Showing posts with label cancer. Show all posts
Showing posts with label cancer. Show all posts
Friday, July 20, 2012
Aged people get more cancers than young ones due to use of Non-homologous end joining instead of homologous recombination for repairing double strand breaks
Friday, July 6, 2012
Choosing negative control of cell division: one of the major cause of problems in animal system
Some weeks back when we were discussing about cell division and cancer we were comparing plant vs animal cell cycle and the interesting question came is “Why animals and plants chose different mode of controlling their cell division ?”. I thought of sharing this with you in this post.
Plants normally do not die (premature death) out of inherent problems (defects in their own genes controlling cell cycle). Mostly their premature death is due to pathogens or stress which are external. In contrast, in animals including human one of the major cause of premature death is the cancer which is due to the defects in cell division control genes. If we take an aerial view of this problem one thing is clear that plant cells are
Friday, June 1, 2012
Tissue Biopsy for cancer detection may disappear soon: Genomic method of cancer detection
Tissue Biopsy for cancer detection may disappear soon: Simple blood plasma assay (a liquid biopsy) may be the method of cancer detection in future
Blood plasma, the straw-colored liquid component of blood that normally holds the blood cells in whole blood in suspension contains dissolved proteins, glucose, clotting factors, mineral ions, hormones and carbon dioxide and DNA. Plasma of cancer patients contains cell-free tumor DNA that carries information on tumor mutations and tumor burden. Though individual mutations have been probed earlier, for the first time a method has been developed ( by a team of researchers from UK) for tagged-amplicon deep sequencing (TAm-Seq) which resulted in screening 5995 genomic bases for low-frequency mutations. Using this method they identified cancer mutations present in circulating DNA at allele frequencies as low as 2%, with sensitivity and specificity of >97%.They identified mutations throughout the tumor
Tuesday, May 29, 2012
What is Cancer Genome Atlas ?
Cancer genome atlas is a very important project aiming to map all genomic variations associated with different cancers and create a comprehensive atlas. This was initiated by The National Cancer Institute (USA)and the National Human Genome Research Institute (USA) and is being carried out by a network of more than 100 researchers at many
Friday, May 25, 2012
BREAKING DISCOVERY: Radiation treatment converts a normal breast cancer cells to breast cancer stem cells which are more tumorigenic
Breast cancers are thought to be organized hierarchically with a small number of breast cancer stem cells (BCSCs) able to regrow a tumor while their progeny lack this ability. Recently, several groups reported enrichment for BCSCs when breast cancers were subjected to classic anticancer treatment. However, the underlying mechanisms leading to this enrichment are incompletely understood.
Friday, May 18, 2012
DNA sequencing found to be better than flow cytometry in predicting cancer relapse
In a recent study Scientists at University of Washington, University of New Mexico Health Sciences Center, University of Virginia, University of California and Fred Hutchinson Cancer Research Center have found that high-throughput sequencing could improve the diagnosis and post-treatment monitoring of leukemia. The sequencing-based method is more sensitive than flow cytometry and cheaper and faster than the quantitative real-time PCR. They used high throughput sequencing (HTS) to the diagnosis of T-lineage acute lymphoblastic leukemia/lymphoma. 43 paired patient samples were used for assessing
Germline low-methylated regions are more prone for structural mutation than methylated regions
The human genome contains many loci with high incidence of structural mutations, including insertions and deletions of chromosomal segments. This excessive mutability has accelerated evolution and contributed to human disease but has yet to be explained.
Segments of DNA repeated in low-copy numbers (LCRs) have been previously implicated in promoting structural mutability in specific disease-associated loci. Lack of methylation (hypo-methylation) of genomic DNA has been previously associated with high structural mutability in gibbons and in human cancer cells, but the association with structural mutability in the human germline has not been explored.
A recent study carried out by Scientists from
Segments of DNA repeated in low-copy numbers (LCRs) have been previously implicated in promoting structural mutability in specific disease-associated loci. Lack of methylation (hypo-methylation) of genomic DNA has been previously associated with high structural mutability in gibbons and in human cancer cells, but the association with structural mutability in the human germline has not been explored.
A recent study carried out by Scientists from
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