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1.
Reprod Biol Endocrinol ; 11: 53, 2013 Jun 19.
Article in English | MEDLINE | ID: mdl-23782518

ABSTRACT

The female reproductive system (FRS) has a great capacity for regeneration. The existence of somatic stem cells (SSC) that are likely to reside in distinct tissue compartments of the FRS is anticipated. Normal SSC are capable of regenerating themselves, produce a progeny of cells that differentiate and maintain tissue architecture and functional characteristics, and respond to homeostatic controls. Among those SSC of the FRS that have been identified are: a) undifferentiated cells capable of differentiating into thecal cells and synthesizing hormones upon transplantation, b) ovarian surface epithelium stem cells, mitotically responsive to ovulation, c) uterine endometrial and myometrial cells, as clonogenic epithelial and stromal cells, and d) epithelial and mesenchymal cells with self-renewal capacity and multipotential from cervical tissues. Importantly, these cells are believed to significantly contribute to the development of different pathologies and tumors of the FRS.It is now widely accepted that cancer stem cells (CSC) are at the origin of many tumors. They are capable of regenerating themselves, produce a progeny that will differentiate aberrantly and do not respond adequately to homeostatic controls. Several cell surface antigens such as CD44, CD117, CD133 and MYD88 have been used to isolate ovarian cancer stem cells. Clonogenic epithelial and stromal endometrial and myometrial cells have been found in normal and cancer tissues, as side population, label-retaining cells, and CD146/PDGF-R beta-positive cells with stem-like features. In summary, here we describe a number of studies supporting the existence of somatic stem cells in the normal tissues and cancer stem cells in tumors of the human female reproductive system.


Subject(s)
Genital Neoplasms, Female/pathology , Genitalia, Female/cytology , Neoplastic Stem Cells/pathology , Stem Cells/cytology , Biomarkers/metabolism , Biomarkers, Tumor/metabolism , Cell Differentiation , Cell Proliferation , Female , Genital Neoplasms, Female/metabolism , Genitalia, Female/metabolism , Humans , Neoplastic Stem Cells/metabolism , Stem Cells/metabolism
2.
Ginecol. obstet. Méx ; 70(1): 11-16, ene. 2002.
Article in Spanish | LILACS | ID: lil-331070

ABSTRACT

The objective of this study was to determine high risk human papillomavirus infection (HPV-RH) and factors with cervical intraepithelial neoplasia appears (CIN). MATERIAL AND METHOD: From October 1998 to January 2000, a case-control study, was made; women with benefit package from Mexican Institute of Social Security. The cases were of the colposcopic clinic of the department of the Hospital Obstetrics and Gynecology Luis Castelazo Ayala, women histologically diagnosed with colposcopy and CIN cervical biopsy, and controls patients with negative cervical uterine cytologic study of the Preventive Medicine Department, Unit of Familiar Medicine No. 8, of Mexico City. Trained personnel obtained information about socioeconomic and reproductive factors did the interview. A cytobrush was used to take the cervical sample for HPV-RH to determine HPV-RH utilizing Hybrid Capture II test. Both bivariate analysis and logistic regression analysis were used for the adjustment of variables. RESULTS: We analyzed 102 cases and 192 controls, 79 (44/56) of the cases with CIN I and 89 (37/42) of CIN II-III as 21 of controls, respectively, were positive for HPV-RH. Global risk for HPV-RH association to CIN was OR = 40.6 (95 CI, = 17-96.8). Women age was determinative for HPV-RH association to CIN. We observed a high correlation between HPV positive magnitude and CIN degree. CONCLUSIONS: Frequency of RH-HPV in controls and CIN I is higher than other reports in the literature. HPV was identified as the most important agent associated with this neoplasia, other factors involved and age is an important modifier in HPV-RH and CIN.


Subject(s)
Humans , Female , Adult , Middle Aged , Carcinoma in Situ , Papillomavirus Infections/complications , Tumor Virus Infections/complications , Papillomaviridae , Case-Control Studies , Risk Factors
3.
Medicina [B.Aires] ; 60(6): 895-901, Dic. 2000.
Article in Spanish | BINACIS | ID: bin-7405

ABSTRACT

The aim of this study w trial randomized as to investigate the frequencies of human papillomavirus (HPV) and mutation in Ha-ras oncogene and tumour suppressor p53 gene in cervical cancer and precursor lesions. A total of 30 invasive carcinomas (IC), 36 cervical intraepithelial neoplasia grade III (CIN III) and 12 normal tissues adjacent to the tumor (NT) were included. HPV typification and scanning of possible mutations in Ha-ras and p 53 genes were made by SSCP-PCR. The IC cases showed 93 HPV positivity, 41 having mobility shifts for Ha-ras mutations and 17 for p53 mutations while in CIN III, these percentages were 80, 18 and 11, respectively. In normal tissues HPV frequency was 17. All Ha-ras mutated samples were HPV positive but 33 of p53 mutated cases were HPV negative. All mutations were heterozygous. HPV 16 was more prevalent (44) than HPV 18 (15) and the high rate of undetermined HPV types (18) would indicate the circulation in our country of other types different from the assayed HPV controls (6, 11, 16, 18, 31 and 33), being variants or mixed infections. The low frequency of p53 mutations (17) strengthens the view that wild type p53 inactivation by HPV probably plays a major role in the pathogenesis of cervical cancer. Because mutated Ha-ras was found in HPV associated premalignant lesions, we speculate that it represents an early marker for progression. Our findings provide additional evidence for an interactive effect between high risk types of HPV and oncogene activation in the development of uterine cervical cancer.(Au)


Subject(s)
Humans , Female , RESEARCH SUPPORT, NON-U.S. GOVT , Uterine Cervical Dysplasia/virology , Uterine Cervical Neoplasms/virology , Genes, p53/genetics , Genes, ras/genetics , Human Papillomavirus Viruses/genetics , /virology , Tumor Virus Infections/virology , Uterine Cervical Neoplasms/genetics , DNA, Viral/genetics , Mutation/genetics , /genetics , Polymerase Chain Reaction , Polymorphism, Single-Stranded Conformational
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