As they age, most men will develop some sort of prostate abnormality, such as enlargement of the prostate or prostate cancer. A drug that is activated by prostate-specific antigen (PSA) “a protein produced by both the normal and diseased prostate gland”could be effective in treating prostate diseases while leaving non-prostate cells unharmed.

Simon Williams, Ph.D., of The Johns Hopkins Oncology Center in Baltimore, and colleagues synthesized a PSA-activated protoxin, called PRX302, and tested it in prostate cancer cells and several animal models. PRX302 caused prostate cancer tumors to shrink when injected directly into mice tumors. Because PRX302 is activated only in the presence of PSA, cells that do not express PSA were unaffected. A phase I clinical trial has already begun to test the toxicity of PRX302.

“The development of novel therapies to treat prostate cancer could be of substantial benefit to large numbers of men,” the authors write. “Current therapies for these local recurrences include techniques that are associated with substantial morbidity, including increased rates of incontinence and impotence.”

Contact: Samuel Denmeade, Johns Hopkins University School of Medicine

Other highlights in the March 7 JNCI

Note: The Journal of the National Cancer Institute is published by Oxford University Press and is not affiliated with the National Cancer Institute. Attribution to the Journal of the National Cancer Institute is requested in all news coverage. Visit the Journal online.

Contact: Liz Savage

Journal of the National Cancer Institute

This large adjuvant trial will compare the effectiveness of oral
lapatinib versus placebo given in high-risk patients following surgery.
SCCHN is the sixth most common cancer worldwide (1): 600,000 people are
diagnosed with SCCHN annually (1), 40,000 in the United States (2) and
100,800 in Europe alone.(3) 40,000 people die from the disease every
year.(3)

The design of this Phase III trial was based on recent results from two
large-scale, independent randomized studies which have established the
addition of chemotherapy to radiation therapy as the new standard of care
in the post-operative treatment of high-risk SCCHN patients with additional
use of chemotherapy.(4, 5) However, research suggests that approximately
one quarter to one third of advanced head and neck cancers that are
primarily treated with surgery and radiation therapy come back following
treatment.(4, 5)

“The initiation of this trial represents another exciting step towards
understanding the role of lapatinib in other tumor types beyond breast
cancer,” says Professor Jean Bourhis, Head of Radiation-Oncology
Department, Institute Gustave Roussy, France and principal investigator for
this trial. “There is a significant group of patients who are at high-risk
of disease recurrence following surgery, and they need new treatments that
can be combined with standard chemoradiation therapy.”

This global, Phase III study will enroll 680 high-risk patients with
locally advanced head and neck cancer (stages II, III and IVa) that have
undergone surgery. Patients will receive, within four to seven weeks after
surgery, either lapatinib (1500 mg) or placebo tablets once-daily with
radiotherapy and cisplatin for seven weeks. After this time, patients will
continue with either lapatinib or placebo treatment for one year. The
principal objective will be to investigate the length of time without
disease symptoms, and overall survival with other clinical factors will
also be measured. Side effects will be assessed using the National Cancer
Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE).

Results from a Phase I dose-escalation study of lapatinib (doses ranged
from 500 mg to 1500 mg) plus chemoradiation in 31 head and neck cancer
patients were also presented at the conference. Results identified 1500 mg
of lapatinib taken once-daily with chemotherapy and radiotherapy as the
optimal dose for this combination, and this dose was selected for the Phase
III study. Additionally, 89% of patients had a tumor response to this
combination treatment. The most common side effects in the Phase I study
were mouth ulcers (87%), radiation skin injury (65%), nausea (61%),
swallowing difficulties (52%) and vomiting (52%).(6)

“Having already shown promise as a breast cancer treatment, we are very
excited to continue investigating lapatinib in SCCHN,” said Paolo Paoletti,
MD, Senior Vice President, Oncology Medicine Development Centre, GSK. “We
recognize the importance of developing a new treatment approach to
difficult- to-treat tumor types, such as head and neck cancer, which may
offer hope to patients in need of a further treatment option.”

Lapatinib blocks the activation of two key receptors, EGFR (ErbB1) and
HER2 (ErbB2), associated with increased growth and development of this type
of head and neck tumor. Stimulation of these receptors is associated with
multiple processes involved in tumor growth. An excessive presence of these
receptors has been reported in a variety of human tumors and is associated
with poor outcome and reduced survival.

About SCCHN

SCCHN is the most common form of cancer of the head and neck, and
approximately two-thirds of all patients are diagnosed with advanced
disease. EGFR and HER2 are two types of receptors found on tumors which
play a key role in the development of this type of head and neck cancer.
Researchers have found that the excessive expression of EGFR receptors is
nearly universal in SCCHN disease, with large numbers of HER2 receptors
present in 20 to 40 percent of tumors.(7,

About Lapatinib

Lapatinib was discovered and developed by GSK as an oral once daily
therapy, and is currently being investigated in breast cancer and other
solid tumors. Phase III results of lapatinib plus capecitabine show
superior efficacy to capecitabine alone in women with HER2 positive
advanced breast cancer who have progressed following prior therapy,
including trastuzumab.(9)

The most frequent side effects related to lapatinib from clinical
trials to date are mild to moderate (grade 1 or 2) diarrhea, nausea,
vomiting, fatigue and rash.(10)

GSK is using advanced technologies, including pharmacogenomics, to
better define patient populations that may respond to lapatinib.

Lapatinib, in combination with capecitabine, has been submitted for
marketing approval in the United States, European Union and Switzerland for
the treatment of advanced or metastatic HER2 positive breast cancer in
women who have progressed despite prior therapy, including trastuzumab.
Registration dossiers have also been filed in Australia, Canada and New
Zealand.

GSK in Oncology

GSK Oncology is dedicated to producing innovations in cancer that will
make profound differences in the lives of patients. Through GSK’s “bench to
bedside” approach, we are transforming the way treatments are discovered
and developed, resulting in one of the most robust pipelines in the
oncology sector. Our worldwide research in oncology includes partnerships
with more than 160 cancer centres. GSK is developing a new generation of
patient focused cancer treatments in prevention, supportive care,
chemotherapy and targeted therapies.

About GlaxoSmithKline

GlaxoSmithKline — one of the world’s leading research-based
pharmaceutical and healthcare companies — is committed to improving the
quality of human life by enabling people to do more, feel better, and live
longer. For company information, visit GlaxoSmithKline at
gsk.

For further information on the trial please visit
clinicaltrials.

TYKERB(R) (lapatinib) is a registered trademark of the GlaxoSmithKline
group of companies in the United States and Europe.

References

(1) Study EGF102988 protocol.

(2) Wang J, Xi L, Hunt J, et al. American Association for Cancer Research.
“Expression Pattern of Chemokine Receptor 6 (CCR6) and CCR7 in
Squamous Cell Carcinoma of the Head and Neck Identifies a Novel
Metastatic Phenotype,” citing Greenlee, R. T., Hill-Harmon, M. B.,
Murray, T., and Thun, M. Cancer statistics, 2001. CA Cancer J. Clin.,
51: 15-36, 2001.

(3) Mouth Cancer Foundation. Initiative of the Restorative Dentistry
Oncology Clinic: rdoc/ accessed 3rd Jan 2007.

(4) Bernier J, Domenge C et al. Postoperative irradiation with or without
concomitant chemotherapy for locally advanced head and neck cancer.
NEJM; 2004 May 6;350(19):1945-52.

(5) Cooper J, Pajak TF et al. Postoperative concurrent radiotherapy and
chemotherapy for high-risk squamous-cell carcinoma of the head and
neck. NEJM; 2004 May 6;350(19):1937-44.

(6) El-Hariry, I., Harrington K. et al. A phase I, open label study
(EGF100262) of lapatinib plus chemoradiation in patients with locally
advanced squamous cell carcinoma of the head and neck (SCCHN). Oral
presentation, 1st International Meeting on Innovative Approaches in
Head & Neck Oncology, Barcelona, Spain. 22nd – 24th February 2007.

(7) Khademi B, Shirazi FM, Vasei M, et al. The expression of p53, cerbB-1
and cerbB-2 molecules and their correlation with prognostic markers in
patients with head and neck tumors. Cancer Letters 2002;184:223-230.

(8) O-Charoenrat P, Modjtahedi H, Rhys-Evans P et al. Epidermal Growth
Factor-like Ligands Differentially Up-Regulate Matrix
Metalloproteinase 9 in Head and Neck Squamous Carcinoma Cells. Cancer
Research, 2000; 60:1121-1128.

(9) Geyer C, Forster J, Lindquist D, Chan S, Romieu C et al. Lapatinib
plus capecitabine for HER2-positive advanced breast cancer. N Engl J
Med 2006; 355;2733-43.

(10) GSK data on file. Ongoing studies to 15 November 2005.

GlaxoSmithKline
gsk

“High cholesterol is a chronic health problem for millions of Americans,” says study author Kory Floyd. “Although many pharmaceutical medications exist to treat this condition, our research shows promise for an additional, non-medical treatment that could provide an added benefit to these patients.” Floyd acknowledges that additional research needs to be completed to confirm the benefits in patients.

According to Floyd, this research is particularly interesting because it highlights the effects of showing affection. “There are many studies showing that patients benefit from receiving care and attention during illness,” says Floyd. “Our research shows that it’s as rewarding to give as it is to receive.”

Kory Floyd, Ph.D., is an Associate Professor of Human Communication at Arizona State University and has studied affectionate communication for over a decade.

Human Communication Research is one of the official journals of the prestigious International Communication Association and concentrates on presenting the best empirical work in the area of human communication. It is a top-ranked communication studies journal and one of the top ten journals in the field of human communication. Major topic areas for the journal include language and social interaction, nonverbal communication, interpersonal communication, organizational communication and new technologies, mass communication, health communication, intercultural communication, and developmental issues in communication. For more information, please visit blackwellpublishing/hcr.

Blackwell Publishing is the world’s leading society publisher, partnering with 665 medical, academic, and professional societies. Blackwell publishes over 800 journals and has over 6,000 books in print. The company employs over 1,000 staff members in offices in the US, UK, Australia, China, Singapore, Denmark, Germany, and Japan and officially merged with John Wiley & Sons, Inc.’s Scientific, Technical, and Medical business in February 2007. Blackwell’s mission as an expert publisher is to create long-term partnerships with our clients that enhance learning, disseminate research, and improve the quality of professional practice. For more information on Blackwell Publishing, please visit blackwellpublishing or blackwell-synergy.

Previous studies have suggested that blacks are at greater risk for colorectal cancer and have a higher mortality rate than whites, but it is unclear whether this disparity is due to biological differences or differences in access to health care. No study has examined racial disparity in colorectal cancer according to both health care utilization and the results of screening.

To look at this question, Adeyinka O. Laiyemo, M.D., of the Division of Cancer Prevention, National Cancer Institute, Bethesda, Md., and colleagues used data from the ongoing Prostate, Lung, Colorectal, and Ovarian Cancer Screening (PLCO) Trial. A total of 60,572 African-American and non-Hispanic white participants in this study underwent flexible sigmoidoscopy screening in ten centers across the United States from November 1993 to July 2001. This initial screening found suspicious lesions in similar percentages of blacks and whites (25.5% vs 23.9%).

Of those screened, 13,743 white and 767 black men and women were referred to their own physicians for a diagnostic colonoscopy. The PLCO did not pay for the follow-up visits. Of those referred, 9,944 (72.4%) whites and 480 (62.6%) blacks went on to see a physician and have a colonoscopy.

The researchers also reviewed the colonoscopy results for these 10,424 subjects. No statistically significant difference between blacks and whites was found in the prevalence of polyps, advanced adenomas, advanced pathology in small adenomas, or colorectal cancer.

“We did not observe any meaningful differences in the yield of colorectal cancer neoplasia by race,” the authors write. “We observed a lower rate of diagnostic evaluation following an abnormal screening among blacks as compared with whites.” Taken together, the two findings “suggest that the biology of colorectal cancer may not be materially different by race, at least in the early stages of carcinogenesis, but instead that healthcare utilization differences among the races may play a more important role in the observed disparities in colorectal cancer.”

In an accompanying editorial, John Z. Ayanian, M.D., M.P.P., of Harvard Medical School, Boston, says the study “identified an important barrier to optimal care – follow-up of abnormal findings on sigmoidoscopy – that affected many white participants and an even larger proportion of black participants.”

He notes that “colorectal cancer is one important disease in which racial and socioeconomic disparities in outcomes can most readily be eliminated by ensuring that all eligible adults are effectively screened and abnormal findings are fully treated.”

Study limitations: Only participants with lesions in the distal colon would be identified by flexible sigmoidoscopy screening.

Reprinted with kind permission from kaisernetwork. You can view the entire Kaiser Daily Health Policy Report, search the archives, or sign up for email delivery at kaisernetwork/dailyreports/healthpolicy. The Kaiser Daily Health Policy Report is published for kaisernetwork, a free service of The Henry J. Kaiser Family Foundation.

© 2009 Advisory Board Company and Kaiser Family Foundation. All rights reserved.

On February 13, Principal Investigator Chiu Wong, M.D., Associate
Professor of Medicine, New York-Presbyterian Hospital/Weill Cornell Medical
Center and a Cordis Corporation Consultant, treated the first patient in
the trial. Prior to the start of the ECLIPSE Trial, the ExoSeal(TM)
Vascular Closure Device had been used in 150 patients participating in a
first-in-human study for the device.

“The results from the first-in-man study were very encouraging, and
this trial will help us determine whether those results can be maintained
in a larger number of patients,” said Dr. Wong. “As an interventional
cardiologist, I welcome the opportunity to investigate a device that could
help patients recover faster from a catheterization procedure.”

The ExoSeal(TM) Vascular Closure Device features a synthetic
bioabsorbable polymer and is being studied to determine whether it can
enable expedited hemostasis (the cessation of bleeding), faster patient
ambulation (ability to walk) and reduced bed-stay after a catheterization
procedure. It also represents Cordis’ entry into the vascular closure
device market. Nearly eight million patients undergo cardiac
catheterization procedures annually.

“The swift progress of the ExoSeal(TM) Vascular Closure Device from the
proof-of-concept stage to a pivotal trial in only seven months marks a
major milestone in Cordis’ efforts to accelerate the development of new
devices to improve the treatment of vascular diseases,” said Campbell
Rogers, M.D., Chief Technology Officer, Cordis Corporation. “The ECLIPSE
Trial will help us evaluate whether the ExoSeal(TM) Vascular Closure Device
could make a significant and positive difference in patients’ comfort as
well as recovery time following a catheterization procedure.”

Catheterization procedures involve the temporary insertion of a
catheter into an artery, usually the femoral artery, through a vascular
puncture. While a variety of methods, such as manual compression, sandbags
and mechanical clamps have been used to close the puncture site and stop
the bleeding after the catheter is removed, many of these methods cause
significant discomfort and require several hours of bed-rest.

About Cordis Corporation

Cordis Corporation, a Johnson & Johnson company, is a worldwide leader
in developing and manufacturing interventional vascular technology. Through
the company’s innovation, research and development, physicians worldwide
are better able to treat the millions of patients who suffer from vascular
disease. For more information, visit cordis.

Cordis Corporation
cordis

Ronald A. DePinho, MD, of Dana-Farber has created mice that form tumors that are more genetically complex and unstable — and therefore a better stand-in for human cancers — than those of conventional genetically engineered mouse models of cancer. To characterize these mouse tumors, DePinho collaborated with Lynda Chin, MD, also at Dana-Farber, to perform high-resolution array-CGH profiling, a genome-scanning technology that can define regions of DNA abnormalities.

The report has been posted as an advanced online by the journal Nature and will appear in a forthcoming print version.

The scientists, working with a large dataset generated by the Chin laboratory during the past several years, compared the patterns of these chromosomal changes in the mice with patterns observed in more than 400 human tumor specimens, including melanoma, lung, colon, and pancreatic cancers, and multiple myeloma.

The comparisons showed that genetic instability in the mouse cancer cells caused DNA alterations that in many cases were identical to such changes in human tumors. This match up, said the researchers, suggested that the new mouse model may be useful in guiding the search for genes that are important for cancer growth. To that end, it may facilitate research associated with the National Institutes of Health-funded Human Cancer Genome Atlas Project, which involves sifting the entire human DNA and identifying the immensely complicated, interacting molecular changes that initiate and maintain tumors.

“We found a rather striking overlap of genetic alterations in the mouse and human cancers, which should greatly help us sort out genetic events that drive cancers from those that are simply irrelevant ‘passenger’ events,” DePinho said.

Indeed, using the new “instability” model of cancer in collaboration with Michael Stratton, PhD, and Andy Futreal, PhD, at the Wellcome Trust Sanger Institute in England, the team discovered a pair of gene mutations involved in a type of human blood cancer.

Stratton, Futreal, Chin, and DePinho are co-senior authors of the report.

As part of the ongoing Cancer Genome Project at the Sanger Institute, its researchers analyzed human cancer cell lines and clinical samples to identify the new mutated genes. These studies have uncovered an unexpectedly large number of genetic alterations present in the typical human cancer genome, presenting challenges in the identification of truly causative events.

DePinho said that the overlap in patterns of genetic abnormalities found in both mouse and human tumors shows that cancer mechanisms in the two species are more alike than had been thought.

Futreal, co-director of the Cancer Genome Project at the Sanger Institute, said that such mouse models and cross-species genomic comparisons will be of “real importance” in facilitating the identification of new human cancer genes and understanding their role in the formation of tumors, “as well as a potential avenue to explore new therapeutic strategies.”

Conventional mouse models are made by transferring a cancer-causing oncogene into a mouse embryo. “You plug it into the mouse, and lo and behold, it gets cancer,” explained Richard Maser, PhD, of Dana-Farber, one of the study’s lead authors. “But that’s rigging the game — it’s not identical to the process by which tumors normally arise,” he said. These tumors lack some key characteristics of human tumors, such as genomic instability — pieces of chromosomes breaking apart and reattaching, which result in widespread abnormalities like missing genes or extra copies of genes some of which are essential to the tumors’ formation.

In the current study, the scientists used gene knockouts to create mice whose cells lacked crucial molecules whose role is to guard the genome from instability and chaos in the DNA. As a result, the mice developed T-cell acute lymphoblastic leukemia/lymphoma, or T-ALL, and the cancer cells exhibited “rampant genome instability” leading to a complex pattern of mutations, chromosomal rearrangements, gene amplifications and gene deletions similar to those in human solid tumors.

The mouse model’s close resemblance to human T-ALL enabled the scientists to rapidly and efficiently identify two genes, FBXW7 and PTEN, to be commonly deleted or mutated in this type of human cancer.

The research was supported by grants from the National Cancer Institute, the Wellcome Trust, and the Center for Applied Cancer Research of the Belfer Institute for Innovative Cancer Science at Dana-Farber, which DePinho heads.

Dana-Farber Cancer Institute (dana-farber) is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute.

Contact: Bill Schaller

Dana-Farber Cancer Institute

These results were published in the May 15, 2009, edition of the journal Transplantation, which is currently in press.

Yun Miao, MD, PhD, Jason Everly, PharmD, Steve Woodle, MD, and colleagues at UC compared lung, colon, breast, prostate, bladder, kidney and skin cancer data in 635 adult transplant recipients from the Israel Penn International Transplant Tumor Registry with that of about 1.2 million adults from the general population in the Surveillance, Epidemiology and End Results (SEER) database.

“It has been known for some time that transplant recipients are at an increased risk of developing cancer, but the outcomes of cancers that arise in organ transplant recipients have not been defined,” says Woodle, professor and chief of transplant surgery and co-author of the study.

“In this study, we wanted to examine the influence of transplantation on the outcomes of individual types of cancers arising in organ transplant recipients,” adds Miao, co-author and research fellow in the division.

The Israel Penn International Transplant Tumor Registry is the largest and most comprehensive transplant tumor registry in the world and was created by doctors at the UC College of Medicine.

The SEER registry collects information on cancer incidence, survival and prevalence for roughly 26 percent of the United States population and compiles reports and statistics based on this information along with cancer mortality rates for the entire nation.

A comparison of results in transplant recipients to the general population also demonstrated that transplant patients were more likely to have early stage renal cell (kidney) cancer and more advanced colon, breast, bladder and skin cancer at the time of diagnosis.

Disease-specific survival was worse in the transplant population for each of these seven cancers analyzed and was a negative risk factor for survival.

Now, researchers want to conduct further studies to find out why this may be the case.

“Transplant patients receive immunosuppressive therapies to prevent them from rejecting transplanted organs,” says Woodle. “We want to see if immunosuppressive therapies contribute to the poorer outcomes in transplant recipients.”

He says the worse outcomes in transplant recipients may have occurred because this population is not as healthy as the general population or because their cancers may be more aggressive as a result of their immunosuppression treatments.

“Some of our data supports this premise, as the extent of the cancers at diagnosis were greater in the transplant recipients,” Woodle continues. “This was surprising since transplant recipients are generally followed more closely than the general population.”

Everly, co-author and board-certified oncology pharmacist in the division, says that this data may change the way physicians screen transplant patients for cancer.

“We found that most cancers developed within five years following transplantation,” he says, noting that more frequent and detailed checks should be made in order to catch the cancer in its earliest stages. “This may alter the way doctors should screen these patients for cancer.”

This study was investigator-initiated and supported by research grants from Astellas Pharmaceuticals.

According to the National Institutes of Health’s National Heart, Lung and Blood Institute (NHLBI), high cholesterol affects more than 65 million Americans. Because high cholesterol does not cause symptoms, individuals may not be aware that they are at increased risk of developing heart disease or experiencing a heart attack. September is National Cholesterol Education Month, and is a good opportunity for people to get their cholesterol levels checked and take steps to lower their levels if they are high.

“This data illustrates that younger adults with high cholesterol are not taking their medication as prescribed, putting them at increased risk for developing heart disease, worsening their long term clinical outcomes and ultimately increasing the cost of their care,” said Troyen A. Brennan, M.D., M.P.H., Executive Vice President and Chief Medical Officer, CVS Caremark. “CVS Caremark engages plan participants with chronic diseases, such as high cholesterol, by addressing barriers to evidence-based care. We engage patients in their care early in the process by providing disease and therapy education and help them improve medication adherence through proactive intervention and outreach.”

The study examined adherence to cholesterol lowering medications by evaluating de-identified data for more than 74,000 adult patients from the CVS Caremark Health Management Claims Database who incurred claims for a cholesterol lowering medication between January 1, 2008 and December 31, 2008. All study participants were continuously eligible for pharmacy benefits for the entire evaluation period. Results found that only 42 percent of patients between the ages of 18-34 were optimally adherent to their medications with a medication possession ratio (MPR) of greater than 80 percent. In addition, among those patients aged 35-44, only 50 percent were identified as optimally adherent to their high cholesterol medication.

The CVS Caremark Proactive Pharmacy Care approach engages patients earlier with education and personalized outreach to improve adherence. The Adherence to Care solution is a mail and retail based program designed to impact patient behavior through timely interventions that include face-to-face, first fill counseling; IVR and Web refill reminders, renewals and pick-up prompts; and personalized letters about the importance of staying on a prescribed therapy sent to those patients who have stopped filling a maintenance prescription and their health care provider. The Adherence to Care program has been shown to help increase adherence to high cholesterol therapies with those members under 45 years of age who participate in the program experiencing an MPR increase of more than 9 percent.

Medication possession ratio (MPR) is the standard statistic used to measure medication adherence via pharmacy claims. MPR assesses if a patient has a sufficient quantity of medication dispensed to suggest the medication is being taken as prescribed. MPR is represented as a ratio of total days supply of medication divided by the total days in the measurement period. In this study, MPR was calculated using the DMAA methodology on pharmacy claims incurred by the study subjects. Patients with an MPR greater than or equal to 80 percent were considered optimally adherent to therapy. This analysis is an observational study only, and the results demonstrate a correlation between patients under age 45 and suboptimal adherence to cholesterol lowering medications; however, as in most observational studies, the causal nature of this relationship cannot be determined.

About CVS Caremark

CVS Caremark is the largest provider of prescriptions in the nation. The Company fills or manages more than 1 billion prescriptions annually. Through its unmatched breadth of service offerings, CVS Caremark is transforming the delivery of health care services in the U.S. The Company is uniquely positioned to effectively manage costs and improve health care outcomes through its more than 6,900 CVS/pharmacy and Longs Drugs stores; its Caremark Pharmacy Services division (pharmacy benefit management, mail order and specialty pharmacy)

The authors reach their conclusion from a study of 279 women with invasive breast cancer. The disease was in the early stages in 204 women, and advanced in the remainder.

Serum levels of vitamin D, parathyroid hormone, and calcium were measured in both groups of women.

The results showed that women with early stage disease had significantly higher levels of vitamin D and significantly lower levels of parathyroid hormone than did the women with advanced disease.

There was little difference in calcium levels between the two groups.

The authors say that the exact reasons for the disparity are unclear, nor is it known whether the low levels of vitamin D among those with advanced disease are a cause or consequence of the cancer itself.

But it is known that vitamin D treatment boosts the activity of certain key genes and dampens it down in others. One gene that is boosted is p21, which has an important role in controlling the cell cycle.

Low levels of vitamin D may therefore promote progression to advanced disease, venture the authors.

Laboratory studies have also shown that vitamin D stops cancer cells from dividing and that it enhances cell death. And the epidemiological evidence points to a link between rates of, and deaths from, breast cancer and exposure to sunlight.

Click here to view the paper in full

Contact:
Dr Carlo Palmieri, Cancer Research UK Laboratories, Department of Cancer Medicine, Faculty of Medicine, Imperial College, Hammersmith Hospital, London, UK