American Association for Cancer Research

Zytiga May Up Mortality Risk in Prostate Cancer Patients With CVD

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Zytiga May Up Mortality Risk in Prostate An increased risk of early death was observed in men with pre-existing cardiovascular disease (CVD) starting abiraterone acetate (Zytiga) for advanced prostate cancer, a registry study found.

Among abiraterone-treated patients, increased mortality ranged from 21.4% for those with ischemic heart disease to 25.6% for those with acute myocardial infarction (MI), compared with 15.8% for those without a heart condition, reported Grace Lu-Yao, PhD, MPH, of the Sidney Kimmel Cancer Center at Thomas Jefferson University in Philadelphia.

“Our data show that patients with existing cardiovascular conditions experience significantly higher 6-month mortality than those without CVD,” Lu-Yao said during a media briefing ahead of the American Association for Cancer Research (AACR) meeting, to be held here March 29-April 3.

Of the 2,845 patients in the study, 67.6% had a pre-existing heart condition (n=1,924). Patients with atrial fibrillation, congestive heart failure, and stroke had increased mortality risks of 24.4%, 23.4%, and 22.1%, respectively, within these first 6 months.

“Typically clinical trials do exclude people who have significant medical problems,” said AACR President Elizabeth Jaffee, MD, of Johns Hopkins Medicine in Baltimore. “I think this has been rationalized as a safety measure by both investigators and sponsors.”

In her presentation, Lu-Yao highlighted that roughly 40% of prostate cancer patients have uncontrolled hypertension. These patients, plus those with a history of major heart conditions, are usually excluded from clinical trials. In the STAMPEDE study, for instance, exclusion criteria included those with a history of severe angina or heart failure, and those with a recent MI.

Jaffe noted that testing new agents in the healthiest patients does not provide the real-world data physicians need.

The researchers used Surveillance, Epidemiology, and End Results (SEER)-Medicare linked data to look at prostate cancer patients treated with abiraterone from 2011 to 2014.

The study also found an increased risk of hospitalizations by examining hospital use in the 6 months before and after starting abiraterone treatment. Risk of hospitalization was increased for patients without a history of CVD for incidence rate ratios (IRR) 1.43 (95% CI 1.30-1.57), as well as for those with pre-existing CVD:

  • Acute MI: IRR 1.44 (95% CI 1.12-1.86)
  • Congestive heart failure: IRR 1.35 (95% CI 1.21-1.51)
  • Stroke: IRR 1.30 (95% CI 1.07-1.57)
  • Atrial fibrillation: IRR 1.27 (95% CI 1.09-1.48)
  • Ischemic heart disease: IRR 1.22 (95% CI 1.01-1.48)

The study captured the period from when abiraterone was first approved by the FDA in 2011 for use in late-stage castration-resistant prostate cancer after prior treatment with docetaxel, and when it was then expanded in 2012 to also include use before chemotherapy. In the study, roughly 20% of the patients had received prior chemotherapy (n=586), with the rest being chemotherapy naive. Lu-Yao said that regardless of prior chemotherapy use, the patterns for both early mortality and hospitalization were “quite similar.”

Jaffee noted that while the study is retrospective, it still provides important data, similar to that of a phase IV study.

“Once a drug’s approved, all physicians can administer these drugs, and we don’t really have a handle on who may have worse side effects from these drugs,” she said. “We know that all therapies have side effects, and we need to be able to predict early, screen early, so we can at least monitor for these side effects and intervene at an early stage before patients have severe consequences from these drugs.”

Study limitations included the possibility of misclassification of patients’ CVD, the fact that treatment efficacy could not be assessed, and that there was no control group to look at expected survival for this patient population. A lack of clinical data also meant that the researchers could not compare the study population against the pivotal trials of abiraterone acetate.

Breast Cancer Gene Test Cuts Use of Chemo

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Many women with high-risk breast cancer by conventional criteria avoided adjuvant chemotherapy with no increased risk of metastatic disease by use of a cancer-genetics test, according to data reported here.

Patients at high clinical/pathologic risk but low risk by the 70-gene MammaPrint assayhad a 5-year distant metastasis-free survival (DMFS) of 94.4% without chemotherapy versus 95.9% with chemotherapy, a difference that did not reach statistical significance (HR 0.78, 95% CI 0.50-1.21). In patients with a low clinical risk but high genetic risk, the 5-year DMFS was 95% to 96% with or without chemotherapy.

Among the 3,348 high-risk patients, use of the gene assay was associated with a 46% reduction in prescriptions for chemotherapy and 14% reduction for all 6,648 patients in the study, Martine Piccart, MD, PhD, of the Jules Bordet Institute in Brussels, Belgium, said at the American Association for Cancer Research (AACR) meeting.

Acknowledging the 22% reduction in the hazard ratio with chemotherapy for the clinical high-risk/genetic low-risk group, Piccart said, “The statistician will tell you that it is not totally impossible that there is a very small chemotherapy benefit, which would translate into a very small absolute benefit that would not justify the risks of chemotherapy.”

In the U.S., breast cancer specialists have access to MammaPrint and the OncoType DXgene test, the latter being more widely used. AACR President Nancy E. Davidson, MD, of the University of Pittsburgh, declined to speculate as to whether the findings could influence clinical practice. Instead, she said the data will help inform decision making for clinicians and their patients.

Piccart said the key issue is that breast cancer patients should have access to a validated gene test to help with clinical decision making.

Three decades of clinical trial results have shown that adjuvant chemotherapy improves survival in early breast cancer by 2% to 12% in absolute terms. However, effective therapy confers its own risks, including secondary cancers, cardiac toxicity, early menopause, and an adverse impact on cognitive function. Chemotherapy also adds to the cost of care

One approach to maximize the benefits and minimize the risks of chemotherapy is to use clinical/pathologic risk criteria, such as a freely available prognostic model validated more than a decade ago as a decision-making aid for adjuvant chemotherapy. More recently, tumor gene expression profiling has added another method to define breast cancer risk.

Whether tumor genomics profiling could improve risk prediction versus clinicopathologic criteria remained unproven, leading to the international MINDACT (Microarray In Node Negative Disease May Avoid Chemotherapy) trial to evaluate the strategies in clinical practice.

“Our hypothesis was that the MammaPrint genomic assay would outperform the clinical criteria by reducing the prescription of adjuvant chemotherapy without impairing patient outcomes,” said Piccart.

From 2007 to 2011, investigators in nine countries enrolled 6,693 who had undergone surgery for early breast cancer. Initially, only patients with node-negative disease status were eligible, but the protocol was subsequently amended to allow women with as many as three positive nodes after the gene assay was validated in such patients.

Every patient was evaluated by the clinicopathologic prognostic model and the genetic test. By consensus, investigators defined “clinical low risk” as a patient who had an estimated 10-year disease-specific survival of 88% without chemotherapy or endocrine therapy for estrogen receptor (ER)-positive disease or 92% for ER-negative disease.

Patients who had low-risk disease by both methods did not receive chemotherapy, and all patients who were high risk by both methods did get chemotherapy. The 3,348 patients with discordant results (high by one method, low by the other) formed the focal point of the investigation.

The patients with discordant results received radiation therapy and were randomized clinical or genetic risk assessment to decide whether they would receive adjuvant chemotherapy. The primary endpoint was 5-year DMFS.

The primary analysis involved the patients with high clinical risk/low genetic risk, randomized to no adjuvant chemotherapy. To reject the null hypothesis, the lower boundary of 95% confidence intervals (CI) had to exceed 92.0%

The patients with discordant results had a median age of 55; 80% had node-negative disease, 58% had T1 tumors, 88% had ER-positive tumors, and 10% had HER2-positive tumors.

After a median follow-up of 5 years, DMFS was 97.6% for patients who had low-risk disease by clinical/pathologic factors and the gene test versus 90.6% for those who had high-risk disease by both criteria. Piccart said women with high-risk disease tended to have larger tumors and were more likely to have node-positive and HER2-positive disease.

For the primary analysis, women with high clinical/low genetic risk had a 5-year DMFS of 94.7% without chemotherapy (95% CI 92.5%-96.2%), which allowed investigators to reject the null hypothesis.

By intention-to-treat analysis, the clinical high-risk/genetic low-risk group had a 5-year DMFS of 94.4% without chemotherapy and 95.9% with chemotherapy. For the clinical low-risk/genetic high-risk group, 5-year DMFS was 95.8% with chemotherapy and 95.0% without.

First-in-class HER3/EGFR Antibody Safe, With Antitumor Activity in Patients With Refractory Epithelial Cancers

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MEHD7945A, a dual-action antibody that targets two members of the epidermal growth factor receptor (EGFR) family, was found to be safe and showed clinical activity in some patients with locally advanced or metastatic refractory epithelial cancers, including cancers of the head and neck, according to phase I clinical trial data published in Clinical Cancer Research, a journal of the American Association for Cancer Research (AACR).

“MEHD7945A is a humanized IgG1 antibody that has the capacity to target two members of the EGFR family, EGFR [also known as HER1] and HER3,” saidJosé Baselga, MD, PhD, physician-in-chief and chief medical officer at theMemorial Sloan Kettering Cancer Center in New York.

Baselga, who is also president of the AACR, explained, “For about 20 years, we have been working on the hypothesis of targeting EGFR in epithelial cancers as a fruitful approach based on our understanding that dysregulated EGFR plays an important role in tumorigenesis. What we have learned since then is that there are other players in the EGFR family, such as HER3, which are functionally similar to EGFR and, therefore, have a significant role in tumor promotion. We felt it is important that we hit not just EGFR alone, but also target HER3, with the goal of achieving more durable responses.”

Binding of growth factors to EGFR and HER3 in a cell leads to activation and downstream signaling to promote cell growth. Dysregulated EGFR and/or HER3 can lead to overactive signaling, causing uncontrolled cell growth and proliferation, as seen in a variety of epithelial cancers. MEHD7945A has two antigen-binding arms, and they bind to unique targets on HER3 and EGFR, thus inhibiting the activity of multiple cancer signaling pathways.

“In a phase I clinical trial, we found that MEHD7945A was well tolerated as a single agent, and we were able to confirm partial responses in patients who had refractory disease, which clearly suggests that this dual-targeting approach is a good strategy moving forward,” Baselga added.

Baselga and colleagues enrolled 66 patients at six sites in the United States and Spain: 30 patients to the dose-escalation study and 36 to the dose-expansion study. All patients had received prior systemic therapies, and about 50 percent of them had received prior anti-EGFR therapies. Patients had incurable, locally advanced, or metastatic epithelial cancer, including colorectal, non-small cell lung, or head and neck cancers, which had progressed despite prior therapies.

Six different dose levels were tested in the dose-escalation study, and patients enrolled in the dose-expansion study received 14 mg/kg b.w. of the drug intravenously, every two weeks until patients experienced toxicity or disease progression.

No dose-limiting toxicities or drug-related grade 4 adverse events were reported in the dose-escalation or the dose-expansion cohorts. Two patients with squamous cell carcinoma of the head and neck (in the tongue and larynx, respectively) had partial responses, and eight patients had stable disease that lasted for 16 weeks or longer.

Patients whose tumors had high levels of the growth factor heregulin, which binds to EGFR, were found to benefit from the drug, according to Baselga. “Presence of high levels of the ligand [heregulin] could be a marker of response to this drug, but this needs further confirmation,” he said.

“We have been using antibodies to treat cancers for a while now, but recent advancements in technology are allowing us to use antibodies in a way we have not done in the past,” Baselga noted. “Dual targeting of HER2 and HER3 was shown to be a promising strategy for breast cancers; this study adds further support to the dual-targeting approach, and also speaks to the increasing opportunities we all have with engineering antibodies for patient benefit.”

Vaccines Do Not Cover Most Common HPV Types in Black Women.

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The HPV subtypes that are most common in black women in the United States are not targeted by the currently available vaccinesGardasil and Cervarix, according to new research.

The findings suggest that current HPV vaccination will be less beneficial for black women in the US than for their white counterparts, said study coauthor Catherine Hoyo, PhD, MPH, of Duke University, in Durham, North Carolina.

She spoke at a press briefing today at the annual International Conference on Frontiers in Cancer Prevention Research, in National Harbor, Maryland. The meeting is sponsored by the American Association for Cancer Research.

“The approved cervical cancer vaccines are effective but may not be effective for everyone,” said Paul Limburg, MD, from the Mayo Clinic, in Rochester, Minnesota, who moderated the press briefing. He was not involved with the study.

Persistent infection with HPV 16 and/or HPV 18 accounts for about 70% of all cervical cancers, said Dr. Hoyo. These are the subtypes targeted by Gardasil and Cervarix. Gardasil also targets HPV 6 and HPV 11.

Some black women in the new study did, in fact, have infections with HPV 16 and/or HPV 18. But much less often — their rate was about half of that of white women.

“Since African-American women don’t seem to be getting the same subtypes of HPV with the same frequency, the vaccines aren’t helping all women equally,” said study coauthor Adriana Vidal, PhD, in a press statement. She is also from Duke University.

The investigators prospectively looked at 572 women at 10 Duke-affiliated clinics with abnormal Pap tests who then underwent colposcopy; the group was about evenly divided among blacks (n = 280) and whites (n = 292). And just about even numbers of the respective racial groups subsequently had evidence of cervical intraepithelial neoplasia 1 (CIN1; 112 vs 118).

For whites with CIN1, the most frequent HPV subtypes were 16, 18, 56, 39, and 66.

But for blacks with CIN1, the most frequent HPV subtypes were 33, 35, 58, and 68.

Thus, in blacks, the most common genotypes were not HPV 16 and 18, which defies conventional wisdom about HPV infection.

There were no data on Hispanics in the new presentation because their numbers were too small at this point to be included, said Dr. Hoyo.

Without HPV 16/18, Are Some Black Women “Getting Dropped”?

The study findings may help explain why black women in the US are harder hit by cervical cancer than white women, said Dr. Hoyo.

She pointed out that both the incidence of invasive cervical cancer and related mortality rates are higher in blacks than in whites.

“We don’t know what is causing the disparity,” Dr. Hoyo told Medscape Medical News in a phone interview after the press conference.

“The problem is not likely detection,” she said, explaining that screening rates for precancerous lesions are comparable for black and white women.

The new data, however, suggest that, if clinicians are strongly focusing on HPV 16 and 18 for more careful follow-up in their black patients, then they may be missing some eventual cervical cancers, Dr. Hoyo said.

“Somewhere along the line, some black women may be getting dropped because they don’t have the HPV subtypes that are considered to be most aggressive,” she summarized.

Her advice to clinicians with black females who HPV infection and CIN is: “Broaden the subtypes that you look at.”

Currently, there is a vaccine in phase 3 clinical trials that targets 9 HPV subtypes (6, 11, 16, 18, 31, 45, 52, and 58). That means that 2 of the 4 most common subtypes in blacks are targeted by the experimental vaccine. “We need more African American women to enroll in trials like this to see how beneficial this new vaccine will be for them,” Dr. Hoyo said.

The new study is not the first to indicate that black women have lower rates of HPV 16 and 18.

A recent report found that black race was a predictor of lower HPV 16 and 18 positivity among women with high-grade cervical lesions (Cancer. 2013;119(16):3052-3058).

However, the new study from the Duke team is the first to indicate that this race-influenced distribution of HPV subtypes also occurs in lower-grade cervical lesions.

The Duke investigators also looked at high-grade lesions (CIN2/3).

In CIN2/3, HPV 16, 18, 33, 39, and 59 were the most common genotypes detected in white women, whereas HPV 31, 35, 45, 56, 58, 66, and 68 were the most prevalent in African American women.

Prostate Cancer Risk Linked To Early-Onset Baldness In New Study.

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African american shaved head

French researchers said it, and now a team from the Center for Clinical Epidemiology and Biostatistics at the University of Pennsylvania in Philadelphia have released new evidence to support their claim: Men who lose their hair early in life have a greater risk of developing prostate cancer.

In a study of 537 African-American men — 318 with prostate cancer and 219 controls — investigators discovered that baldness of any kind was associated with a 69 percent increased risk of prostate cancer, particularly among African-American men.

According to the study, which was published in Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research, black men with frontal baldness, and not vertex baldness, were more than twice as likely to have been diagnosed with advanced prostate cancer. The association was even stronger among those who were diagnosed when younger than 60, with a sixfold increase in high-stage prostate cancer and a fourfold increase in high-grade prostate cancer.

The findings concur with a 2011 report showing that men who start to go bald at age 20 may be more likely to develop prostate cancer in later life. Though grim, the team conducting that study suggested that their findings be used as a basis for early screening or preventative therapy for those at higher risk.

“Early-onset baldness may be a risk factor for early-onset prostate cancer in African-American men, particularly younger men,” said Charnita Zeigler-Johnson, Ph.D., research assistant professor at the Center for Clinical Epidemiology and Biostatistics at UPenn and lead author of the study. “Pending future studies to confirm our results, there is a potential to use early-onset baldness as a clinical indicator of increased risk for prostate cancer in some populations of men,” he added.

Black men have the highest incidence rate for prostate cancer in the United States and are more than twice as likely as White men to die of the disease, according to the National Cancer Institute.

 

The role of vitamin D in chronic heart failure .

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Vitamin D is an emerging agent with tremendous potential and may represent a novel target for therapy in congestive heart failure (CHF). Further studies are needed to identify the mechanism(s) involved in the pathophysiology as well as to adequately examine the role of Vitamin D measurement and supplementation in patients with CHF.

  • Despite advanced medical and device–based therapies, congestive heart failure (CHF) remains a major medical problem, associated with significant morbidity and mortality.
  • Vitamin D deficiency is prevalent in CHF and is associated with poor outcomes.
  • In this manuscript the authors review the evidence linking vitamin D deficiency and CHF and discuss potential mechanisms involved, as well the clinical data on vitamin D supplementation in CHF patients.
  • A clear relationship has been established between Vitamin D deficiency and increased mortality and morbidity in CHF.
  • However, the mechanism involved is not clearly understood.
  • Recent clinical and experimental evidence have identified the renin–angiotensin–aldosterone system and inflammatory cytokines as likely mediators that can lead to poor clinical outcomes via the cardiorenal syndrome.
  • Clinical data on vitamin D supplementation also remain unestablished, with potential clinical benefits recently reported in patients with vitamin D deficiency.
  • Nonetheless, large–scale randomized clinical trials are lacking.

Source: Current Opinion in Cardiology

Breast Cancer Risks Acquired in Pregnancy May Pass to Next 3 Generations.

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What a woman eats and is exposed to during pregnancy can impact not only the future health of her child, but also that of her grandchildren and even great-grandchildren.

It’s difficult to really get your mind around this concept, as it is quite astonishing to think that what your grandmother or great grandmother was exposed to during pregnancy may have an impact on your health today… but that is what the research is showing…

Breast Cancer Risks May Carry Over for Three Generations

In a study on rats, those exposed to chemicals or foods that raise estrogen levels during pregnancy produce daughters that have a higher than normal risk for breast cancer – and that risk is passed on to the next two generations. It was not genetic mutations that were passed on, but rather epigenetic alterations that influence the expression of your genes.

The researchers analyzed DNA methylation, a normal process that allows cells to perform different actions by turning gene expression off. The rat descendants with increased breast cancer risk had “several hundred common DNA regions that were methylated differently than in a control group, providing statistically convincing evidence that breast cancer risk can be transmitted via epigenetic means.”1

Dramatic Impact of Diet on Multiple Generations Revealed in the 1930s…

Starting in the 1930’s, Francis M. Pottenger, Jr., M.D., conducted a now classic study on cats, which showed the power of nutrition in impacting multiple generations. Over a period of 10 years, Pottenger conducted studies involving upwards of 900 cats, which were fed either a healthy raw-food diet or a “junk-food” diet consisting mostly of cooked meat.

The cats on the raw-food diet thrived while those eating the cooked meat developed health problems – and the effects persisted in their offspring. While the cooked-meat cats of the first generation developed degenerative diseases later in life (and reportedly became lazy), the second-generation cats started to get sick in mid-life.

By the third generation, the cats developed degenerative diseases very early in life, had a shorter lifespan, and some were born blind. Many of the third-generation cats could not reproduce, and those that did produced even sicker offspring that often died within six months. By the fourth generation, the “junk food” cats died off completely.

You can read the details for yourself in the book Pottenger’s Cats: A Study in Nutrition – the fact of the matter is, epigenetic changes have been found to be passed down through generations for decades now…

In 2010, research presented at the 101st 2010 meeting of the American Association for Cancer Research in Washington DC similarly showed that when pregnant rats were fed an unhealthy diet, both their daughters and granddaughters proved to be at greater risk of breast cancer.2 Even if the daughters of the first generation of rats ate healthy, their offspring – the third generation – were still at greater risk of disease.

Additional research has shown that rat fetuses that received poor nutrition while in the womb experienced epigenetic changes that primed them for a nutrition-poor environment once they were born, thereby increasing their risk of health problems ranging from diabetes and heart disease to obesity3 – and it’s been shown now that these changes may last for two generations or more…

Are Rising Breast Cancer Rates the Product of Modern-Day “Food”?

It’s easy to forget that the processed, pre-packaged foods and fast food restaurants of today are actually a radical change in terms of the history of food production. The modern frozen food business didn’t begin until the mid 1920’s when the General Seafoods Company set up shop and began selling crudely frozen fish filets, and fast food restaurants didn’t get a foothold until after World War II.

So it could be that we’re now looking right at these generational effects, caused by our grandparents’ – and for the younger generations, great grandparents’ – dietary changes.

If that’s the case, then we have even more incentive to make drastic changes, and soon, because the disease trends we’re now seeing are only going to get worse as much of the processed foods consumed today are not even food-based! Who knows what kind of genetic mutations and malfunctions we’re creating for our future generations when a MAJORITY of our diet consists of highly processed and artificial foods.

Exposures to Synthetic Estrogens on the Rise

Substances that mimic estrogen in your body, and may increase breast cancer risk, are found liberally in the modern-day diet, in soy products, bovine growth hormones (rBGH, found in dairy prodcuts), and even in food additives like the preservative propyl gallate, and 4-hexylresorcinol, which is used to prevent discoloration in shrimp and other shellfish.

But you’re also exposed to estrogen-mimicking chemicals from plastic food containers, personal care products, non-stick cookware, and other common sources.

The problem is so bad that researchers have expressed concern that children may be exposed to so many synthetic hormone-mimicking chemicals they could potentially overtake the actions of his or her natural hormones! And considering pregnant women are also exposed to these chemicals, the effects in utero cannot be ignored.

For instance, parabens – hormone-mimicking chemicals that are widely used in personal care products like shampoo, lotion, deodorant, shaving gel and cosmetics – have been detected in breast cancer tissues at concentrations up to 1 million times higher than the estrogen (estradiol) levels naturally found in human breast tissue.4 And, the presence of paraben esters have been detected in 99 percent of breast cancer tissues sampled…5

As breast cancer rates continue to climb, it’s quite clear that our future generations could pay the biggest price of all if our food and environment continue to be contaminated with synthetic estrogens and other toxins.

The Good News: You Can Influence the Expression of Your Genes

Even if you know your mother (or grandmother) had a terrible diet while pregnant, or was exposed to a significant amount of synthetic estrogens or other toxins, it doesn’t mean the die has been cast for your health.

As you age, your genome does not change but your epigenome changes dramatically, especially during critical periods of life, such as adolescence. It is influenced by lifestyle, diet, and physical and emotional stresses – how you respond to everything that happens in your environment, from climate change to childhood abuse.

The secret is in the methyl groups that modulate the DNA in your body, which is the realm of the epigenome. When a gene is turned off epigenetically, the DNA has usually been “methylated,” the biological equivalent of being silenced. When methyl groups adhere to a segment of DNA, they inhibit the gene from being expressed.

For the most part you do not manifest disease merely by a defective gene, but by the regulation or expression of your gene by epigenetic influences. Even if you inherited a certain increased disease risk from your mother or grandmother, you can therefore change it.

How to Optimize Your Genetic Expression

A healthy diet is a wonderful start. For instance, we all have tumor suppressor genes, and these genes are capable of stopping cancer cells in their tracks. These genes are present in every cell in your body, but so are proteins called “histones.” As Dr. Jean-Pierre Issa at the M.D. Anderson Cancer Center explained, histones can “hug” DNA so tightly that it becomes “hidden from view for the cell.”6 If a tumor suppressor gene is hidden, it cannot be utilized, and in this way too much histone will “turn off” these cancer suppressors, and allow cancer cells to proliferate.

Now here’s where epigenetics comes in… certain foods, such as broccoli and other cruciferous vegetables, garlic, and onions contain substances that act as histone inhibitors, which essentially block the histone, allowing your tumor suppressor genes to activate and fight cancer. By regularly consuming these foods, you are naturally supporting your body’s ability to fight tumors.

Certain alternative oncologists also tap directly into the epigenetic mechanism, such as Dr. Nicholas Gonzalez, who uses a three-pronged approach to cancer based primarily on nutrition and detoxification, and Dr. Stanislaw Burzynski, who treats cancer with a gene-targeted approach. His treatment uses non-toxic peptides and amino acids, known as antineoplastons, which act as genetic switches that turn your tumor suppressor genes “on.”

If you’re ready to address your dietary choices, read through my comprehensive and recently revised nutrition plan, which will give you tips and tools for eating healthy, dealing with stress, and living a lifestyle that will support your epigenetic health.

You can also turn your genes off and on with your emotions too. Many, if not most people carry emotional scars — traumas that can adversely affect health. Using techniques like energy psychology, you can go in and correct the trauma and help regulate your genetic expression. My favorite technique for this is the Emotional Freedom Technique (EFT).

Finally, if you are looking for tips to reduce your breast cancer risk specifically, you can find my eight top tips for breast cancer prevention here.

Source: Dr. Mercola.

 

 

 

Systematic lymphadenectomy in ovarian cancer at second-look surgery: a randomised clinical trial.

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The role of systematic aortic and pelvic lymphadenectomy (SAPL) at second-look surgery in early stage or optimally debulked advanced ovarian cancer is unclear and never addressed by randomised studies.

Methods:

From January 1991 through May 2001, 308 patients with the International Federation of Gynaecology and Obstetrics stage IA–IV epithelial ovarian carcinoma were randomly assigned to undergo SAPL (n=158) or resection of bulky nodes only (n=150). Primary end point was overall survival (OS).

Results:

The median operating time, blood loss, percentage of patients requiring blood transfusions and hospital stay were higher in the SAPL than in the control arm (P<0.001). The median number of resected nodes and the percentage of women with nodal metastases were higher in the SAPL arm as well (44% vs 8%, P<0.001 and 24.2% vs 13.3%, P:0.02). After a median follow-up of 111 months, 171 events (i.e., recurrences or deaths) were observed, and 124 patients had died. Sites of first recurrences were similar in both arms. The adjusted risk for progression and death were not statistically different (hazard ratio (HR) for progression=1.18, 95% confidence interval (CI)=0.87–1.59; P=0.29; 5-year progression-free survival (PFS)=40.9% and 53.8%; HR for death=1.04, 95% CI=0.733–1.49; P=0.81; 5-year OS=63.5% and 67.4%, in the SAPL and in the control arm, respectively).

Conclusion:

SAPL in second-look surgery for advanced ovarian cancer did not improve PFS and OS.

Source: British journal of oncology