November 13, 2011
BRCA1 is a gene whose name is among the most familiar to the general public of all genes – for the unfortunate reason that mutations of BRCA1 are associated with significantly increased hereditary risk for breast cancer (as the name suggests). Strangely, however, it’s still not known exactly how mutations of BRCA1 confer this greater risk for cancer. But recent research has narrowed down the possibilities.
The protein that the gene codes for, BRCA1, is a fairly long chain of 1863 amino acids. BRCA1 is known to be involved in repair of damaged DNA. If BRCA1 is defective (due to a gene mutation), the failure to properly repair DNA (which can become damaged for many possible reasons) can lead to a cell becoming cancerous.
Previous research has identified around 1500 different mutations of BRCA1 associated with cancer risk. But most of these mutations directly affect the amino acids of only two different regions of BRCA1. Every protein has an amine group at one end of its chain and a carboxyl group at the other end. One of the two regions in which mutations lead to cancer is at the amino end and is called the “RING domain”. The other region, near the carboxyl end, is called BRCT (BRCA1 carboxyl-terminal tandem repeats).
The RING domain is known to have a role in the process that attaches a marker called ubiquitin to a protein in order to identify the protein as ready for recycling. The BRCT region is associated with the process of protein phosphorylation, which is a key element of chemical signaling within cells. What hasn’t been known is what aspects of DNA repair are disrupted by defects in one or both of these regions.
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September 15, 2011
Stem cells and cancer cells seem to have more in common besides an ability to divide much more freely than normal adult cells – the persistence of structures called midbodies that are, as currently understood, important only in cell division. This raises the question of whether midbodies have functions, besides helping in cell division, that are common to both stem cells and cancer cells.
Obscure Organelle in Stem Cells and Cancer – The Scientist
Cellular structures known as midbodies, formed during cell division, appear to accumulate in stem cells and cancer cells, hinting at a potential function for these once-disregarded organelles.
Midbodies, once considered the rubbish of cell division, might have a function beyond their role in getting daughter cells to separate. Researchers show in today’s Nature Cell Biology that stem cells and cancer cells collect used midbodies, whereas differentiated cells digest the organelle through autophagy.
Midbody accumulation through evasion of autophagy contributes to cellular reprogramming and tumorigenicity
September 8, 2011
The gene in question, BRCA1, is the one which, when mutated, makes women who inherit the mutated form much more susceptible to breast and ovarian cancer. Up till now, a good understanding has been lacking of how the protein produced by unmutated BRCA1 acts as a tumor suppressor.
Breast-cancer gene keeps DNA under wraps – Nature News
The protein encoded by the tumour-suppressor gene BRCA1 may keep breast and ovarian cancer in check by preventing transcription of repetitive DNA sequences, says a study published today in Nature. This explanation brings together many disparate theories about how the gene functions and could also shed light on how other tumour suppressors work.
Since the discovery in the mid-1990s that defects in BRCA1 strongly predispose women to breast and ovarian cancer, researchers have suggested numerous ways in which the protein might stop cells from becoming cancerous. Some have focused on its ability to repair DNA damage, whereas others have studied how it regulates cell-cycle checkpoints, transcription or cell proliferation. But until now, no unifying theory of how these different functions might prevent breast and ovarian cancer has emerged.
Cancer: Let sleeping DNA lie
BRCA1 tumour suppression occurs via heterochromatin-mediated silencing
September 8, 2011
Antibodies are proteins produced by the immune system to seek out and attach to other proteins. These latter proteins may be part of a bacterium, a virus, or found on the surface of cancer cells. Cells of the immune system can then use the antibody as a signal to neutralize of destroy whatever the antibody has attached to. The research here indicates that antibodies can perhaps get inside a cell and attach to a target. In the case of cancer cells, this might neutralize the activity of targeted proteins (such as signaling proteins) that drive cell proliferation.
Antibodies Target Cancer’s Insides – ScienceNOW
Researchers may have found a way to get inside cancer’s head—or at least its body. The cancer cell has been long believed to be impermeable to antibodies that could target it for destruction. But a new study suggests that some antibodies can get through after all, potentially opening up a vast new array of cancer therapies.
A*STAR scientists make headway for cancer treatment and cancer prevention with landmark discovery