Prognostic significance of COX-2 and beta-catenin in colorectal carcinoma

The high prevalence of colorectal carcinoma [CRC] is a driver to understand the underlying molecular mechanisms. Chemoprevention strategy using non-steroidal anti- inflammatory drugs [NSAIDs] revealed that these drugs suppress colorectal carcinoma. The best known targets of NSAIDs are cyclooxygenase [COX] enzymes. The function of prostaglandins and cyclooxygenase in cancer pathogenesis is unclear. COX-2 regulation of proliferation, apoptosis, and tumor-blood vessel interaction has been suggested. beta-Catenin is a component of the WNT [wing1ss type] signaling pathway, increased protein concentrations promote transcription of genes important in regulating the cell cycle. To determine the significance of COX-2 and beta-catenin expression in colorectal carcinogenesis and prognosis. Thirty patients with colorectal carcinomas treated by colonic resection were studied for the expression of both COX-2 and beta-catenin by immunohistochemistry. Their expression was interpreted in relation to adjacent normal colonic mucosa and analyzed in correlation with various clinicopathologic parameters and patient's survival after a follow up period of 24 months. Our results showed that in normal adjacent colonic mucosa, COX-2 was completely absent, whereas beta-catenin was specifically located in the plasma membranes. Both proteins were expressed in tumorous tissues, COX-2 showed diffuse cytoplasmic positivity, whereas 3-catenin accumulated in both the cytoplasm and nuclei. We established statistically significant relationships between pathological grade and both beta-catenin, and COX-2 positivity scores, being at the higher end for poorly-differentiated tumors. beta-Catenin expression also correlated significantly with higher tumor stage and LN metastasis. Both COX-2 and beta-catenin expression correlated with a higher incidence of shorter disease free survival

role of angiogenesis assessment in the prognosis of breast carcinoma and in the evaluation of the therapeutic effect of "shark care" drug as an angiogenesis inhibitor

There is still uncertainty about angiogenesis as a prognostic factor in breast cancer. To evaluate the prognostic value of microvascular density [MVD] in breast carcinoma and soluble vascular cell adhesion molecule-1 [sVCAM-1], leptin, estradiol and total testosterone as angiogenic markers. Efficacy of shark care drug was assessed by patient's overall survival. 30 premenopausal breast cancer patients [group II] and 15 controls [group I]. Group II was subgrouped into 15 patients receiving chemotherapy alone [IIA] and 15 patients receiving chemotherapy + shark care drug [IIB]. After modified radical mastectomy, microvessels were counted by staining tissues for factor VIII. For surrogate markers, enzyme-linked immunosorbant assay or radiommunoassay kits were used. A high MVD was found only in areas of carcinoma. MVD and sVCAM-1 correlated significantly with each other and with lymph node involvement. After the follow-up, all subgroup IIB patients were alive compared to 66.6% of subgroup IIA [p=0.02]. A high MVD may be a poor prognostic marker of breast carcinoma and a target for antiangiogenic therapy sVCAM-1 is useful for diagnosis and for monitoring response to therapy. Chemotherapy + shark care drug seem to ameliorate the outcome of these patients

Study of the dielectric properties of breast cancer and the surrounding tissue

Relative permittivity and conductivity of infiltrating breast carcinoma and the surrounding tissue were measured. The experiments were performed at frequencies 1 kHz- 100 kHz at 25[degree sign] C using an automatic network analyzer LCR. Cole-Cole dielectric parameters were calculated by curve fitting using a computer program. Statistical analysis showed significant differences between cancerous and normal tissues which confirmed that impedance spectroscopy can be considered as potentially suitable for breast cancer detection. Results obtained from the dielectric properties on the basis of the net tissue water content were discussed. Result have shown that the permittivity and conductivity values in breast carcinoma are higher than those in normal tissue. Histological analysis showed an infiltrating ductal carcinoma with a focal papillary component or a lobular carcinoma. In some specimens, the tumor formed a hard core of different density and size

Apoptosis, proliferation, and FAS/FASL expression in pancreatic adenocarcinoma

Deregulation of normal cell cycle machinery is integral to neoplastic growth. There is now compelling evidence implicating the loss of cell kinetic balance in the development and progression of most human cancers, including pancreatic carcinoma which caries extremely poor prognosis. Understanding the pathogenesis of pancreatic cancer seems to be of great value in order to determine the mechanisms of the aggressive growth and metastasis. As the tumor growth depends upon the balance between apoptosis and proliferation, herein, we analyzed by immunohistochemistry the expression of Fas and FasL in 20 operative specimens of pancreatic ductal adenocarcinoma. The apoptotic index [AI] was evaluated by TUNEL in relation to the proliferation index [PI] as estimated by Ki67 aiming to correlate [AI and PI] with clinicopathologic variables and apoptosis-regulating proteins Fas and Fas-L. Fas and FasL were inversely correlated and were detected in 40% and 65% of cases respectively. The mean apoptotic index [AI] was 1.40 +/- 0.74%, and the mean proliferation index [PI] was 42.7 +/- 14%. Fas and AI were closely associated and decreased significantly in higher tumor grade and stage; whereas, FasL and PI increased significantly in higher grade and stage. Tumor infiltrating lymphocytes [TIL] showed higher mean apoptotic index in FasL positive than FasL negative tumor tissues. Therefore, it could be suggested that the apoptotic and proliferation indices could be useful prognostic markers in pancreatic ductal adenocarcinoma. Fas expression plays a key role in apoptosis in pancreatic cancer and FasL expressing carcinomas induce marked apoptosis in TIL allowing them to evade immune surveillance. Therefore, we recommend designing new therapeutic approaches for pancreatic adenocarcinoma based on reinforcement of Fas/FasL-induced tumor apoptosis