FDA approves first molecular-based lab test to detect metastatic breast cancer

The US Food and Drug Administration has approved the first molecular-based laboratory test for detecting whether breast cancer has spread (metastasized) to nearby lymph nodes. The GeneSearch BLN Assay detects molecules that are abundant in breast tissue but scarce in a normal lymph node. The presence or absence of breast cancer cells in underarm lymph nodes is a powerful predictor of whether the cancer has spread and is used to help decide appropriate therapy for a woman with metastatic breast cancer. Lymph nodes are part of the system that helps protect the body against infection. The first lymph node that filters fluid from the breast is called the 'sentinel node,' because that is where breast cancer cells are likely to spread first. During a lumpectomy or mastectomy to remove a breast tumor, surgeons commonly remove the sentinel node for examination under a microscope. Sometimes the sentinel node is examined immediately and if tumor cells are found, additional lymph nodes are removed. A more extensive microscopic examination, requiring one to two days for results, is almost always performed. If tumor cells are only found with the later microscopic examination, the patient may require a second surgery to remove the remaining lymph nodes. --Click the title of this post to read the full article from its source--

FOXP3 gene suppresses tumor growth, HER-2 expression

Researchers at the University of Michigan Comprehensive Cancer Center have identified a gene linked to the development of an aggressive form of breast cancer. The researchers found that the gene, FOXP3, suppresses tumor growth. FOXP3 is located on the X chromosome, which means a single mutation can effectively silence the gene. This is unusual, as only one other gene linked to cancer has been found on the X chromosome.When one copy of the FOXP3 gene is silenced, the researchers found in studying mice, 90 percent of the mice spontaneously developed cancerous tumors. The researchers also looked at FOXP3 in human breast tissue cells, comparing cancerous and non-cancerous cells. FOXP3 was found to be either deleted or mutated in a substantial portion of the cancer sample: about 80 percent of the cancer tissues studied did not express the gene at all. --Click the title of this post to read the full article from its source--

4 New Breast Cancer Genes Identified

Scientists have identified four new breast cancer genes and predict that more clues on the genetics of breast cancer await discovery. The findings may ultimately help scientists understand who's at risk for breast cancer and what to do about it. Doctors already know that variations in the BRCA1 and BRCA2 genes make breast cancer and ovarian cancer more likely. But experts have long suspected that other genes also affect breast cancer. Now, researchers say they've found four genes that affect breast cancer risk. But the new findings don't explain all cases of breast cancer. A complex mix of genetic and lifestyle factors likely affect breast cancer risk....Easton's team screened the genes of nearly 4,400 women with breast cancer and 4,300 women without breast cancer. They checked their results in more than 44,400 other women, roughly half of whom had breast cancer. Four genes -- the FGFR2, TNRC9, MAP3K1, and LSP1 genes -- had variations that were more common in women with breast cancer than in women without breast cancer, the study shows. --Click the title of this post to read the full article from its source--

Gene profiling predicts resistance to breast cancer drug Herceptin

Using gene chips to profile tumors before treatment, researchers at Harvard and Yale Universities found markers that identified breast cancer subtypes resistant to Herceptin, the primary treatment for HER2-positive breast cancer. They say this advance could help further refine therapy for the 25 to 30 percent of breast cancer patients with this class of tumor. --Click the title of this post to read the full article from its source--

Rogue Gene Linked To Breast And Childhood Cancer Risk

Women who inherit one damaged copy of a gene called PALB2 have double the risk of developing breast cancer. And children who inherit two damaged copies have a newly identified serious disorder linked to childhood tumours, according to the findings from two papers published by scientists in Nature Genetics. --Click the title of this post to read the full article from its source--

Breast Cancer Stem Cells Seem to Survive Radiation Therapy

Breast cancer stem cells, a type of cell that scientists have recently discovered is difficult to kill, may be especially resistant to radiation therapy, a new study suggests. In fact, the radiation can even increase the growth of these stubborn stem cells, report researchers from the University of California, Los Angeles, David Geffen School of Medicine. "This population of stem cells is more radiation-resistant than are non-stem cells," said Dr. Frank Pajonk, an assistant adjunct professor of radiation oncology at UCLA and corresponding author on the study. "We are the first to report this." Radiation treatment involves exposure to high-energy rays or particles that destroy cancerous cells. It is often recommended after surgery for breast cancer, according to the American Cancer Society. --Click the title of this post to read the full article from its source--

Epigenetic drugs, promising for breast cancer treatment

Worldwide, cancer persists as one of the most important diseases that affect the human being. The knowledge on the molecular bases of cancer generated during the last decades has been successfully translated into small but significant gains in overall cancer survival rates due to better primary prevention measures, improved diagnostic methods and the development of more effective and specific therapies, collectively termed "molecular targeted therapies". In the context of these new forms of treatment, epigenetic or transcriptional cancer therapy is clearly promising. Epigenetics refers to the function of DNA that does not depend on the coding DNA sequence itself but on the accessory molecules and mechanisms affected by DNA. It is known that epigenetic alterations are equally if not more important than classical genetic alterations to disrupt the function of tumour suppressor genes. The two most studied epigenetic aberrations common to all types of cancer are DNA hypermethylation and histone deacetylation, which cooperate to silence the expression of tumour suppressor genes, just as gene mutations and gene deletions do. The big difference between these two alternative ways that tumour cells use to inactivate tumour suppressor genes is that, while the reversal of genetic alterations is technically almost unfeasible in clinical scenarios, the function of these epigenetically inactivated suppressor genes is easily reactivated by pharmacological means. In this inaugural issue of PLoS ONE, Dr. Dueñas-Gonzalez's group from the Instituto de Investi gaciones Biomédicas of the Universidad Nacional Autónoma de México and the Instituto Nacional de Cancerología, Mexico, demonstrate, for the first time, that a combination of a DNA methylation and a histone deacetylase inhibitor, can reactivate the expression of more than a thousand genes in primary tumours of breast cancer patients. --Click the title of this post to read the full article from its source--

Genomic Health Announces Multiple New Findings On Oncotype DX(TM) Based On Evaluation Of More Than 20,000 Tumor Samples

Genomic Health, Inc. (Nasdaq: GHDX) today announced the results of several studies looking at the roles and relationships of genes measured by the company's Oncotype DX breast cancer assay, including an analysis of more than 10,000 node-negative tumors indicating that all 21 genes impact the assessment of an individual woman's tumor. This research was presented at the 29th Annual San Antonio Breast Cancer Symposium.Oncotype DX measures the expression of 16 cancer-related genes plus 5 reference genes of an individual tumor to generate a "Recurrence Score" to quantify risk of recurrence and likelihood of response to chemotherapy. To assess the degree to which components of this multi-gene assay influence the Recurrence Score, researchers measured expression of the 16 individual cancer genes relative to reference genes in 10,618 tumor specimens on a scale of 0 to 15, where a one-unit increment is associated with a twofold change in expression. Results suggest that every cancer gene used in the Oncotype DX 21-gene panel impacts the Recurrence Score due to the potentially large variation in quantitative expression for each gene in different patients. The study found this result even though expression of certain genes and gene families; including ER, HER2 and a group of five genes linked to proliferation, have the largest coefficients used in calculating the Recurrence Score. --Click the title of this post to read the full article from its source--