Twenty years of screening for breast and prostate cancer – the most diagnosed cancer for women and men – have not brought the anticipated decline in deaths from these diseases, argue experts from the University of California, San Francisco and the University of Texas Health Science Center at San Antonio in an opinion piece published in the "Journal of the American Medical Association."

There is concern that mastectomy is over-utilized in the United States, which raises questions about the role of surgeons and patient preference in treatment selection for breast cancer. New data from an observational study found that breast-conserving surgery was presented and provided in the majority of patients evaluated. Surgeon recommendations, patient decisions, and failure of breast-conserving surgery were all found to be contributing factors to the mastectomy rate.

DURHAM, N.C. -- One person's breast cancer is not the same as another person's, because the gene mutations differ in each tumor. That makes it difficult to match the best therapy with the individual patient.

Using a finding that the genetic complexity of tumors in mice parallels that in humans, researchers at the Duke University Institute for Genome Sciences and Policy and Duke University Medical Center are starting trial studies in mice, just like human clinical trials, to evaluate whether understanding tumor diversity can improve cancer treatment.

HOUSTON - Researchers at The University of Texas M. D. Anderson Cancer Center have identified a protein that marks the tumor suppressor p53 for destruction, providing a potential new avenue for restoring p53 in cancer cells.

The new protein, called Trim24, feeds p53 to a protein-shredding complex known as the proteasome by attaching targeting molecules called ubiquitins to the tumor suppressor, the team reported this week in the Proceedings of the National Academy of Sciences Online Early Edition.

The enzyme target, Brk, is shown to be an accelerator of HER2-positive tumors

Tumor cells in a particular subset of breast cancer patients churn out too much of a protein called ErbB2 -- also often called HER2 -- which drives the cells to proliferate unchecked. Patients unlucky enough to be in this group -- about one in four -- have poorer prognoses and clinical outcomes than those who don't.

The drugs Herceptin and Lapatinib, prescribed in combination with other chemotherapeutic agents, have improved this picture significantly, but leave plenty of room for improvement: they suppress ErbB2 but are effective against less than half of ErbB2-producing tumors. Moreover, patients with tumors that do respond usually develop resistance to these drugs.

Australian scientists have identified a way to 'switch off' a molecule, a key player in the molecular processes that trigger breast cancer and certain forms of leukaemiaterm.

The molecule, known as Gab2, operates downstream of a major breast cancer oncogene, HER2, the target of the drug Herceptin.

A research team from the Garvan Institute of Medical Research, led by Professor Roger Daly, has found a novel way of blocking signals to and from Gab2, preventing it from fulfilling its role in cell proliferation. The finding is published online today in the EMBO Journal.

In 2002, Professor Daly identified the important role of Gab2 in breast cancer. His task since then has been to work out exactly how Gab2 functions, and how to stop it.

An organized population-based breast cancer screening program in Norway and an approach to screening that relies on physician- and self-referrals in Vermont are equally sensitive for detecting cancer, researchers report in the July 29 online issue of the Journal of the National Cancer Institute. But the recall rate for abnormal mammograms was lower in Norway.

Breast cancer screening in the United States is usually initiated in response to a physician's recommendation (known as "opportunistic screening"), and women are advised to have annual screening mammograms. By contrast, breast cancer screening programs in Norway and in some other European countries regularly send letters to all women in a specific age range inviting them to have a screening mammogram. The Norway program aims for women to be screened every two years. The differences between the two approaches make it relatively difficult to compare their effectiveness, and few studies have aimed to do so previously.

The identification of five genes involve in the metastasistermterm of breast tumours to the lung is the principal finding of a scientific team made up of two bodies from the University of Navarra, the Applied Medical Research Centre (CIMA) and the University Hospital of the University of Navarra.

Doctor Alfonso Calvo, researcher in the area of Oncology at the CIMA, led the work with the special collaboration of Doctor Ignacio Gil Bazo, cancer specialist from the University Hospital. The study made up a significant part of Mr Raúl Catena’s PhD thesis.

For this research, recently published in the scientific journal Oncogene, a transgenic mouse model which presented a greater tendency for developing metastasis was employed. The increase in what is known as the Vascular Endothelial Growth Factor (VEGFterm) in its mammary glands triggered profound changes in the tumoural structure, which enabled the malignant cells to leave the tumour and invade the lungs.

The invasion and spread of cancer cells to other parts of the body, known as metastasistermterm, is a principal cause of death in patients diagnosed with breast cancer. Although patients with early stage, small, breast tumours have an excellent short term prognosis, more than 15 to 20 per cent of them will eventually develop distant metastases, and die from the disease. Vascular invasion — through lymphatic and blood vessels — is the major route for cancer spreading to regional lymph nodes and to the rest of the body.

Researchers have discovered a new family of agents that inhibit the growth of estrogen-dependent breast cancer cells. The finding, described today at a meeting of the Endocrine Society, has opened an avenue of research into new drugs to combat estrogen-dependent breast cancers.

“Tamoxifen is useful in that it is very effective at blocking recurrence of breast cancer in patients for whom the entire tumor is removed,” Shapiro said. “But for patients who still have existing tumors, eventually those tumors will become resistant.”

Shapiro’s team sought to target other steps in the pathway of estrogen action. Using a technique they developed that can quickly determine whether the target DNA is – or is not – bound by the estrogen-receptor complex, the team was able to screen a long list of potential therapeutic compounds to see if they inhibited the binding of the complex to the DNA. They then tested these agents in ER-positive breast cancer cells.

The collaboration included researchers from the University of Colorado, the University of North Carolina, and the departments of molecular and integrative physiology and of chemistry at Illinois.

St. Louis, May 21, 2008 — A unique genetic signature can alert physicians to high-risk breast tumors that are masquerading as low-risk tumors, according to research at Washington University School of Medicine in St. Louis and collaborating institutions. Although these tumors are apparently estrogen-receptor positive — meaning they should depend on estrogen to grow — they don't respond well to anti-estrogen therapy.

Until now, doctors had no way to know these tumors would be unresponsive because their pathology is deceptive — the tumors appear to be more easily treatable estrogen-receptor-positive tumors, but they rapidly lose their estrogen receptors. The researchers demonstrated that the chance for cancer recurrence in such patients is significantly higher, and standard post-operative care with long-term anti-estrogen therapy is often not effective. The genetic signature defined by the researchers will permit doctors to identify their high-risk patients and direct them to more effective therapy.

PHILADELPHIA – Women with breast cancer have more aggressive disease and lower survival rates if they are overweight or obese, according to findings published in the March 15 issue of Clinical Cancer Research, a journal of the American Association for Cancer Research.

“The more obese a patient is, the more aggressive the disease,” said Massimo Cristofanilli, MD, associate professor of medicine in the Department of Breast Medical Oncology at The University of Texas M.D. Anderson Cancer Center. “We are learning that the fat tissue may increase inflammation that leads to more aggressive disease.”

Anti-inflammatory drugs like aspirin may reduce breast cancer by up to 20 per cent, according to an extensive review carried out by experts at London’s Guy’s Hospital and published in the March issue of IJCP, the International Journal of Clinical Practice.

But they stress that further research is needed to determine the best type, dose and duration and whether the benefits of regularly using non-steroidal anti-inflammatory drugs (NSAIDs) outweigh the side effectsterm, especially for high-risk groups.

“Our review of research published over the last 27 years suggests that, in addition to possible prevention, there may also be a role for NSAIDs in the treatment of women with established breast cancer” says Professor Ian Fentiman from the Hedley Atkins Breast Unit at the hospital, part of Guy's and St Thomas' NHS Foundation Trust.

Women whose breast cancer came back after treatment had almost twice as much estrogen in their blood than did women who remained cancer-free – despite treatment with anti-estrogen drugs in a majority of the women –according to researchers in a study published in the March issue of Cancer Epidemiology, Biomarkers and Prevention, a journal of the American Association for Cancer Research.

The findings suggest that high levels of estrogen contribute to an increased risk of cancer recurrence, just as they lead to the initial development of breast cancer, said the study’s lead author, Cheryl L. Rock, Ph.D., a professor in the Department of Family and Preventive Medicine at the University of California, San Diego.

Targeting and killing the non-malignant cells that surround and support a cancer can stop tumor growth in mice, reports a research team based at the University of Chicago Medical Center in the March 1, 2008, issue of the journal Cancer Research. The discovery offers a new approach to treating cancers that are resistant to standard therapy.

Many solid tumors develop elaborate mechanisms to prevent recognition and elimination by the immune system. Due to their genetic instability they often discard the tumor antigen-presenting cell-surface structures that alert the immune system that these cells are harmful. Without these “flags,” the white blood cells fail to recognize and kill infected or cancerous cells. These tumors then often grow rapidly and resist treatment with chemotherapyterm or efforts to boost the immune system's response to the tumor.