The aim of this study was to investigate pRb2/p130, p107 and p53 expressions in precancerous lesions and squamous cell carcinoma (SCC) of the uterine cervix. We evaluated Human Papillomavirus (HPV) testing and typing and pRb2/p130, p107 and p53 expressions (antibody D07) of 48 patients showing low-grade cervical intraepithelial neoplasia (LCIN, 18 cases), high-grade CIN (HCIN, 13 cases) and SCC (17 cases). Paraffin-embedded tissue sections were analyzed for the study. High-risk HPV types were present in 67%, 89% and in 100% of HPV-positive LCIN, HCIN and SCC, respectively (Spearman's correlation coefficient: 0.393, p=0.035). Positive pRb2/p130 expression was detected in 89% of LCIN, 77% of HCIN and in 35% of SCC (p=0.001), whereas diffuse p107 expression was 72%, 62% and 100%, respectively (p=0.024). The results of p53 expression in CINs and SCCs showed values (not statistically significant) comparable with the literature data concerning the antibody D07. For the first time, we tested pRb2/p130 and p107 expressions in CINs and SCCs. We found a progressive decrease in pRb2 expression from CINs to SCCs that suggests an important role of pRb2 in cervical carcinogenesis. Indeed, p107 expression does not seem to be a useful factor. In our opinion, confirmed by the literature data, p53 immunostaining helps to biologically characterize CIN (in particular LCIN) when each case is evaluated separately considering HPV testing/typing.
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J Exp Clin Cancer Res
November 2015
Department of Veterinary Public Health & Food Safety, Istituto Superiore di Sanità, 00161, Rome, Italy.
Background: Hepatitis C Virus (HCV) infection is associated with chronically evolving disease and development of hepatocellular carcinoma (HCC), albeit the mechanism of HCC induction by HCV is still controversial. The nucleocapsid (core) protein of HCV has been shown to be directly implicated in cellular transformation and immortalization, enhancing the effect of oncogenes and decreasing the one of tumor suppressor genes, as RB1 and its protein product pRB. With the aim of identifying novel molecular mechanisms of hepatocyte transformation by HCV, we examined the effect of HCV core protein on the expression of the whole Retinoblastoma (RB) family of tumor and growth suppressor factors, i.
View Article and Find Full Text PDFJ Cell Physiol
February 2013
Research Laboratories, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.
The retinoblastoma (RB) family consists of three genes, RB1, RBL1, and RBL2, that code for the pRb, p107, and pRb2/p130 proteins, respectively. All these factors have pivotal roles in controlling fundamental cellular mechanisms such as cell cycle, differentiation and apoptosis. The founder and the most investigated RB family protein is pRb, which is considered to be the paradigm of tumor suppressors.
View Article and Find Full Text PDFPediatr Blood Cancer
February 2012
Department of Pathology, Tata Memorial Centre, Mumbai, India.
Background: The prevalence of human papillomavirus (HPV) infection in India is high. HPV infection is known to cause cervical cancer and has also been implicated in the pathogenesis of retinoblastoma (RB), a common intraocular malignant tumor of childhood which can be familial or sporadic. Despite the high incidence of RB in India, its familial form is rare.
View Article and Find Full Text PDFOncol Rep
December 2010
CROM-Center of Oncology Research Mercogliano, Avellino, Italy.
Gastric cancer is one of the most diffuse neoplastic pathologies in the world whose environmental and molecular causes, although deeply investigated, have not been completely clarified. Besides some well-established etiological factors, such as Helicobacter pylori and E-cadherin mutations, investigations on other possible causes gave contrasting results. Rb family proteins (including pRb/p105, pRb2/p130 and p107) are involved in cell cycle regulation and their function and/or expression is often lost in various kinds of tumours such as lung, bladder, breast and brain cancer.
View Article and Find Full Text PDFJ Cell Biochem
May 2010
Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, Pennsylvania 19122, USA.
The formation and progression of mudulloblastoma (MB) is poorly understood. However, somatic inactivation of pRb/p105, in combination with a somatic or a germ-line TP53 inactivation, leads to MB in a mouse model. Presently, there is no specific evidence of pathway/s alterations for the other two members of the retinoblastoma family, pRb2/p130 and/or p107 in MB.
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