and caspase-3 enzymatic activity. The apoptotic effect of citral depended on the α,β-unsaturated aldehyde group.

Citral inhibits cell proliferation and induces apoptosis and cell cycle arrest in MCF-7 cells.
In this study, we investigated the effect of citral (3,7-dimethyl-2,6-octadienal), a key component of essential oils extracted from several herbal plants, on the proliferation rate, cell cycle distribution, and apoptosis of the human breast cancer cell line MCF-7. The effects of this compound were also tested on cyclo-oxygenase activity. Citral treatment caused inhibition of MCF-7 cell growth (IC(50)-48 h: 18 x 10(-5)m), with a cycle arrest in G(2)/M phase and apoptosis induction. Moreover, we observed a decrease in prostaglandin E(2) synthesis 48 h after citral treatment. These findings suggest that citral has a potential chemopreventive effect.

Cod Liver Oil

Women and Lung Cancer - Could Cod Liver Oil Improve Survival
My Scandinavian, cod-liver-oil-serving grandma was right again – based on the results of a new Norwegian study. Women who used cod liver oil daily for a year prior to their diagnosis of lung cancer, had a 44% lower chance of dying. Though my grandmother would have turned 100 last week, support for her advice will be published next month in the International Journal of Cancer. Researchers looked at questionnaires completed by over 68,000 women between 1996 and 1999. They then analyzed 2,242 women who developed cancer following the questionnaire and up to the year 2007. Women who used cod liver oil daily, had a 23% lower chance of dying from solid tumors in general (breast, colorectal, and lung cancers), and a 44% reduced risk of dying from lung cancer.

Coenzyme Q10

Foods: Fish, chicken, peanuts, seasame seeds, pistachios, olive oil, soy beans, grapeseed, parsley, perilla, broccoli (and relatives).

How does CoQ10 work against cancer?
Co-Q10 is present in most "eukaryotic" cells (muscle tissues and more). It's produced naturally in the body, which uses it for cell growth and to protect cells from damage that could lead to cancer. In animals it's most concentrated in the heart. Co-Q10 both boosts the immune system, and has been shown to induce apoptosis.
A Gentle Cancer Killer
In laboratory and animal studies, the UM researchers found that by delivering CoQ10 to cancer cells and tissues, the molecule induced apoptosis, which is the normal programmed cell death that goes awry in the disease process.
Coenzyme Q10 (PDQ®)–Patient Version
Low blood levels of coenzyme Q10 have been found in patients with myeloma, lymphoma, and cancers of the breast, lung, prostate, pancreas, colon, kidney, and head and neck. Studies suggest that coenzyme Q10 may help the immune system work better. Partly because of this, coenzyme Q10 is used as adjuvant therapy for cancer. Adjuvant therapy is treatment given following the primary treatment to increase the chances of a cure.
Clinical trials have shown that coenzyme Q10 helps protect the heart from the damaging side effects of doxorubicin, a drug used to treat cancer.

Normalizattion of BCL-2 family members in breast cancer by Coenzyme Q10
Because of their integral role in intrinsic apoptosis any imbalance can lead to a variety of diseases; under expression can lead to degenerative diseases while over expression can lead to cancer and autoimmune disease. Due to their life or death role in the cell, Bcl-2 family members are currently the targets of many therapies in various disease states. Bcl-2 itself is over expressed in most tumors and all anti-apoptotic Bcl-2 family members are considered to have oncogenic potential. Conversely, the pro-apoptotic members are considered to be tumor suppressors and many mimetics are foci for cancer research. ...Both pro- and anti-apoptotic protein levels were measured in the two breast cancer cell lines after Q10 exposure. Protein levels were measured at 4,8,12, and 24 hours respectively in order to capture evidence of Q10's normalizing influence on disrupted apoptotic function. In the MCF-7 cell line Bcl-2 levels were seen to significantly drop after only 4 hours of Q10 exposure.


Food: Cumin Seeds.

Primary ingredient in Chili Powder.

Cumin: natures potent cancer combatant
This herb has been seen to effectively decrease the incidence of chemically induced tumors of the stomach, colon, and cervix. Its significant antioxidant activity and the ability to modulate the metabolism of carcinogens (toxins) explain its cancer-preventive prowess. Cumin seeds are known to induce the activity of glutathione-S-transferase, a protective enzyme that helps eliminate cancer-causing substances. Cumin offers a significant level of caffeic, chlorogenic, ferulic, and other phenolic acids that have anti-inflammatory potential.


Foods: Tumeric roots / powder, curry powder, yellow mustard.
Sources: Health food stores (extracts), large farmers markets (roots), Indian grocery stores (tumeric powder in bulk).

Induction of apoptosis in human lung cancer cells by curcumin
This study investigated the cellular and molecular changes induced by curcumin leading to the induction of apoptosis in human lung cancer cell lines—A549 and H1299. A549 is p53 proficient and H1299 is p53 null mutant. The lung cancer cells were treated with curcumin (0–160 μM) for 12–72 h. Curcumin inhibited the growth of both the cell lines in a concentration dependent manner. Growth inhibition of H1299 cell lines was both time and concentration dependent. Curcumin induced apoptosis in both the lung cancer cell lines. A decrease in expression of p53, bcl-2, and bcl-XL was observed after 12 h exposure of 40 μM curcumin. Bak and Caspase genes remained unchanged up to 60 μM curcumin but showed decrease in expression levels at 80–160 μM. The data also suggest a p53 independent induction of apoptosis in lung cancer cells.

Curcumin induces apoptosis in immortalized NIH 3T3 and malignant cancer cell lines
Curcumin, which is a widely used dietary pigment and spice, has been demonstrated to be an effective inhibitor of tumor promotion in mouse skin carcinogenesis. We report that curcumin induces cell shrinkage, chromatin condensation, and DNA fragmentation, characteristics of apoptosis, in immortalized mouse embryo fibroblast NIH 3T3 erb B2 oncogene-transformed NIH 3T3, mouse sarcoma S180, human colon cancer cell HT-29, human kidney cancer cell 293, and human hepatocellular carcinoma Hep G2 cells

Curcumin induces apoptosis in human breast cancer cells
The aim of this study was to determine the mechanisms of curcumin-induced human breast cancer cell apoptosis. From quantitative image analysis data showing an increase in the percentage of cells with a sub-G0/G1 DNA content, we demonstrated curcumin-induced apoptosis in the breast cancer cell line MCF-7, in which expression of wild-type p53 could be induced. Apoptosis was accompanied by an increase in p53 level as well as its DNA-binding activity followed by Bax expression at the protein level. Further experiments using p53-null MDAH041 cell as well as low and high p53-expressing TR9-7 cell, in which p53 expression is under tight control of tetracycline, established that curcumin induced apoptosis in tumor cells via a p53-dependent pathway in which Bax is the downstream effector of p53. This property of curcumin suggests that this molecule could have a possible therapeutic potential in breast cancer patients.
Chemopreventive Effect of Curcumin, a Naturally Occurring Anti-Inflammatory Agent, during the Promotion/Progression Stages of Colon Cancer
The inhibition of adenocarcinomas of the colon was, in fact, dose dependent. Administration of curcumin to the rats during the initiation and postinitiation stages and throughout the promotion/progression stage increased apoptosis in the colon tumors as compared to colon tumors in the groups receiving AOM and the control diet. Thus, chemopreventive activity of curcumin is observed when it is administered prior to, during, and after carcinogen treatment as well as when it is given only during the promotion/progression phase (starting late in premalignant stage) of colon carcinogenesis.

Antiproliferation and apoptosis induced by curcumin in human ovarian cancer cells

Curcumin, an active ingredient from the rhizome of the plant, Curcuma longa, has antioxidant, anti-inflammatory and anti-cancer activities. It has recently been demonstrated that the chemopreventive activities of curcumin might be due to its ability to inhibit cell growth and induce apoptosis. In the present study, we have investigated the effects of curcumin on growth and apoptosis in the human ovarian cancer cell line Ho-8910 by MTT assay, fluorescence microscopy, flow cytometry and Western blotting. Our data revealed that curcumin could significantly inhibit the growth and induce apoptosis in Ho-8910 cells. A decrease in expression of Bcl-2, Bcl-X(L) and pro-caspase-3 was observed after exposure to 40 microM curcumin, while the levels of p53 and Bax were increased in the curcumin-treated cells. These activities may contribute to the anticarcinogenic action of curcumin.
Curcumin, an antioxidant and anti-tumor promoter, induces apoptosis in human leukemia cells

Curcumin, widely used as a spice and coloring agent in food, possesses potent antioxidant, anti-inflammatory and anti-tumor promoting activities. In the present study, curcumin was found to induce apoptotic cell death in promyelocytic leukemia HL-60 cells at concentrations as low as 3.5 micrograms/ml.
Notch-1 down-regulation by curcumin is associated with the inhibition of cell growth and the induction of apoptosis in pancreatic cancer cells
Curcumin inhibited cell growth and induced apoptosis in pancreatic cancer cells. Notch-1, Hes-1, and Bcl-XL expression levels concomitantly were down-regulated by curcumin treatment. These results correlated with the inactivation of NF-κB activity and increased apoptosis induced by curcumin. The down-regulation of Notch-1 by small-interfering RNA prior to curcumin treatment resulted in enhanced cell growth inhibition and apoptosis.

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