Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mass closure of midline incisions with a running large-bore permanent monofilament polypropylene suture has been used in general surgery and gynecology patients with a reported small incidence of fascial dehiscence. Late-occurring wound sinus formation is one problem reported with the use of this permanent suture material. Over a 22-month period, 285 patients had midline incisions closed with a continuous, running no. 1 polyglyconate monofilament delayed absorbable suture. Closely spaced bites (about 1.5 cm apart) were taken and placed 2 cm lateral to the fascial edge. Over 60% of the patients had surgery because of gynecologic cancer. Other high-risk factors included obesity in 62%, diabetes in 19%, and previous irradiation or chemotherapy in 22%. An ovarian cancer staging procedure was done in 16% of the patients. Of the remaining patients, almost half had extensive operative procedures that ranged from exenterations to hysterectomies with lymph node dissection. Wound complications were noted in nine patients (3.2%). Seven had superficial infections, one had an evisceration, and one developed a ventral hernia. Wound sinuses did not occur. The closure technique is safe and expedient and distributes tension equally over a continuous line. It has the additional advantage of eventual absorption of the suture material, thereby avoiding the wound sinus problems occasionally reported with large-bore permanent sutures.
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PMID:Primary mass closure of midline incisions with a continuous polyglyconate monofilament absorbable suture. 221 39

Over a 42-month period, 210 patients had a lower midline incision, usually extending around the umbilicus, that was closed with a continuous, running number 2 polypropylene suture. Patients in this study had various predisposing factors for wound disruption. Over 60% were operated upon because of gynecologic cancer. Additional high-risk factors included obesity in 56%, diabetes in 28%, previous irradiation or chemotherapy in 17%, and ascites in 8%. The operative procedures performed ranged from hysterectomies with node sampling to bowel resections and exenterations; wound complications were noted in seven patients. One patient had an incisional hernia. No eviscerations occurred. The closure is safe, expedient, and cost-efficient, and distributes tension equally over a continuous line.
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PMID:Primary mass closure of midline incisions with a continuous running monofilament suture in gynecologic patients. 264 26

Endometrial carcinoma is now the most common gynecologic cancer in the United States and its incidence is increasing. Many investigators attribute this to exogenous factors over which little control has been exerted in the western world. Obesity, dietary fat content, and changing patterns of parity and lifestyle seem significant. Moreover, there appears to be an emerging virulence noted, particularly in some centers. Improved surgical staging and a better understanding of virulence factors will increase the number of patients requiring treatment to fields larger than heretofore recognized. We can expect that one third of the patients with endometrial cancer will require treatment for widespread disease or recurrent disease. Progestational treatment is useful in approximately one-third of all patients with recurrent disease. Thus, systemic nonhormonal chemotherapy must be developed if cure rates in this disease are to improve appreciably. In 1974, only 126 patients had been reported to have been treated with cytotoxic chemotherapy for endometrial cancer. Since that time, experience has demonstrated that the most active single agents are adriamycin, cisplatin, and hexamethylmelamine. These drugs produce a 30-40% response rate when used individually. Multidrug regimens employing various combinations have achieved responses of 15-85% with and without the inclusion of a progestational agent. The median duration of response has been increased but cures are still relatively few. Adverse effects are tolerable and age is not a contraindication to the administration of cytotoxic chemotherapy. Adjuvant treatment is being tested and optimism for future success is justified.
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PMID:Cytotoxic chemotherapy for patients with endometrial carcinoma. 379 31

The incidence of newly diagnosed breast cancer cases world-wide is expected to double by 2020. Risk-reducing strategies for breast cancer include lifestyle modifications, chemoprevention and surgery (bilateral mastectomy and/or oophorectomy). Lifestyle modifications include avoidance of postmenopausal obesity and hormone replacement therapy (HRT), regular physical activity, and restriction of alcohol and animal fat intake. Tamoxifen is a selective estrogen receptor modulator (SERM) shown in randomized controlled trials to reduce the incidence of estrogen receptor (ER)-positive breast cancer in high-risk healthy women. However, its routine use cannot be recommended for breast cancer prevention in healthy women due to its significant adverse effects, specifically in terms of endometrial carcinoma and thromboembolism. On the other hand, tamoxifen may be used for chemoprevention in women at high risk of developing ER-positive breast cancer and at low risk of developing complications. Raloxifene, another SERM, also appears to be effective in reducing breast cancer risk, and lacks the unwanted stimulatory effect on the uterus. Other promising chemopreventive agents currently under investigation include cyclo-oxygenase 2 (COX-2) inhibitors, fenretinide, aromatase inhibitors, and goserelin. Prophylactic mastectomy can reduce breast cancer risk by 90% in high-risk women. Bilateral oophorectomy has the potential of reducing the risk of both breast and gynecologic cancer in women carrying BRCA-1 or BRCA-2 mutations. Further research is required to identify novel strategies to prevent ER-negative breast cancer, minimize the adverse effects of tamoxifen and other SERMs, and evaluate the role of mammary ductal lavage and ductoscopy in guiding risk-reducing strategies.
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PMID:Risk-reducing strategies for breast cancer--a review of recent literature. 1564 97

Office visits centering on preventive and gynecologic concerns compose a significant proportion of any primary care practice. The detection and prevention of gynecologic cancers are topics that often predominate such visits. The trend of increasing obesity in the general population and the exploding public awareness of the prevalence of human papillomavirus are examples of topics that affect the primary care physician's approach toward gynecologic cancer screening for women. Changing incidence rates in endometrial cancer and cervical cancer challenge the traditional approach to screening, guiding the primary care physician to consider individual risk factors during the routine health maintenance examination. In this article, the epidemiology, screening guidelines, and a review of management are presented for vulvar, cervical, ovarian, and endometrial cancer.
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PMID:Gynecologic cancers. 1923 5

Epithelial ovarian cancer (EOC) is the most lethal gynecologic cancer and also one of the most poorly understood. Other health issues that are affecting women with increasing frequency are obesity and diabetes, which are associated with dysglycemia and increased blood glucose. The Warburg Effect describes the ability of fast-growing cancer cells to preferentially metabolize glucose via anaerobic glycolysis rather than oxidative phosphorylation. Recent epidemiological studies have suggested a role for hyperglycemia in the pathogenesis of a number of cancers. If hyperglycemia contributes to tumour growth and progression, then it is intuitive that antihyperglycemic drugs may also have an important antitumour role. Preliminary reports suggest that these drugs not only reduce available plasma glucose, but also have direct effects on cancer cell viability through modification of molecular energy-sensing pathways. This review investigates the effect that hyperglycemia may have on EOC and the potential of antihyperglycemic drugs as therapeutic adjuncts.
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PMID:The role of dysregulated glucose metabolism in epithelial ovarian cancer. 2018 31

Diet, physical activity, and weight may affect prognosis among women who are diagnosed with breast or gynecologic cancer. Observational studies show associations between being overweight or obese and weight gain with several measures of reduced prognosis in women with breast cancer and some suggestion of poor prognosis in underweight women. Observational studies have shown an association between higher levels of physical activity and improved breast cancer-specific and all-cause mortality, although a dose-response relationship has not been established. One large randomized controlled trial reported increased disease-free survival after a mean of 5 years in patients with breast cancer randomly assigned to a low-fat diet versus control. However, another trial of similar size found no effect from a high vegetable/fruit, low-fat diet on breast cancer prognosis. The few reported studies suggest that obesity negatively affects endometrial cancer survival, while the limited data are mixed for associations of weight with ovarian cancer prognosis. Insufficient data exist for assessing associations of weight, physical activity, or diet with prognosis in other gynecologic cancers. Associations of particular micronutrient intake and alcohol use with prognosis are not defined for any of these cancers. The effects of dietary weight loss and increase in physical activity on survival or recurrence in breast and gynecologic cancers are not yet established, and randomized controlled trials are needed for definitive data.
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PMID:Weight, physical activity, diet, and prognosis in breast and gynecologic cancers. 2064 95

The prevalence of overweight and obesity in the United States and elsewhere has increased dramatically in recent decades. It has long been known that obese women have an increased risk of developing endometrial cancer, but recent studies suggest this association is strongest for the most common low-grade endometrioid endometrial cancers and weaker for the other histologic subtypes. There are insufficient data to assess whether obesity affects endometrial cancer-specific survival or whether the relation with all-cause mortality is similar to that seen in the general population. Recent data suggest obesity also increases risk of ovarian cancer, although it may not influence risk of the high-grade serous cancers that account for the majority of ovarian cancer deaths, and that it is also associated with poorer outcomes. There is currently insufficient evidence to draw any clear conclusions regarding the relation between obesity and risk of/survival from other gynecologic cancers although there are suggestions that obesity may increase risk of cervical cancer, particularly adenocarcinoma, and perhaps vulvar cancer. Possible mechanisms whereby obesity might influence gynecologic cancer risk and survival include: its strong association with endogenous estrogen levels among postmenopausal women, its effects on glucose metabolism, its effects on the wide range of adipocytokines and inflammatory mediators that are produced by adipose tissue and altered in concentration among obese individuals, and its potential effects on patient management, particularly with regard to chemotherapy dosing.
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PMID:Obesity and gynecologic cancer etiology and survival. 2371 8

Women are living longer after a cancer diagnosis because of advances in early detection and treatment. However, although our ability to effectively treat gynecologic malignancies has improved, survivors of gynecologic cancer often face profound physical, emotional, sexual, and psychosocial challenges as a result of their cancer diagnosis and treatment. In this article, we discuss how patient comorbidities (i.e., obesity) and cancer treatment effects may adversely affect sexual health outcomes, gastrointestinal function, and general health among survivors of gynecologic cancer. The importance of a multidisciplinary, patient-centered approach to survivorship care is emphasized.
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PMID:Survivorship in gynecologic cancer: enduring the treatment toward a new normal. 2485 15

Rates of the most common gynecologic cancer, endometrioid adenocarcinoma (EAC), continue to rise, mirroring the global epidemic of obesity, a well-known EAC risk factor. Thus, identifying novel molecular targets to prevent and/or mitigate EAC is imperative. The prevalent Type 1 EAC commonly harbors loss of the tumor suppressor, Pten, leading to AKT activation. The major endoplasmic reticulum (ER) chaperone, GRP78, is a potent pro-survival protein to maintain ER homeostasis, and as a cell surface protein, is known to regulate the phosphatidylinositol 3-kinase (PI3K)/AKT pathway. To determine whether targeting GRP78 could suppress EAC development, we created a conditional knockout mouse model using progesterone receptor-Cre-recombinase to achieve Pten and Grp78 (cPten(f/f)Grp78(f/f)) deletion in the endometrial epithelium. Mice with a single Pten (cPten(f/f)) deletion developed well-differentiated EAC by 4 weeks. In contrast, no cPten(f/f)Grp78(f/f) mice developed EAC, even after more than 8 months of observation. Histologic examination of uteri from cPten(f/f)Grp78(f/f) mice also revealed no complex atypical hyperplasia, a well-established EAC precursor. These histologic observations among the cPten(f/f)Grp78(f/f) murine uteri also corresponded to abrogation of AKT activation within the endometrium. We further observed that GRP78 co-localized with activated AKT on the surface of EAC, thus providing an opportunity for therapeutic targeting. Consistent with previous findings that cell surface GRP78 is an upstream regulator of PI3K/AKT signaling, we show here that in vivo short-term systemic treatment with a highly specific monoclonal antibody against GRP78 suppressed AKT activation and increased apoptosis in the cPten(f/f) tumors. Collectively, these findings present GRP78-targeting therapy as an efficacious therapeutic option for EAC.
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PMID:Targeting the glucose-regulated protein-78 abrogates Pten-null driven AKT activation and endometrioid tumorigenesis. 2568 38


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