James Watson: A Geneticist’s View of Cancer

Picture L-R: Dr Michael Murphy, President, UCC and Pro Vice Chancellor, NUI with Nobel Laureate, Dr James Watson and Professor Gerald O’Sullivan, Director of the Cork Cancer Research Centre at UCC.

At 82 years old, you might imagine James Watson would be taking life easy. After a spectacular scientific career, during which he was part of a duo which made , as his fellow Nobel Laureate Sir Peter Medawar described it, “the greatest achievement of science in the 20th century”, a relaxing retirement might be in order. Not so for Watson, it seems.

Speaking at University College Cork last night, while presenting the inaugural Cancer Lecture of the Cork Cancer Research Centre (CCRC), Watson told a packed audience of his ongoing research into finding a cure for cancer at the Cold Spring Harbor Laboratory in New York where he is now Chancellor Emeritus.

Striking a highly optimistic note, the Nobel Laureate bemoaned some pessimistic cancer researchers who he said were more interested in merely researching cancer and didn’t realise that they had an obligation to cure people and to save lives.

“We are nearly there“, was his message for the evening, having suggested that the medicines to do the job might already be in use for a variety of ailments, but that doctors and scientists may not have recognised their anti-cancer properties yet.

Watson explained how he initially became interested in cancer research early on in his career. So much so, that he included a whole chapter on cancer in the first edition of his seminal textbook Molecular Biology of the Gene, which was originally published in 1965. The book was based on a a ten-lecture series he had been giving at Harvard for six years to introductory biology students and its format was ground-breaking at the time.

In the preface to the 1965 edition, Watson proclaimed that “it is time to reorient our teaching and to produce the new texts that will give the biologist of the future the rigor, the perspective, and the enthusiasm that will be needed to bridge the gap between the single cell and the complexities of higher organisms. The we may expect hard facts about today’s most challenging biological problems: the structure of the cell, the nature of cancer, the fundamental mechanism(s) of differentiation, and how the ability to think arises from the organization of the central nervous system“.

Writing in the final chapter of the first edition, Watson explains his hopes for elucidating the causes of cancers and beginning to treat them effectively. In “A Geneticist’s View of Cancer“, he writes that scientists at the time were just beginning to understand the genetic makeup of the diseases.

“If we are still a colossally long way from understanding a healthy animal cell at the molecular level, have we any chance of gaining an insight into the diseased cell?”

Even at the time, just over a decade after the publication of the double-helical structure of DNA, Watson was optimistic that “an understanding of at least some aspects of uncontrolled cell growth may soon be achieved at the molecular level. Such optimism arises from recent, spectacular results on the induction of tumors by viruses“.

‘Only today are we beginning to gain some confidence that we are close to understanding the essential molecular features upon which the life of even the simplest bacterial cell depends’ – James Watson, 1965As a young scientist, at the time, he recognised the obstacles that lay ahead: “Only today are we beginning to gain some confidence that we are close to understanding the essential molecular features upon which the life of even the simplest bacterial cell depends. The jump to an attempt to understand the much more complex vertebrate cell with its thousandfold greater amount of DNA has only begun“.

Born in Chicago in 1928, James Dewey Watson received his degree from the University of Chicago in 1947, having enrolled in university at the age of just 15. A PhD from Indiana University followed in 1950 and the young scientist then spent two years doing postdoctoral work in Copenhagen before moving to the Cavendish Laboratory at Cambridge University.

In the Spring of 1953, while still at Cambridge, Watson and his colleague Francis Crick published the results of their collaboration – the elucidation of the double helical structure of DNA.

Watson has had several high-profile roles over the years, including serving as the director, president and chancellor of Cold Spring Harbor Laboratory in New York where he focused on the study of the genetic basis for cancer. He resigned as chancellor in 2007 after a controversy erupted over comments he made in an interview regarding race and intelligence. He was also involved in the Human Genome Project and was only the second person to publish his full genome publicly online.

‘I think the ethics committees are out of control’ – James Watson, 2010Prior to receiving an  Honorary Doctorate from University College Cork last evening, Watson spoke to journalists telling them that he was in favour of less regulation for clinical trials as this could speed up the process of finding a cure for cancer: “We’re terribly held back on clinical tests by regulations which say that no one should die unnecessarily during trials; but they are going to die anyway unless we do something radical. I think the ethics committees are out of control and that it should be put back in the hands of the doctors. There is an extraordinary amount of red tape which is slowing us down. We could go five times faster without these committees“.

Speaking in an introductory address to the gathered audience, Prof. Gerald O’Sullivan of CCRC praised Watson: “His accomplishments and contributions transcend boundaries, disciplines, and generations. One of the greatest scientists ever, he is also a respected leader, a gifted administrator, a brilliant author and a beacon in the Gaelic Diaspora“. Watson mentioned his mother’s family during his speech who left Co. Tipperary during the famine.

Prof. O’Sullivan continued, “Hopefully mankind will also constructively use its increasing technical capability to live peacefully. If so,  the humans in future millennia  may not know of  many from our time but they will know of the structure of DNA and of Watson and Crick as by then the ramifications of its discovery will have impinged on life in ways that we cannot yet imagine“.

The Inaugural Cancer Lecture of the Cork Cancer Research Centre by James Watson is available as a series of video clips here.

An edited version of this article appears on the Guardian.co.uk Science Blog. You can read it here.

Posted by Eoin Lettice at 8:45 AM

Labels: Cancer, CCRC, DNA, Guardian, James Watson, UCC, Watson and Crick

Detection of circulating and disseminated tumor cells in blood is a promising methodology to diagnose cancer dissemination or to follow up cancer patients during therapy. Today, the detection analyses of these cells are performed in medical laboratories requiring labor intensive, expensive and time-consuming sample processing and cell isolation steps. A full tumor cell detection analysis can take more than a day. A lab-on-chip, integrating the many processing steps, would enable a faster, easy-to-use, cost-effective detection of tumor cells in blood. They are therefore labor-saving and minimally invasive, increasing the patient’s comfort and the efficiency of today’s healthcare.

In a preceding joint project by some of the partners (MASCOT FP6-027652), individual microfluidic modules for cell isolation, cell counting, DNA amplification and detection have been developed. Based on this expertise and strengthened by additional partners, the development of a fully automated, lab-on-chip platform to isolate, count and genotype CTCs is envisaged within the framework of the MIRACLE project. For genotyping, genetic material (i.e. the mRNA) will be extracted from the cells and multiple cancer related markers will be amplified based on multiplex ligation dependent probe amplification (MLPA) followed by their detection using an array of electrochemical sensors. Full integration of all steps requires innovative research and processing steps that need a combination of the multidisciplinary and unique expertise of the different project partners (ranging from microfluidics to interfacing, miniaturization, and integration skills). The resulting lab-on-chip tumor detection system will be well ahead of the current state-of-the-art, revolutionizing cancer diagnostics and individualized theranostics.

Within the framework of the MIRACLE project, imec as project coordinator, collaborates with the Universitat Rovira I Virgili (Spain), the Institut für Mikrotechnik Mainz, AdnaGen, ThinXXs and Consultech (Germany), MRC Holland (The Netherlands), the Oslo University Hospital (Norway), the KTH Royal Institute of Technology, Multi-D and Fujirebio Diagnostics (Sweden), ECCO the European CanCer Organisation and ICsense (Belgium) and Labman (UK). The project aims at developing a fully automated and integrated microsystem providing the genotype (gene expression profile) of CTCs and DTCs starting from clinical samples. MIRACLE is partly funded by the European Commission (FP7-ICT-2009.3.9).

Source: Interuniversity Microelectronics Centre (IMEC)

Main News Category: Cancer / Oncology

Also Appears In:  Medical Devices / Diagnostics,  Blood / Hematology,

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From left, cancer researchers Jim Dimitroulakos, Dr. Glen Goss and Ian Lorimer will be able to develop and refine their discoveries under one roof after they move to the new $15.8-million facility, the Ottawa Hospital Cancer Centre.

Photograph by: Wayne Cuddington, The Ottawa Citizen

OTTAWA — It took John Bell more than a decade to turn his cancer-killing virus into a treatment that could be tested in patients. And it could take another two years before Bell and his research team know for sure if the genetically engineered virus destroys tumours effectively.

But with a new lab about to open at The Ottawa Hospital Cancer Centre, Bell expects that for future medical discoveries, the road to early-stage testing could be shortened dramatically, giving patients a faster route to experimental therapies to fight cancer.

“Instead of 10 years, it would be down to two years,” said Bell, a senior scientist at the affiliated Ottawa Hospital Research Institute.

The expanded third floor of the cancer centre is still an active construction zone, although new lab benches have been installed and a dozen offices carved out. But by

October, when work on the $15.8-million lab is due to be completed, the facility will finally allow cancer researchers to develop and refine their discoveries under one roof.

And for the first time, all the specialized facilities and equipment will be in place for researchers to test experimental therapies for their safety and effectiveness in patients.

Such tests, an exhaustive effort in three phases, require labs to follow the strict standards of drug regulators such as Health Canada and the U.S. Food and Drug Administration. Regulation manufacturing suites are needed to handle the experimental drugs, while self-contained testing suites are required to analyze genetic and tumour samples collected from patients.

In short, the new facility will enable researchers to shepherd their own discoveries through a longer section of the drug-development pipeline.

“As far as cancer-drug development is concerned, we’ll finally be able to do everything onsite, from target validation to Phase 3 clinical trials, which is really fantastic given that 10 years ago, we couldn’t do any of that,” said Dr. Glen Goss, a medical oncologist and one of the researchers who will benefit from the new lab.

The state-of-the-art facility will also allow the institute to compete with top-ranked cancer research centres such Toronto’s Princess Margaret Hospital, Montreal’s Jewish General Hospital and Vancouver’s B.C. Cancer Agency.

Mike McBurney, director of Ottawa’s cancer-research program, said having a world-class lab, where scientists and oncologists work side by side, makes it easier to recruit young talent.

“This creates a melting pot, where if you want to have coffee, you’re going to have to talk to somebody from either the clinical or laboratory side,” said McBurney. “And those kinds of unstructured discussions are what breed discoveries and innovation.”

More than 300 scientists, oncologists, technicians and graduate students work cheek-by-jowl in the existing research lab. The expanded facility allows McBurney to plan for as many as 100 more people to be hired over the next five years.

The new lab lays the groundwork for the cancer centre’s plan to position Ottawa as a hub of “translational research,” that critical stage at which scientists attempt to turn medical discoveries into useful therapies for patients.

Researchers call it the “bench-to-bedside” approach.

According to McBurney, nine out of 10 discoveries languish in the lab, never to be turned into actual treatments. Federal and provincial governments agree and have pumped in millions of new dollars to help bring more medical discoveries to market.

Under the federal Conservatives, $32 million has flowed to Ottawa researchers for new labs and equipment — the single largest health grant awarded to the city’s researchers. An additional $18.5 million has come from the provincial Liberals. The cancer centre has been a major beneficiary, receiving a total of $16.3 million, with most of it going to support work on Bell’s tumour-killing virus, known as JX594.

The virus, genetically engineered from a version used to vaccinate against smallpox, has been designed to kill cancer cells, but spare normal ones. This means it can be injected into tumours in heavy doses without causing harm to the patient. Experience with the new drug is too short to permit any conclusion about its ultimate effectiveness, but physicians who have used it are encouraged so far.

Bell said his team has at least 20 other viruses with cancer-fighting potential under development, meaning more clinical trials are planned in the coming years.

Meanwhile, Goss and his collaborators are planning a clinical trial of their own in the new lab. Starting this fall, the team will test whether statins, drugs normally used to lower cholesterol levels, can be used to fight cancer in combination with Tarceva, a new-generation lung-cancer therapy.

Tarceva entered the cancer arsenal in the past few years after studies showed it lengthened survival among patients who didn’t respond to other treatments. It’s among a new wave of “targeted therapies” that zero in on particular cells and cell processes closely tied to the growth or spread of tumours.

For some patients, these treatments are more effective and have more tolerable side effects than traditional chemotherapy, which attacks both healthy and cancerous cells in the hopes of wiping out the cancerous ones.

Biochemist Jim Dimitroulakos, one of Goss’s collaborators, has done test-tube and animal studies showing that when used in combination, Tarceva and statins have the potential to shrink tumours.

The trial, being conducted with fellow biochemist Ian Lorimer, is expected to involve up to 40 patients with lung, head or neck cancer. As an experimental therapy that has not yet been approved by government regulators, the trial is restricted to patients who have exhausted conventional treatments.

By the Numbers

$15.8 million — Total cost of new lab

$6.3 million — Federal government contribution

$9.5 million — Money to come from fundraising

$10 million — Funding for clinical trials into cancer-killing viruses and other anti-cancer therapies to come from Ontario government

$750,000 — Funding for clinical trials into cancer-killing viruses and other anti-cancer therapies to come from drug-maker Roche

ptam@thecitizen.canwest.com

–Ralph W. Moss, Ph.D.
Cancer Decisions

References:

Song KY, Wong J, Gonzalez L, et al. Antitumor efficacy of viral therapy using genetically engineered Newcastle disease virus [NDV(F3aa)-GFP] for peritoneally disseminated gastric cancer. J. Mol. Med. 2010;88(6):589-596.
Csatary LK, Gosztonyi G, Szeberenyi J, et al. MTH-68/H oncolytic viral treatment in human high-grade gliomas. J. Neurooncol. 2004;67(1-2):83-93.
Csatary LK, Csatary E, Moss RW. Re: Scientific interest in newcastle disease virus is reviving. J Natl Cancer Inst. 2000 Mar 15;92(6):493-4.
Csatary LK, Moss RW, Beuth J, Töröcsik B, Szeberenyi J, Bakacs T. Beneficial treatment of patients with advanced cancer using a Newcastle disease virus vaccine (MTH-68/H). Anticancer Res. 1999 Jan-Feb;19(1B):635-8.
Schulze T, Kemmner W, Weitz J, et al. Efficiency of adjuvant active specific immunization with Newcastle disease virus modified tumor cells in colorectal cancer patients following resection of liver metastases: results of a prospective randomized trial. Cancer Immunol. Immunother. 2009;58(1):61-69.
Wagner S, Csatary CM, Gosztonyi G, et al. Combined treatment of pediatric high-grade glioma with the oncolytic viral strain MTH-68/H and oral valproic acid. APMIS. 2006;114(10):731-743.

ORLANDO, FL (UroToday.com) – Prostate cancer is an ideal target for chemoprevention strategies that, at present, may be the best approach, according to a group of Italian researchers. They cite a growing body of evidence that compounds from green tea (catechins: the most common are EGCG, EGC, ECG and EC) might posses anti-tumor activity.

Recently they showed that a Green Tea Catechins extract (GTCs) was very effective at inhibiting cancer growth in vitro and in animal model, triggering apoptotic death in cancer cells probably through induction of the nuclear form of Clusterin. In 2006 they published the result of a clinical trial demonstrating that about 90% inhibition of CaP development was indeed achievable by oral administration of GTCs to humans for one year.

Although this was the first study showing that GTCs are safe and very effective for treating pre-malignant lesions, it is evident that this important result needs confirmation with a larger study. But another important issue is still open: understanding whether CaP onset was definitively prevented or simply delayed by treatment. The purpose of this study was to evaluate results the after 2 years.

In the 2006 study, a cohort of 60 human volunteers bearing HG-PIN, the main pre-malignant lesion of CaP, were given 600mg/die of GTCs (n = 30) or placebo (n = 30) for 1y. At the end of the study, only 1 tumor was diagnosed among the GTCs-treated men, while 9 cancers were found among the placebo-treated men, with no significant side or adverse effects recorded. To check whether CaP onset was definitely prevented or simply delayed by treatment, the researchers managed to convince about 50% of patients from both arms (all asymptomatic) to undergo another round of prostate mapping by needle biopsy 2ys after suspension of GTCs administration.

They detected 1 more cancer in the cohort previously belonging to the GTCs-arm, and 2 more in that once belonging to the placebo-arm. Thus, 3 years after the beginning of the study and 2 years after suspension of GTCs administration, final results were: 11cancers in untreated volunteers versus 2 in those given GTCs for 1 year.

This novel data further strengthen the researchers previous result, strongly suggesting that CaP development might be definitely inhibited in men bearing HG-PIN (High-Grade Prostatic Intraepithelial Neoplasia) by administration of 600mg/day of GTCs for just 1year.

Rev Urol. 2002 Summer; 4(3): 157–158.

PMCID: PMC1475983
Copyright © 2002 MedReviews, LLC
High-Grade Prostatic Intraepithelial Neoplasia on a Prostate Biopsy—What Does It Mean?
Alan W Partin, MD, PhD
Department of Urology, Johns Hopkins University School of Medicine, Baltimore, MD
Top
Predicting Cancer Following a Diagnosis of High-Grade Prostatic Intraepithelial Neoplasia on Needle Biopsy: Data on Men with More than One Follow-Up Biopsy

Investigators in the field of urology, oncology, and pathology have been attempting to unravel the mystery of early diagnosis, treatment, and monitoring of men with prostate cancer for several decades. Recently a great deal of attention has been focused on obtaining a better understanding, both pathologically as well as clinically, of the pre-malignant lesion of prostatic intraepithelial neoplasia. Although not diagnostic of prostate cancer on a needle biopsy, many morphologic, molecular, histopathological, epidemiological, and genetic studies have offered strong evidence that high-grade prostatic intraepithelial neoplasia (HGPIN) is in fact a precursor lesion to development of invasive prostatic adenocarcinoma. Early studies in the literature that first characterized this relationship suggested that histologic evidence of HGPIN on a prostate biopsy predicted a nearly 50% risk of finding prostate cancer on a subsequent prostate biopsy. Through the years, much larger, prospective, population-based studies have suggested that this likelihood is more in the range of 25% to 30%. Knowing that the likelihood of finding prostate cancer after a “negative prostate biopsy” ranges between 10% and 25% if a repeat biopsy were performed brings into question the need or clinical utility of recommending immediate repeat prostate biopsy when HGPIN is seen on initial prostate biopsy.

Kronz and associates from the Department of Pathology at the Johns Hopkins Hospital in Baltimore, Maryland have recently published their work investigating how various HGPIN-related factors other than clinical and pathological variables can be used for cancer prediction following an initial diagnosis of HGPIN on a needle biopsy. This important research, published in The American Journal of Surgical Pathology this year, should be required reading for all urologists performing and interpreting the results of prostate needle biopsies within their practice.

The authors conclude that HGPIN does in fact carry with it a clinically significant likelihood of finding cancer in a subsequent prostate biopsy (30% overall), and that with increasing number of cores with HGPIN the likelihood of finding prostate cancer increases (to as much as 75% when more than three cores are found to have this histologic abnormality). They also caution that if cancer is not found on the first two follow-up biopsies after the initial diagnosis of HGPIN, it is unlikely that cancer will be found with subsequent biopsies, and the patient should be followed appropriately with yearly exams and PSA testing.

Presented by Brausi Maurizio, MD, Bettuzzi Saverio, MD, Peracchia Giancarlo, MD, Rizzi Federica, MD, and Corti Arnaldo, MD, at the Annual Meeting of the American Urological Association (AUA) – May 17 – 22, 2008. Orange County Convention Center – Orlando, Florida, USA.

Reported by UroToday.com Contributing Editor Christopher P. Evans, MD, FACS

UroToday – the only urology website with original content written by global urology key opinion leaders actively engaged in clinical practice.

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Copyright © 2008 – UroToday

Article URL: http://www.medicalnewstoday.com/articles/111208.php

If you visit a Chevy dealer to buy a new car, the odds are pretty good that he is not going to recommend that you purchase a Ford. And he is even more likely not to recommend that you hang on to the perfectly good car you already own. Perhaps not surprisingly, the situation is very similar when men visit physicians who treat localized prostate cancer: Surgeons are more likely to recommend surgery, and radiation specialists will call for X-rays or proton beams, researchers reported Monday in the Archives of Internal Medicine. Only if a man visits a disinterested primary-care physician is he more likely to be offered the alternative that some experts consider optimal — no treatment at all until the tumor has begun to progress into a more life-threatening form, a concept known as watchful waiting.

The situation may arise, at least in part, because there is such a smorgasbord of potential treatments available, including surgery, radiation, chemotherapy and watchful waiting. If a man chooses surgery, it can be performed by conventional surgery, laparoscopically or with the assistance of a robot. If radiation, it can be delivered conventionally, with proton beams, or by implantation of radioactive seeds, an approach called brachytherapy. What makes the decision even harder, Dr. Michael J. Barry of the Foundation for Informed Medical Decision Making in Boston wrote in an editorial accompanying the report, is that there is an “embarrassing” absence of clinical trials comparing the therapies. The only trial for men over 65, in fact, found that surgical removal of the tumor was no more likely to improve survival than watchful waiting. The National Cancer Institute is now sponsoring a trial to compare treatment to monitoring, but results are not expected until later this year. Until those results are available, however, men rely on their physicians to help them make a decision, and those decisions, framed by anecdotal experience, are likely to be biased.

A 1988 survey of radiation oncologists and urologists — who perform most prostate surgeries — asked them which treatment they would prefer if they developed localized prostate cancer. A full 92% of radiation oncologists said they would prefer radiation, while 79% of urologists would opt for a radical prostatectomy. In a 2000 survey, researchers asked the two groups how they would prefer to treat patients, and the results were very similar.

To determine if the doctors’ actions jibed with their words, Dr. Thomas L. Jang, now at the Cancer Institute of New Jersey in New Brunswick, and his colleagues used data from the government’s Surveillance, Epidemiology and End Results (SEER) database to study 85,088 men over the age of 65 who were diagnosed with localized prostate cancer. Half were seen only by urologists, 44% by urologists and radiation oncologists, 3% by urologists and medical oncologists and 3% by all three groups. Only 22% of the men visited a primary-care physician during the period between diagnosis and treatment, and only 17% visited one they had an established relationship with.

Among men ages 65 to 69, 70% of men who saw only a urologist had a radical prostatectomy. If they also saw a radiation oncologist, however, 78% had radiation therapy. Among men who saw a urologist and a medical oncologist, 53% had surgery, 17% had radiation therapy, 16% had watchful waiting and 14% had chemotherapy–androgen-deprivation therapy to starve the tumor of needed hormones. Men who also visited a primary-care physician were more likely to be prescribed watchful waiting, which is the only one of the treatment regimens without side effects. Older men were also more likely to be prescribed watchful waiting, reflecting a growing adherence to treatment guidelines that recommend against aggressive therapy in men who may have less than 10 years to live.

Part of the reason for the emphasis on treatment, Barry said, is the large capital investments surgeons make for robotically assisted surgery and that radiation therapists make for proton beam therapy or newer techniques of radiation therapy. Moreover, current reimbursement rules do not allow physicians adequate time to educate patients about the pros and cons of the various procedures.

So, if you are diagnosed with prostate cancer and considering therapy, the recommendation is to do the same kind of background research you might do in buying a car. Consider all the options, decide which side effects you are prepared to live with or, in the final analysis, think about whether you really need it in the first place.

– Thomas H. Maugh II

Clinica di Oncoematologia Pediatrica, Azienda Ospedaliera-Universita di Padova, Padova, Italy.

BACKGROUND: A boy age 14 years who was in complete remission from Stage IIB small cell osteosarcoma, which was misdiagnosed as Ewing sarcoma and consequently was treated, developed inoperable lung metastases when he was off therapy. He received second-line treatment for recurrent Ewing sarcoma, including chemotherapy and radiotherapy, and obtained only a temporary response. A compassionate treatment with all-trans retinoic acid (ATRA) and interferon-alpha (IFNalpha) was then undertaken. METHODS: The patient initially was treated according to the national SE91 protocol for nonmetastatic Ewing sarcoma. After a bilateral pulmonary recurrence, he received second-line chemotherapy and irradiation of the largest metastasis, with a temporary partial response. The patient was then treated with a combination of oral ATRA (90 mg/m(2) for 3 days per week) and subcutaneous IFNalpha (3 x 10(6) U/m(2) 5 days per week) for 4 months. The same therapy also was administered for the control of residual disease after surgery for a total duration of 1 year of ATRA/IFN treatment. During the first 3 weeks of therapy, ATRA pharmacokinetics were studied. RESULTS: After progression of the patient’s disease, despite the administration of first-line and second-line chemotherapy, combined treatment with ATRA/IFNalpha yielded a partial remission, which allowed surgical resection of the largest metastasis. The same therapy was effective in preventing tumor recurrence after incomplete removal of the remaining metastases. Treatment was well tolerated, and the patient is in stable complete remission 14 months after the end of therapy. The pharmacokinetics results confirmed the indication of an intermittent schedule for oral ATRA therapy. CONCLUSIONS: ATRA/IFNalpha treatment may be considered as an alternative approach in the treatment of patients with metastatic osteosarcoma who have disease that is resistant to conventional chemotherapy and in the treatment of patients with minimal tumor residue. Copyright 2000 American Cancer Society.

American Journal of Clinical Nutrition, Vol. 87, No. 4, 985-992, April 2008

Katharina Nimptsch, Sabine Rohrmann and Jakob Linseisen

1 From the Division of Cancer Epidemiology, German Cancer Research Centre, Heidelberg, Germany

Background:Anticarcinogenic activities of vitamin K have been observed in various cancer cell lines, including prostate cancer cells. Epidemiologic studies linking dietary intake of vitamin K with the development of prostate cancer have not yet been conducted.

Objective:We evaluated the association between dietary intake of phylloquinone (vitamin K1) and menaquinones (vitamin K2) and total and advanced prostate cancer in the Heidelberg cohort of the European Prospective Investigation into Cancer and Nutrition.

Design:At baseline, habitual dietary intake was assessed by means of a food-frequency questionnaire. Dietary intake of phylloquinone and menaquinones (MK-4–14) was estimated by using previously published HPLC-based food-content data. Multivariate-adjusted relative risks of total and advanced prostate cancer in relation to intakes of phylloquinone and menaquinones were calculated in 11 319 men by means of Cox proportional hazards regression.

Results:During a mean follow-up time of 8.6 y, 268 incident cases of prostate cancer, including 113 advanced cases, were identified. We observed a nonsignificant inverse association between total prostate cancer and total menaquinone intake [multivariate relative risk (highest compared with lowest quartile): 0.65; 95% CI: 0.39, 1.06]. The association was stronger for advanced prostate cancer (0.37; 0.16, 0.88; P for trend = 0.03). Menaquinones (Vitamin K2) from dairy products had a stronger inverse association with advanced prostate cancer than did menaquinones from meat. Phylloquinone (Vitamin K1) intake was unrelated to prostate cancer incidence (1.02; 0.70, 1.48).

Conclusions:Our results suggest an inverse association between the intake of menaquinones, but not that of phylloquinone, and prostate cancer. Further studies of dietary vitamin K and prostate cancer are warranted.

The Natural Products Association (NPA) is filing an amicus curiae brief in the U.S. Supreme Court defending the dietary supplement industry against an overreaching and potentially damaging decision by the Ninth Circuit Court of Appeals.

The case, Matrixx Initiatives, Inc. v. Siracusano, presents the critical question of whether mere nondisclosure of adverse event reports (AERs) can give rise to liability under federal securities laws – even when those reports are not statistically significant. In an unprecedented decision, the Ninth Circuit held that the answer is “yes,” and permitted a class action lawsuit to proceed.

“While the case involves an over-the-counter product, there are clear implications for the supplement industry, especially as the reporting requirements for OTCs and supplements were enacted in the same piece of legislation” said John Gay, Executive Director and CEO of the Natural Products Association. “In this brief, we were able to focus on our industry’s perspective, and bring to bear NPA’s experience with the legislative history of the law that created the AER system.”

“The decision is wrong because evaluation of safety signals is a scientific judgment ultimately made by the FDA. Companies cannot possibly guess in advance what will be deemed adequate disclosure years later in collateral litigation,” said Scott Bass, of NPA’s counsel Sidley Austin LLP. “The statute explicitly states that AERs are not proof of causation.”

“The practical consequence of the Ninth Circuit’s decision, if it is not reversed, is that manufacturers of dietary supplements very likely will be forced to disclose all AERs, however insignificant, in order to avoid meritless – but expensive – strike suits against the supplement industry,” said Jonathan Cohn, who authored the brief for Sidley Austin.

“The Ninth Circuit’s action is not good for manufacturers, not good for consumers, and just is not good law. We hope the Supreme Court will agree,” said Gay.

Source:
Natural Products Association

Main News Category: Complementary Medicine / Alternative Medicine

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