Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many occupations in which women comprise the majority of the workforce involve exposure to biological, physical, and chemical hazards. Potential reproductive effects of work-related substances include impaired reproductive capacity, mutagenesis, teratogenesis, and transplacental carcinogenesis. However, female-dominated occupations tend to be only minimally regulated by the US Occupational Safety and Health Administration, and the corporate response to the issue of reproductive and fetal health has been to institute "protective discrimination policies" such as the demotion or exclusion of women of childbearing age from certain jobs. This article rates the effectiveness of alternate policy responses to increase women's occupational health and safety through use of a series of analysis criteria: equity, efficiency, preference satisfaction, right to privacy, avoidance of stigma, and unintended consequences. Policy options include the following: 1) do nothing, 2) leave current policies intact while supporting a research program to document the health consequences of specific occupational risks to women's reproductive health, 3) restrict women for who pregnancy is not ruled out from occupations or work areas known or suspected to be hazardous, 4) improve working conditions for all women, and 5) improve working conditions for all workers. Policy analysis suggests the working conditions of all workers should be improved. This alternative reduces inequity, eliminates stigma, maintains privacy, and honors preferences. Implementation of this policy would be expensive, requiring an increase in knowledge of the effects of industrial substances on female and male reproductive health, expansion of the technical capacity to control occupational hazards, and an increase in the resources of programs that monitor and regulate occupational health. However, this approach is in accord with growing concern that workers should not have to compromise their health to keep their jobs.
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PMID:A policy analysis of the problem of the reproductive health of women in the workplace. 647 Jan 31

Although ovarian mechanisms of ovulation have been a subject of investigation for more than a century, essential regulatory pathways remain uncertain. A role for the ovarian surface epithelium in ovulation has recently been demonstrated. Ovarian surface epithelial cells in close contact with the apical wall of preovulatory ovine follicles secrete a urokinase-type plasminogen activator in response to surge concentrations of (locally delivered) gonadotrophins. Urokinase activates latent collagenases and stimulates release of tumour necrosis factor alpha from thecal endothelium. Tumour necrosis factor alpha progressively induces matrix metalloproteinase gene expression, apoptosis and inflammatory necrosis. Collagenolysis and cellular death are a prelude to stigma formation and ovarian rupture. Epithelium exfoliated from the dome of ovulatory follicles is replenished by generative stem cell replication and migration from the wound edges. Common epithelial ovarian cancer has been related to successive bouts of ovulation and mitosis. The integrity of the DNA of surface cells circumjacent to the ovarian rupture site is compromised during the ovulatory process. Clonal expansion of an epithelial cell with damaged (unrepaired) DNA is a putative factor in carcinogenesis. Ovarian cancer is a deadly insidious disease because typically it is asymptomatic until the malignancy has reached beyond the ovaries.
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PMID:Roles of the ovarian surface epithelium in ovulation and carcinogenesis. 1205 28