Woodland, TX ( AP ) News ----- How can some people smoke all of their adult life and not get lung or breast cancer and others people and their families’ will get lung cancer. Brought To You By Julie Beth Hangbags--- Rodeo ReadyGenomics and personalized medicine for lung cancer is being used more and more to diagnose and treat lung and breast cancer. What is new in this area of science and medicine is the SYK Gene. Yes -- Spleen tyrosine kinase (SYK) researcher’s has given Scientist around the world new information and a major step to a cure. With the advent of genomic science, scientist has added to the P53 gene --- SYK gene.
Spleen tyrosine kinase (SYK) is a non-receptor type cytoplasmic protein and a known tumor suppressor gene in breast and lung cancer. When a copy of your SYK gene is lost,Brought To You By: Fashion Woodlands 51 other genes are directly affected. This leads to genetic disruption. A tumor suppressor gene, or antioncogene, is a gene that protects a cell from one step on the path to cancer. When this gene mutates to cause a loss or reduction in its function, the cell can progress to lung and breast cancer.
Researcher has discovered patients with lung adenocarcinomas diagnosed each year in the United States have tumors that carry a mutation called V600E BRAF. The BRAF gene makes a protein that affects how cancer cells divide and grows. The powerful tumor suppressor gene, SYK, as wellas genetic alterations in 51 other genes that are directly affected by the loss of a copy of the SYK gene and the absence of its protein is a major cause of breast cancer. Genomic science is gaining popularity and many Doctors throughout the United States and around the world. Genomics is a discipline in genetics that applies recombinant DNA, DNA sequencing methods, and bioinformatics to sequence, assemble, and analyze the function and structure of genomes (the complete set of DNA within a single cell of an organism). With so many folks getting diagnosed with lung cancer, personalized medicine core foundation uses genes. Our genes are the molecular unit of heredity of a living organism. It is used extensively by the scientific community as a name given to some stretches of deoxyribonucleic acids (DNA) and ribonucleic acids (RNA) that code for apolypeptide or for an RNA chain that has a function in the organism.
Proteins are large biological molecules, or macromolecules, consisting of one or more long chains of amino acid residues. The key elements of an amino acid are carbon, hydrogen, oxygen, and nitrogen, though other elements are found in the side-chains of certain amino acids. About 500 amino acids are known and can be classified in many ways. Lung cancer is the leading cause of cancer-related deaths among men and women. According to the National Cancer Institute, an estimated 224,210 Americans will be diagnosed with lung cancer, and 159,260 will die from the disease this year. About 85 percent of lung cancers are NSCLC, making it the most common type of lung cancer. However, only 2-7 percent of patients with NSCLC are ALK-positive.
How we use to treated lung Cancer in 1975, the incidence rate for all cancers combined in the United States was 400 new cases for every 100,000 people in the population; the mortality rate was 199 deaths for every 100,000 persons. Among adults diagnosed with cancer during the period from 1974 through 1976, the 5-year relative survival rate for all cancers combined was 50%. Among whites, it was 51%; among blacks, it was approximately 40%. During the same period, the 5-year relative survival rate for all childhood cancers combined was about 62%. (Note: Relative survival compares the survival of a cancer patient to that of an average person of the same age and sex.) For the five most common cancers diagnosed in adults, the 5-year survival rates were: breast, 75%; prostate, 69%; lung, 13%; colorectal, 51%; and bladder, 74%.
In the mid-1970s, approximately 37% of U.S. adults were current smokers. In 1975, the lung cancer mortality rate among men was about 76 deaths per 100,000 persons; among women, it was about 18 deaths per 100,000 persons. In the mid-1960s, clinical investigation of combination chemotherapy, using multiple drugs with different mechanisms of action, in the treatment of cancer was just beginning. Clinical studies of anticancer vaccines (treatment or prevention) had not yet begun.
Through The Cancer Genome Atlas (TCGA) (http://tcga.cancer.gov/), a joint effort of the National Cancer Institute and the National Human Genome Research Institute, we will greatly expand our understanding of the genetic basis of more than 20 cancers that affect adults and identify specific molecular changes that can be targeted for the development of new treatments or exploited to detect cancer earlier or prevent its occurrence. If you have lung, the great news is Vemurafenib received FDA approval for the treatment of late-stage melanoma on August 17, 2011. Dabrafenib a drug for the treatment of cancers associated with a mutated version of the gene BRAF. Dabrafenib acts as an inhibitor of the associated enzyme B-Raf, which plays a role in the regulation of cell growth. In 2014 Zykadia (ceritinib) for patients with a certain type of late-stage (metastatic) non-small cell lung cancer (NSCLC).
Discovery of key genes and proteins that spark and fuel lung cancers (ie, driver genes) has shifted the focus of lung cancer treatment toward targeted therapies. This year, strategies of screening for genetic changes in lung tumors and matching patients to appropriate targeted treatments were reported, thus delivering on the promise of personalized medicine. Early results showed encouraging antitumor effects of dabrafenib against BRAF-positive lung cancers and LDK378 and AF802 for ALK-positive lung cancers.
A total of 1,007 patients with metastatic adenocarcinomas (the most common subtype of NSCLC) were tested for at least one genomic mutation, and 733 underwent testing for all 10 known lung cancer oncogenic drivers: KRAS, EGFR, HER2, BRAF, PIK3CA, AKT1, MEK1, NRAS, ALK, and MET. A driver was detected in 622 (62%) of 1,007 patients with at least one gene tested, and 465 (63%) of 733 patients who underwent testing for all 10 genes. Mutations in KRAS, EGFR, and ALK genes accounted for approximately half of all driver mutations detected. Twenty-nine patients (4%) had mutations in two driver genes.
These findings were then used to select available targeted therapies or appropriate clinical trials testing new targeted therapies in 279 patients with a driver mutation. Clinical follow-up and treatment information was assessed for 938 patients. Among the 622 patients with a driver mutation detected, those treated with targeted therapy (264 patients) had a median survival of 3.5 years, and those who did not have a targeted therapy available (313 patients) had a median survival of 2.4 years. The 361 patients withoutidentified driver mutations had a median survival of 2.1 years. This study demonstrates that close to two thirds of all patients with lung adenocarcinomas harbor mutations in known lung cancer driver genes and that matching patients with treatments targeted specifically to those drivers leads to improvements in survival.
Nearly 3,000 patients with lung adenocarcinomas diagnosed each year in the United States have tumors that carry a mutation called V600E BRAF. The BRAF gene makes a protein that affects how cancer cells divide and grow. An oral drug that blocks the BRAF protein, dabrafenib, has recently shown dramatic effects in patients with BRAF V600E– positive metastatic melanoma.
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