Apr 03, 2009 - 12:24 pm
This piece of research is really hard to understand, but builds on some earlier research I did on epidermal growth factor type II receptor. This 'factor' can be tested for with fresh tissue samples taken during your hysterectomy, and KNOWING you had this factor would be VERY important information, as there are drugs that can work with this factor. The danger of NOT knowing you have it, is that your survival rate drops about 90% for UPSC patients who have it and do not get the additional chemo drugs that can attack it. (My understanding is that this 'factor' makes your cancer cells resistant to chemo. But the special additional drugs can weaken the cancer cells and make them more 'kill-able'.) Anyway, here's the new stuff, for those of you who can understand it. (If you can, PLEASE explain it to me!!):
There are other significant differences between endometrioid carcinomas and papillary serous carcinomas. Women with papillary serous carcinoma tend to be older (median age 65-70), nonobese and parous. Atypical hyperplasia is not a precursor lesion for this disease, these tumors are not associated with estrogen excess, usually do not express ER or PR, but they frequently have p53 mutations and high degrees of aneuploidy. In contrast to endometrioid adenocarcinoma, microsatellite instability, k-RAS and PTEN mutations are uncommon in papillary serous carcinoma (24)
A significant percentage of poorly differentiated tumors, often with serous papillary or clear cell histology, have been found to overexpress the epidermal growth factor type II receptor. Anti-HER-2/neu-targeted therapy might be a novel and attractive therapeutic strategy in patients harboring this biologically aggressive variant of endometrial cancer.
(and here's one more interesting todbit from my morning of research):
Endometrial carcinoma is the most common neoplasm of the female reproductive tract and it accounts for nearly one-half of all gynecologic malignancies. Although usually curable with surgery, sometimes aggressive tumors such as uterine papillary serous carcinomas (UPSC) are seen. Immunohistochemical studies suggest that p53 is aberrant in 50–90% of UPSC tumors in comparison to 10–30% in typical endometrioid adenocarcinomas. In a recent study, adenoviral delivery of p53 or p21 resulted in growth suppression and induction of apoptosis in a UPSC cell line71.
An alternative approach to inhibiting the growth of cervical cancer cells is based on the observation that tumor suppressor p53 functions are downregulated in most cervical cancer cells. The product of HPV oncogene E6 binds to and inactivates p53 by promoting its degradation. p73 is similar to p53 in structure and function but not degraded by the HPV E6 gene product. Das et al. demonstrated growth inhibition of E6-positive cell lines in vitro following infection with Ad-p7369.