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
• 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
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.
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