Ovarian cancer surgery can not eradicate the risk of women

By | January 20, 2012

U.S. researchers have said before, due to BRCA1 and BRCA2 gene mutations in women with high risk of cancer in the ovaries and fallopian tubes to do surgery, the risk of ovarian cancer and fallopian tube cancer risk will be reduced by 80%, but they may still be suffering from breast cancer, that ovarian surgery can not eradicate the risk of female cancers.
From previous studies the researchers to collect data, found that women suffering from breast cancer surgery can reduce the chance of 50%, but women suffering from ovarian cancer or fallopian tube cancers can only be reduced by 80%, because even if the removal of these organs, but also Some remnants of cells, there is still disease risk.
This research report was published in the "U.S. National Cancer Institute" on. "As long as very little can lead to ovarian cancer cells." Of the article, Timothy Rebbeck, University of Pennsylvania, said in an interview, "Although the risk is greatly reduced, but still there. Ovarian surgery can not eradicate cancer risk women, previous studies shows that surgery can remove 95% or 100% of the disease risk, but is not the case. "
Studies have shown that BRCA1 and BRCA2 genes are mutated women, some of them too late to do surgery, and surgeon should also ensure that all surgical removal of the ovaries and fallopian tubes in the cells.
Ovarian surgery can not eradicate cancer risk women, the researchers believe that this study raises the question how to reduce risk, the solution is to improve the surgical technique, or early surgery.
Rebbeck said: "The evidence shows that surgery still has effect. Female patients need surgery, but also to do it right."

Knowledge: tumor suppressor gene
Tumor suppressor gene, also known as anti-cancer gene. As early as 1960, some kinds of cancer cells and normal fibroblast cells with the fusion, the offspring obtained hybrid cells retain some normal as long as the parent chromosomes can be expressed as normal when the phenotype, but with the loss of chromosomes can be re-emerging malignant cells. This phenomenon indicates that there may be some of the normal chromosome genes that suppress tumors, and their loss, mutation or loss of function, so that play a role in activation of oncogenes and cancer.
Multiple genes involved in cancer formation and genetic changes other than a separate mutations in a gene not sufficient to cause cancer, the accumulation of multiple genetic changes can lead Zhi control mechanism of cell growth and differentiation disorder, so out of control and cancer cell proliferation. Changes in these genes in the two most common abnormal gene changes are: cancer gene (oncogenes) and tumor suppressor genes (cancer suppressor genes, also known as tumor suppressor genes, tumor supp ressor genes, or cancer genes, anti- oncogenes) changes.
Oncogene is a product of the encoding and transformation of tumor cells, the genes involved. Dominant role in the way it is, the positive effect on cell growth, and promote cell transformation. Many cancer genes due to a single base mutation, resulting in cancer gene product in a single amino acid substitution, and the loss of its regulatory activity. The first identified the human ras oncogene is a gene. ras gene family of three closely related members of the: H-ras, K-ras and N-ras is the most common human tumor oncogenes, they are about 15% of human evil of tumor was detected, including 50% 25% of colon cancer and lung cancer.
From the normal tumor suppressor genes inhibit cell proliferation and tumor role. Many tumors were found in two allelic loss of tumor suppressor gene or inactivation, loss of negative regulator of cell proliferation, and thus the transformation of tumor cells and abnormal proliferation of work. The Rb gene on chromosome 13p14 is the first discovered and identified the tumor suppressor gene, which is rare in children in the study of retinoblastoma found.
Was also some of the common adult tumors, such as bladder, breast and lung cancer found that loss or inactivation. Some tumor suppressor gene mutations leading to human tumors the most common molecular changes. If a second tumor suppressor gene p53 were identified in the majority of human cancers such as leukemia, lymphoma, sarcoma, brain tumor, breast cancer, gastrointestinal cancer and lung cancer often has deactivation. p53 mutations found in up to 50% of the people cancer, it is human evil, the most common of tumor genetic changes.
The new tumor suppressor genes are emerging, such as with breast cancer is closely related to BRCA1 and BRCA2, and pancreatic cancer-related DPC4, and renal cell carcinoma and other VHL-related tumor suppressor gene has been found; also related with liver cancer M6P/IGF2r gene, located on chromosome 3p14.2 is also on the tumor suppressor gene FHIT gene and other candidate.
Tumor suppressor gene product is the inhibition of cell proliferation, promote cell differentiation, and inhibition of cell migration, it plays a negative regulatory role, mutations in tumor suppressor genes that normally is hidden.
Including tumor suppressor gene products (Table 16-2): transcription factors, such as Rb, p53; negative regulator of transcription factors, such as WT; cyclin-dependent kinase inhibitor (CKI), such as p15, p16, p21; signaling pathway inhibitor, such as the ras GTP activating protein (NF-1), phospholipase (PTEN); DNA repair factors, such as BRCA1, BRCA2. and development and stem cell proliferation-related signaling pathway components, such as: APC, Axin and so on.
Inactivation of tumor suppressor genes ways: recessive alleles of the role, inactivation of tumor suppressor genes play a recessive allele role in the cell, that is a copy of the deactivation, there is another copy of the still wild-type cells showed a normal phenotype. Only when another copy of the lead after inactivation of tumor, such as the Rb gene. dominant negative effect of tumor suppressor genes (dominant negative): a copy of tumor suppressor gene mutation in another wild-type copy of the existence and expression of the circumstances, can make cells appear malignant phenotype and cancer, and to wild-type copy function inactivation. This effect is called dominant negative effect or anti-dominant role. If confirmed in recent years, mutant p53 and APC proteins were combined with wild-type protein and its inactivation, and then into cells. haploid deficiency hypothesis (Haplo-insufficiency): Some anti-cancer gene expression level is very important, if a copy of the inactivation, another copy may not be sufficient to maintain normal cell function, leading to tumorigenesis. Such as the DCC gene can make a copy of the missing functionality with significantly reduced mucosal cells, thus the loss of cell contact inhibition, the cells were malignant clonal expansion or phenotype.

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