Saturday, July 26, 2014

New Gene BRCAX Help Women Live Longer With Breast Cancer

Barron’s Medical Journal Reporting From Rice University Houston, Texas USA

New Gene BRCAX Help Women Live Longer With Breast Cancer


HOUSTON (AP ) ----- Barron’s Medical Journal at A Susan G Komen Fundraising event in Houston Texas at the world famous Hotel ZA ZA reporting on a major concern among scientist, why is there a slight increase in breast cancer rates with Black Women ? The American Cancer Society provides an overview of female breast cancer statistics in the United States, including data on incidence, mortality, survival, and screening. Approximately 232,340 new cases of invasive breast cancer and 39,620 breast cancer deaths are expected to occur among US women in 2013. One in 8 women in the United States will develop breast cancer in her lifetime. Breast cancer incidence rates increased slightly among African American women; decreased among Hispanic women; and were stable among whites, Asian Americans/Pacific Islanders, and American Indians/Alaska Natives from 2006 to 2010. Historically, white women have had the highest breast cancer incidence rates among women aged 40 years and older; however, incidence rates are converging among white and African American women, particularly among women aged 50 years to 59 years. Incidence rates increased for estrogen receptor-positive breast cancers in the youngest white women, Hispanic women aged 60 years to 69 years, and all but the oldest African American women. In contrast, estrogen receptor-negative breast cancers declined among most age and racial/ethnic groups. These divergent trends may reflect etiologic heterogeneity and the differing effects of some factors, such as obesity and parity, on risk by tumor subtype. Since 1990, breast cancer death rates have dropped by 34% and this decrease was evident in all racial/ethnic groups except American Indians/Alaska Natives. Nevertheless, survival disparities persist by race/ethnicity, with African American women having the poorest breast cancer survival of any racial/ethnic group. Continued progress in the control of breast cancer will require sustained and increased efforts to provide high-quality screening, diagnosis, and treatment to all segments of the population.

Not all hereditary breast cancers are caused by BRCA1 and BRCA2. In fact, researchers now believe that at least half of hereditary breast cancers are not linked to these genes. Scientists also now think that these remaining cases of hereditary breast cancer are not caused by another single, unidentified gene, but rather by many genes, each accounting for a small fraction of breast cancers In 1995 and 1996, studies of DNA samples revealed that Ashkenazi (Eastern European) Jews are 10 times more likely to have mutations in BRCA1 and BRCA 2 genes than the general population. Approximately 2.65 percent of the Ashkenazi Jewish population has a mutation in these genes, while only 0.2 percent of the general population carries these mutations.

Further research showed that three specific mutations in these genes accounted for 90 percent of the BRCA1 and BRCA2 variants within this ethnic group. This contrasts with hundreds of unique mutations of these two genes within the general population. However, despite the relatively high prevalence of these genetic mutations in Ashkenazi Jews, only seven percent of breast cancers in Ashkenazi women are caused by alterations in BRCA1 and BRCA2.

Researchers in Finland, Iceland and Sweden, working with scientists at the National Human Genome Research Institute (NHGRI) of the National Institutes of Health (NIH), have found evidence of a gene that appears to increase susceptibility to hereditary breast cancer. The study examined women who live in Nordic countries and who have three or more female family members with breast cancer. Published in the August 15, 2000 issue of the Brought To You By 2014 Cadillac ELR

Proceedings of the National Academy of Sciences (PNAS), this finding may help to explain why some women with a family history of hereditary breast cancer are at particularly high risk of developing the potentially fatal disease, even when they lack mutations in two previously identified breast cancer susceptibility genes, BRCA1 and BRCA2.

While scientists have not yet identified a third BRCA gene, they have succeeded in pinpointing its probable location to chromosome 13, the same chromosome that contains the previously identified BRCA2 gene. Mutations of BRCA1 and BRCA2 impair the body's cell production of tumor suppressor proteins.

"We've located what looks like a very good region in the human genome in which to search for a third breast cancer susceptibility gene," said Dr. Olli Kallioniemi, former senior scientist at NHGRI. He is one of 35 scientists in 14 laboratories in the United States, Finland, Sweden, Iceland and Germany who collaborated on the study.

Sam Houston Biotech approximately 30% of malignant breast cancers demonstrate overamplification of the human epidermal receptor type 2 (HER2) gene. HER-2 can be resistant to low-doses of anthracycline-based chemotherapy.

The Good News is that science has advanced. Sections of microarray provide targets for parallel in situ detection of DNA, RNA and protein targets in each specimen on the array. The better News is that Genomics is on the Clock. Genomics provide a faster cheaper more effective way to detect the Her2 gene by using Semiconductor Sequencing. A example of this technique is Gennxeix Biotech Inc Semiconductor Sequencing. “Quantum Theory” In Action for Breast Cancer Patients. One of the major player and touch down makers for breast cancer is Houston Texas Methodist Hospital. In A clinical Trial A Rev. Noel Denison, a retired Methodist minister, was diagnosed with locally advanced HER2-positive breast cancer and is enrolled in the study at Methodist, one of only two locations in the United States. The clinical trial is for locally advanced or metastatic HER2-positive breast cancer and combines standard chemotherapy with trastuzumab emtansine, better known in the breast cancer world as T-DM1, and pertuzumab, a monoclonal antibody that also attaches to HER2 on cancer cells. Using Genomics and semiconductors to detect breast cancer plus T-DM1 to treat breast cancer is a winning combination. What is T-DM1? T-DM1 is in a new class of cancer-fighting agents called antibody drug conjugates. By combining the antibody trastuzumab directly with docetaxel (standard chemotherapy) and/or pertuzumab, the T-DMI is designed to attack the tumor cells directly and deliver the chemotherapy. Trastuzumab emtansine (T-DM1) consists of our proprietary DM1 cancer-killing agent attached to the HER2-binding antibody, trastuzumab, developed by Genentech (a member of the Roche Group) using our linker and methods of attachment. Trastuzumab emtansine is in global development by Roche under a collaboration agreement between ImmunoGen and Genentech. Marketing applications for trastuzumab emtansine are under review in the US and Europe. The Defense and the most dangerous aspect of breast cancer is its ability to spread to distant sites, most tumors are initially unable to do that Learning more specifically what triggers metastases may provide additional targets for preventing and treating the malignant process that causes cancer deaths. It’s widely accepted that cancers acquire the ability to spread through the gradual accumulation of genetic changes, and experiments have also shown that these changes occur in parallel with changes in the protein content and 3-dimensional patterning of the protein meshwork that creates their immediate surroundings Gene that stops the growth of KCNK9 Genes is gene is p53. p53 is a fundamental determinant of cancer susceptibility, p53 integrates stress signals and elicits apoplectic responses that maintain genomic stability. When cells sense a decrease in oxygen availability (hypoxia), they develop adaptive responses in order to sustain this condition and survive. If hypoxia lasts too long or is too severe, the cells eventually die. Hypoxia is also known to modulate the p53 pathway, in a manner dependent or not of HIF-1 (hypoxia-inducible factor-1), the main transcription factor activated by hypoxia. The p53 protein is a transcription factor, which is rapidly stabilized by cellular stresses

Breast cancer is a common disease. Each year, approximately 200,000 women in the United States are diagnosed with breast cancer, and one in nine American women will develop breast cancer in her lifetime. But hereditary breast cancer - caused by a mutant gene passed from parents to their children - is rare. Estimates of the incidence of hereditary breast cancer range from between 5 to 10 percent to as many as 27 percent of all breast cancers.

In 1994, the first gene associated with breast cancer - BRCA1 (for Breast Cancer1) was identified on chromosome 17. A year later, a second gene associated with breast cancer - BRCA2 - was discovered on chromosome 13. When individuals carry a mutated form of either BRCA1 or BRCA2, they have an increased risk of developing breast or ovarian cancer at some point in their lives. Children of parents with a BRCA1 or BRCA2 mutation have a 50 percent chance of inheriting the gene mutation

Wednesday, July 2, 2014

BMJ Has Under Covered How Patients Can live 14 % longer With Breast Cancer


Barrons Medical Journal Reporting from Columbia University New York City, NY USA

BMJ Has Under Covered How Patients Can live 14 % longer With Breast Cancer:


New York City ( AP ) How does breast cancer get to the point where patients have to surrender to the disease. For friends and family members to be able to help breast cancer patients with treatment and other options. BMJ has under covered how patients can live 74 % longer with breast cancer. Breast

cancer patients now have a new best friend. Genomics research is making a major difference, Oncologist can now pin point your genes, help stop the spread of breast cancer and extend the life of so many patients. The three ways breast cancer spreads is Tissues, Lymph systems and blood.

• Tissue. The cancer spreads from where it began by growing into nearby areas.

• Lymph system. The cancer spreads from where it began by getting into the lymph system. The cancer travels through the lymph vessels to other parts of the body.

Blood. The cancer spreads from where it began by getting into the blood. The cancer travels through the blood vessels to other parts of the body.

The sentinel lymph node is the first lymph node or group of nodes draining breast cancer. In case of established cancerous dissemination it is postulated that the sentinel lymph node/s is/are the target organs primarily reached by metastasizing cancer cells from the tumor. Thus, sentinel lymph nodes can be totally void of cancer, due to the fact that they were detected prior to dissemination. Historically, complete axillary lymph node dissections had been performed with lumpectomy or mastectomy primarily for staging purposes, providing information that was used to determine adjuvant chemotherapy. The complete axillary lymph node dissection (CALND) may not change the course of the disease, although with removal of involved axillary nodes, the control of local recurrence in the axilla is easier. The morbidity associated with this procedure is substantial in terms of limitation of arm motion, arm pain, and chronic lymphedema. The concept of a sentinel lymph node (SLN) was spawned by Cabanas his study of penile carcinoma.The pioneering studies of sentinel lymph node metastasis (SLNM) originated with the study of melanoma patients; the goal was to spare these patients the morbidity of large regional lymph node dissections. Patients with melanomas who had SLN surgery were found to have a relatively orderly progression of lymph node metastases.

Lymphangiogenomics is an Integrated Project of the European Commission´s Sixth Framework Programme for Life Sciences, Genomics, and Biotechnology for Health (LSHG-CT-2004-503573) with 13 participating consortium members. Its aim is to thoroughly dissect the processes of lymphangiogenesis and to compare them with angiogenesis at the genetic, molecular, cellular, and functional level.

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The lymphatic vasculature is essential for the maintenance of fluid balance in the body, for immune defence, and for the uptake of dietary fat. Absent or damaged lymphatic vessels may lead to lymphedema, a chronic and disfiguring swelling of the extremities, sometimes necessitating the amputation of the affected limb. In addition, lymphatic vessels promote metastatic spread of cancer cells to distant organs - a leading cause of death in patients with cancer, and a major obstacle in the design of effective therapies. The lymphatic vessels were identified hundreds of years ago, yet very limited understanding exists of their development, function, and molecular mechanisms underlying their disease process. The aim of this project is to discover novel genes important for lymphatic vascular versus blood vascular development and function and to study the functional role and therapeutic potential of their gene products in lymphangiogenesis using state-of-the-art technologies. The methods we use

include large-scale knockout and knock-down of the mouse genome, the embryonic stem (ES) technology, knock-down of zebra fish genes by morpholino-antisense and positional cloning of disease susceptibility genes involved in lymphangiogenesis. These studies will provide fundamental new understanding of the molecular and cellular basis of lymphangiogenesis and therefore enable scientists to develop therapies to suppress the growth of lymphatic vessels (e.g. for cancer, inflammatory diseases) or to stimulate their growth (e.g. for tissue ischemia, lymphedema). The Integrated Project “Lymphangiogenomics” puts forward ambitious, competitive research objectives addressing biological processes of high medical importance using a multidisciplinary analysis and validation approach.

Scientist researched Genome-wide association studies looking for genetic variations known as single nucleotide polymorphisms (SNP). SNPs are alterations in the genetic code in which a single nucleotide, the individual building blocks that make up DNA, is changed. The researchers found that variations in four SNPs located in a region of chromosome 6 were present more often in the breast cancer patients, suggesting that genes in this region might contribute to the risk of breast cancer. The researchers also confirmed the finding of previous studies indicating that the locus named FGFR2 is associated with a 20 percent increased risk of breast cancer. Panoincell uses Semiconductor Sequencing Chips that create a direct connection between Biochemical and digital information, bringing these two languages together.Hybrid's chips are designed like any other semiconductor chips.

Pairing proprietary semiconductor technology with sequencing chemistry a nucleotide is incorporated into a strand of DNA by a polymerase, a hydrogen ion is released.

Sam Houston Biotech used a high-density array of micro-machined wells for bioctechnology process in a massive way. Each well holds a different DNA template. Beneath the wells is an ion-sensitive layer and beneath that a proprietary Ion sensor. When a nucleotide, is added to a DNA template and is then incorporated into a strand of DNA, a hydrogen ion will be released. The charge from that ion will change the pH of the solution, which can be detected. Hybrid's sequencer—essentially will call the base, going directly from Biochemical information to digital information. If there are two identical bases on the DNA strand, the voltage will be double, and the chip will record two identical bases called. This process uses no scanners, no cameras, no light—each Nucleotide incorporation is recorded in a real time process. Panoincell uppressed p53, as it is in many cancers, defective cells multiply, fueling Breast Cancer. p53 can't order a bad cell to kill itself without p63 and p73 also being active. When metastatic Breast Cancer occurs p63 is inactive.The reactivation of TAp63 could benefit patients with metastatic breast cancer. Viral transduction of a few genes for the reprogramming of human somatic cells into induced pluripotent stem (iPS) cells.Identifying conditions that can replace viral transduction of oncogenic transcription factors (TFs) and enhance reprogramming efficiency. Hybrid Pharma have found that neural progenitor cells can be reprogrammed with fewer genetic manipulations than previously reported somatic cells, and in the other we have found that small molecules may be able to replace viral integration of certain transcription factors and promote the reprogramming process.

Life Science has taken the next step. Genome, Epigenome In a paper published in Genome Medicine, a team of researchers from University College London (UCL) found an epigenetic signature that is associated with all breast cancer cases, not just those that are linked to a BRCA mutation. "We identified an epigenetic signature in women with a mutated BRCA-1 gene that was linked to increased cancer risk and lower survival rates,” said Professor Martin Widschwendter, the study's lead author and head of UCL's Department of Women's Cancer, in a press release. “Surprisingly, we found the same signature in large cohorts of women without the BRCA-1 mutation and it was able to predict breast cancer risk several years before diagnosis."

Although your DNA, called the genome, determines what proteins your body’s cells can produce, you also have an epigenome, a series of molecules that attach themselves to your DNA to increase or decrease the activity of specific genes. The most well-studied form of epigenetics is methylation, in which environmental factors cause methyl groups to bond to DNA. Usually, the methyl groups bond with the promoter region of a gene, a set of DNA at the beginning of the gene that instructs the cell to turn the gene on. Methyl groups tend to down regulate genes, meaning that if a promoter normally instructed a gene to express itself 20 times, a methylated gene might only express itself 10 times instead. In humans, most epigenetic changes occur during fetal development and early childhood, and they are influenced by any number of environmental factors.

An Epigenetic Difference To find an epigenetic signature linked to breast cancer, the scientists examined a large group of blood samples from women with a certain cancer-causing BRCA-1 mutation. Among the women who went on to develop breast cancer, they found that a certain gene cluster was methylated. The genes in question are involved in helping stem cells to differentiate. Stem cells can divide endlessly and become any type of cell the body might need. If this process goes awry and these super-cells start working against the body instead of for it, the result is cancer. Although the exact process is unknown, methylation of these genes is linked to higher rates of cancer. But the real question was, do women without a BRCA-1 mutation who go on to develop cancer also have these same methylated genes? The researchers were surprised and pleased to discover that they do. Widschwendter’s team isn’t yet sure whether the methylated DNA is one of the factors that directly causes breast cancer, or if the methyl signature is just a handy biomarker. Still, his team's research could be part of a new wave of early breast cancer detection.

Barron’s Medical Journal concludes, data is encouraging since it shows the potential of a blood based epigenetic test to identify breast cancer risk in women without known predisposing genetic mutations.