Posts tagged ‘gene mutation’

Researchers from the Eli and Edythe Broad Centre of Regenerative Medicine & Stem Cell Research at UCLA have found a certain protein which is responsible for the transformation of healthy cells into prostate cancer cells. This protein normally controls the self-renewal of the prostate cells or the restoration of normal cells destroyed by the withdrawal therapy for cancer.

According to previous studies,this protein, known as Bmi-1, has been previously associated with higher grade cancers and is also responsible for poor prognosis. Recent studies and experiments by the team have also revealed that a less Bmi-1 expression hinders the self renewal activities of prostate cells and diminishing its power of abnormal growth changes, thus leading to cancers.

As put by Dr.Owen Witte, the leading author of the study and the director of the Broad stem Cell Research Centre, ‘We conclude by these results that Bmi-1 is a crucial regulator of self renewal in adult prostate cells and plays important roles in prostate cancer initiation and progression’.

With years of active empirical research and studies of the whole mechanism of self-renewal in prostate cells and how their ability to do so is often seized by cancer cells, the scientists have thrown light on the spread of these malignant cells. Dr. Witte even expressed that if  some more information could be developed about this renewal process, it would have been easier for the researchers to hinder the process once the cancerous cells set in.

Finding more insight into the regulation of the self-renewal process seems to be the primary objective of the team. According to Rita Lukacs, a doctoral student in Dr. Witte’s team, ‘Prostate cancer can be initiated by so many different mutations, if we can find a key regulator of self renewal, we can partially control the growth of the cancer no matter what the mutation is’.

Source: http://www.eurekalert.org/pub_releases/2010-12/uoc–usd120110.php

Researchers have now discovered an ideal way of detecting the advanced ovarian cancer by checking the point mutations, which is actually a mis-spelling in a single character of the  genetic code  leading to the development and growth of the cancerous cells. The technique employed successfully for the detection is known as OncoMap. This finding opens up the possibilities of personalized treatment wherein the cancerous tumor can be targeted for each patient, their mutations checked and specific drugs given to stop further growth of the tumor.

The researchers are expected to present the details of how the use of OncoMap can help them to identify the mutations in cancerous tumor samples obtained from women with advanced, high grade, serous  ovarian cancer. The procedure wil be explained at the Molecular Targets and Cancer Therapeutics to be held at Berlin on 17th November 2010. The presentation will be included in the 22nd EORTC-NCI-AACR [1] Symposium there.

Dr Ursula  Matulonis of the Dana Farber Cancer Institute,  Boston, USA,  along with  her colleagues utilized the OncoMap to find out the various mutation status of the high grade, serous ovarian cancer which are not caused by the mutations in the inherited BCRA ½ genes. The researchers found the KRAS, BRAF, CTNNB1 and PIK3CA mutations which had previously been linked to ovarian cancer. They also found  KRAS and PIK3CA to be quite common while the  BRAF mutations were rarer. The researchers also identified low frequency of such mutations in a number of other oncogenes.

The study also revealed that it was possible to use the OncoMap in order to identify a specific mutation within the oncogenes of an affected woman. Targeting the gene by known drugs will then help to keep a check on the cancer. The members involved in the study now hope to utilize the OncoMap as a clinical test resource in order to obtain the genetic information of the patients. The treatment would be based on the information thus obtained and would be totally personalized.


Source: Public Release by ECCO-the European CanCer Organisation on 16th November, 2010