Publications by authors named "H Alazzouzi"
Article Synopsis
- The study investigates the genetic characteristics of rapidly proliferating colorectal cancer cells to discover potential new treatment targets, focusing on the relationship between cell growth rates and gene expression.
- Analysis of 52 colorectal cancer cell lines revealed that faster growth is linked to poor differentiation and specific genetic markers, with 1,290 genes correlated to growth rates, notably including GAPDH and PPOX.
- Experimental inhibition of GAPDH and PPOX showed promise in slowing cancer cell growth, suggesting these genes could serve as innovative therapeutic targets in colorectal cancer management.
Article Synopsis
- Brush border Myosin Ia (MYO1A) is frequently mutated in colorectal tumors with microsatellite instability (MSI), and mutations in the gene were found at a higher rate in gastric tumors compared to endometrial tumors (46.8% vs. 6.2%).
- In gastric cancer, mutant MYO1A(7A) loses its membrane localization and shows reduced protein stability, suggesting a mechanism by which it might promote tumor growth.
- Promoter hypermethylation of MYO1A negatively affects its expression in non-MSI gastric tumors, indicating that both genetic and epigenetic changes in MYO1A could provide growth advantages to gastric cancer cells.
Brush border myosin Ia has tumor suppressor activity in the intestine.
Proc Natl Acad Sci U S A
January 2012
The loss of the epithelial architecture and cell polarity/differentiation is known to be important during the tumorigenic process. Here we demonstrate that the brush border protein Myosin Ia (MYO1A) is important for polarization and differentiation of colon cancer cells and is frequently inactivated in colorectal tumors by genetic and epigenetic mechanisms. MYO1A frame-shift mutations were observed in 32% (37 of 116) of the colorectal tumors with microsatellite instability analyzed, and evidence of promoter methylation was observed in a significant proportion of colon cancer cell lines and primary colorectal tumors.
View Article and Find Full Text PDFNovel molecular profiles of endometrial cancer-new light through old windows.
J Steroid Biochem Mol Biol
February 2008
Endometrial carcinoma (EC) is the most common gynecological malignancy in the western world. A widely accepted dualistic model, which has been established on a morphological basis, differentiates EC into two broad categories: Type I oestrogen-dependent adenocarcinoma with an endometrioid morphology and Type II non-oestrogen-dependent EC with a serous papillary or clear cell morphology. Molecular genetic evidence indicates that endometrial carcinoma, as described in other malignancies, likely develops as the result of a stepwise accumulation of alterations in cellular regulatory pathways, such as oncogene activation and tumor suppressor gene inactivation, which lead to dysfunctional cell growth.
View Article and Find Full Text PDFWe have described recently the Ets family transcription factor, ERM/ETV5, specifically up-regulated in endometrioid endometrial carcinoma (EEC) and associated with myometrial infiltration. Ets family members have been correlated to tumor progression by up-regulating the expression of matrix-degrading proteases. In the present study, we investigated the possibility that in EEC, ERM/ETV5 may act by inducing the expression of genes involved in extracellular matrix remodeling.
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