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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vulvar neoplasia as seen at the Johns Hopkins Hospital during a 38-year period (1935-1972) is reviewed. Of 1385 tissue specimens, 1053 were benign and 332 were malignant lesions. Of the malignant lesions, 246 were squamous cell carcinoma, both in situ and invasive. Of these, 192 were treated and followed and are reported on. There were 71 cases of in situ and 121 of invasive cancer. Of the patients, 64% were white and 36% were nonwhite, which corresponds to the patient population treated at the hospital. Ages of patients ranged from 21 to 86 years, with a median of 50 years. Of those with invasive cancer, 75% were postmenopausal and none was under the age of 30 years. There was a 29% incidence of nulliparity and a 64% incidence of obesity. Diabetes was noted in 64%. Syphilis was discovered in 26%. These patients had a high risk of being exposed to other venereal infections, particularly herpes which is suspect as a precursor of neoplasia. Vurrucous carcinoma are also likely to be of viral origin. Other malignancies were also present in 20% of patients. There was 1 case of chronic clyphocytic leukemia. Presenting symptoms were a lump, a white patch, pruritus, or bleeding. Pruritus was present in 46%. A leukoplakialike appearance was noted in most of the in situ lesions. Multicentric foci of origin were demonstrated in 35%, mostly in the in situ cases. Of the invasive cancers 60% were well differentiated and 11% were verrucous. Multiple histologic patterns were present in many cases. In 167 patients (67%), the initial treatment was surgical. Postoperative radiation was used in 30% of those with invasive cancer. Local recurrences followed in 22%. In those with multicentric foci the recurrence rate was 48%. 44 patients were known to have died, mostly from other causes. Survival was directly related to the stage of the disease at the time of initial diagnosis and treatment.
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PMID:Primary vulvar neoplasia: a review of in situ and invasive carcinoma, 1935-1972. 85 43

It may be possible to delay the step-by-step progression towards frank invasive cancer by avoiding one or more of the well-known clinical risk factors. In addition current clinical trials in the USA and Europe are assessing whether the use of tamoxifen, vitamin analogues or a low-fat diet can delay the appearance of overt disease in women known to be at high risk, but it will be several years before such trials can be evaluated. For women seeking advice on prevention, non-toxic supplements to the diet such as beta-carotene, vitamin A analogues or selenium compounds, and the avoidance of alcohol and obesity, are examples of practical advice which can do no harm yet may help to protect against breast cancer development. In the case of the very anxious first degree relative of a breast cancer patient, the current choice lies essentially between regular monitoring, mastectomy with reconstruction, early termination of ovarian activity and anti-oestrogen therapy. Currently, considerable research is being directed towards identifying oncogenes and growth factors which are involved in the growth of breast cancer. In the meantime, more research needs to be devoted to the effect of various progestagens in counteracting oestrogen support of breast cancer growth, and to biological observations on different formulations and doses of combined oestrogen/progestagen preparations which may reduce breast cancer risk both in pre- and postmenopausal women.
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PMID:Approaches to breast cancer prevention. 226 93

A case-control study conducted within the Breast Cancer Detection Demonstration Project allowed comparison of epidemiologic factors for benign breast diseases (n = 1,404), in situ cancer (n = 199), small (less than or equal to 1 cm) invasive cancer (n = 210), and larger invasive cancer (n = 788). Control subjects consisted of program participants who were not recommended for breast biopsy. Relationships were similar for small and larger invasive tumors, both showing associations with family history of breast cancer, age at first live birth, history of bilateral oophorectomoy, and obesity. In situ cancer was affected by family history and age at first childbirth but not by oophorectomy or obesity. These findings support the notion that "minimal" breast cancer is indeed cancer. In addition, the results suggest that hormonal influences early in life may initiate the carcinogenic process, while those that operate later may enhance the progression from in situ to invasive disease.
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PMID:Epidemiology of minimal breast cancer. 684 48

Cancer prevention as related to the problem of cervical and endometrial cancer involves a great number of factors that are considered contributory to the development of neoplasms in the uterus. Lifestyles encouraging the development of cervical cancer are different from those encouraging endometrial cancer. Cancer of the cervix is a disease of the inner city. It is seen in those staring intercourse in their teens, having multiple partners, having many children, and coming from the low socioeconomic groups. Semen and herpes virus II may have an adverse effect on immature cells, but there are no hard data to confirm these roles. Cancer of the endometrium is a disease of suburbia. The American Cancer Society estimates that there will be 38,000 new cases of endometrial carcinoma in 1980, making it the most common female genital cancer. Women at highest risk for later carcinoma of the endometrium are those who have obesity, diabetes, infertility, irregular menses and failure of ovulation, adenomatous hyperplasia, and/or prolonged estrogen administration. For both cervical and endometrial cancers, it is possible to identify the high-risk patient, to detect changes at an early stage, and, by instituting appropriate therapy, to prevent a more serious problem. It is obvious that prevention, detection, and treatment are all closely intertwined. This paper identifies the patient at high risk and makes suggestions for correcting any imbalance that may predipose to the development of invasive cancer.
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PMID:Uterine cancer (prevention). 723 68

Adenocarcinoma of the endometrium is the most common gynecologic malignancy in the United States, accounting for some 36,000 cases of invasive cancer each year. Hyperplastic lesions of the endometrium follow a continuum, with the risk of progression to carcinoma being related to the severity of the disorder. Risk factors associated with the development of adenocarcinoma include hyperplasia, obesity, menstrual abnormalities, diabetes, hypertension, prior pelvic irradiation, sequential oral contraceptive use, diet, and exogenous estrogen use. There is also some evidence of genetic predisposition, and some data indicating the possibility of specific genetic abnormalities and activation of oncogenes as factors determining the etiology of the disease. At this time there is no accepted screening test for endometrial carcinoma, though the role of immunochemistry techniques for screening and follow-up has just begun to be realized. Dilatation and curettage along with hysteroscopy remain the major means of diagnosis. A variety of prognostic variables including tumor cell type, histologic grade, depth of myometrial invasion, status of peritoneal cytology, presence of disease in preformed vascular spaces, presence of adnexal metastases, and presence of cervical involvement have been defined. Although the treatment plan for each patient must be individualized, the mainstay of treatment remains total abdominal hysterectomy with bilateral salpingo-oophorectomy. Metastatic and recurrent disease is usually treated with hormonal therapy and systemic chemotherapy. Radiation therapy like surgery in recurrent disease is only applicable for the treatment of local recurrences.
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PMID:Endometrial adenocarcinoma. 840 Apr 24

Chemoprevention refers to the use of specific natural or synthetic chemical agents to reverse, suppress, or prevent the progression to invasive cancer. The ideal chemopreventive agent is safe and nontoxic over the long term. It should be easy to take and demonstrated to be effective in randomized trials in humans. Aspirin and NSAIDs meet many of the criteria for an ideal agent. The literature on aspirin and NSAIDs makes it clear that these agents can prevent colorectal cancer and precursor adenomas. That does not mean that we should make general recommendations for their use. First, we do not know the proper dose or duration. More important, these medications are accompanied by adverse effects that can be considerable. Indeed, the Medical Letter, an authoritative, unbiased publication on drugs and therapeutics, concluded that "for primary prevention in low-risk patients, more studies are required to establish whether the beneficial effect of aspirin is great enough to compensate for the possible increased risk of hemorrhagic stroke." These recommendations were directed at the use of these medications for prevention of myocardial infarction, but the same conclusions apply to colorectal cancer: although aspirin may prevent the disease, it may increase the risk of hemorrhagic strokes or cause other adverse effects. We must accurately balance the benefits and risks of these drugs, based on the results of ongoing randomized studies, before recommending aspirin for prevention of colorectal cancer. Is there anything that we can recommend to our patients for prevention of colorectal cancer? Based on observational epidemiologic studies, it is clear that individuals who consume a diet high in vegetables and natural fibers and low in fat have a reduced risk of colon cancer and polyps. Optimal nutrient intakes for the prevention of cancer might be more readily achieved via food fortification or supplementation, but this requires more research. Regular physical exercise and maintenance of normal body weight are also protective. Until the results of definitive studies of chemopreventive agents are available, we can recommend that our patients eat a sensible diet, exercise, and avoid obesity. Such an approach should protect them from cardiovascular disease, an even deadlier condition than colorectal cancer. In the future, we need randomized prevention trials that, for logistic reasons, may need to focus on the occurrence and progression of colorectal adenomas rather than carcinoma itself. Studies that test more than one compound at a time, using factorial designs, will be more efficient. We will need better information about duration and dose, adverse side effects, molecular mechanisms, and cellular sites of NSAID activity. Ultimately, we will need to know more about the biology and molecular biology of colorectal cancer and its precursors. That information will, perhaps, permit us to design agents to interrupt the pathway to cancer and to use intermediate markers more intelligently.
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PMID:Aspirin and other nonsteroidal anti-inflammatory agents in the prevention of colorectal cancer. 879 Nov 32

Biological markers associated with in situ carcinoma and atypical intraductal hyperplasia in the breast are examined to help in identifying a subgroup of premalignant lesions whose natural history may be influenced by epigenetic factors. The biomarkers may be used as indices in clinical trials aiming to assess the effect of weight reduction, dietary intervention or hormone replacement therapy on the risk of progression to invasive breast cancer. In the current state of knowledge, the expression of oestrogen receptors, p53, bcl-2 and HER-2 neu oncogenes and the Ki-67 index of proliferative activity, are the most useful biomarkers for this purpose. In situ carcinoma of the breast manifests a variety of morphological phenotypes with specific biological characteristics. There is evidence that only a proportion of premalignant lesions are committed to progression to invasive cancer while other lesions undergo spontaneous regression at the time of the menopause. Cross-cultural studies suggest that it is the late-stage epigenetic promoting factors which are responsible for the high incidence of postmenopausal breast cancer in Western women. Obesity in middle life and the Western diet favour the development of hyperinsulinaemic insulin resistance, and the metabolic-endocrine effects of its concomitants may promote mammary carcinogenesis around the time of the menopause and increase the incidence of invasive cancer after the menopause. Because biomarker changes in premalignant lesions are nearer in time to these promoting influences, they could provide intermediate endpoints for testing the hypothesis.
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PMID:Premalignant breast lesions: role for biological markers in predicting progression to cancer. 1050 26

Risk factors for breast carcinoma in situ and invasive breast cancer were compared using data from 61,844 women (61% post-menopausal) with no prior breast cancer and at least one screening mammogram between April 1, 1996 and June 30, 2001. The women were followed until a subsequent mammogram before July 1, 2001, or a benign biopsy or breast cancer diagnosis before June 30, 2002. A total of 1,191 breast cancers (300 in situ and 891 invasive) were diagnosed during an average follow-up of 3.1 years. Multivariate Cox regression models were used to estimate the relative risks (RR) of in situ and invasive cancer associated with family history of breast cancer, age at first childbirth or nulliparity, post-menopausal hormone use, body mass index (BMI), and mammographic breast density. Separate analyses were done for pre- and post-menopausal women. BMI was unrelated to risk of in situ cancer regardless of menopausal status, but was associated with an increased risk of invasive cancer in post-menopausal women (RR = 1.9 for BMI > or = 30 vs. BMI < 22, 95% confidence interval 1.4-2.5). Later childbearing and nulliparity were more strongly associated with in situ than invasive cancer in pre-menopausal women. Post-menopausal hormone use was more strongly associated with invasive disease. RR associated with family history and breast density were similar for in situ cancer and invasive cancer. Results indicating that BMI is related to post-menopausal invasive cancers but unrelated to in situ cancers are consistent with the hypothesis that concomitants of obesity activate proliferation.
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PMID:Risk factors for breast carcinoma in situ versus invasive breast cancer in a prospective study of pre- and post-menopausal women. 1706 72

Submucosal cysts (SMCs) might result from severe gastritis and be related to gastric carcinogenesis, although direct evidence is limited. We studied clinicopathologic findings for gastric cancers arising in mucosa with SMC and the relation to gastritis. In 504 submucosal invasive cancer cases, SMC was found in 100. Comparison of degrees of gastritis using the Updated Sydney system, thickness of muscularis mucosae, and the patients' smoking and drinking habits and obesity showed significant variation between cases of cancer with and without SMC. In the stomach with SMCs, cancers were predominantly differentiated-type adenocarcinomas in men and showed a significant tendency for location in the upper gastric region. Intestinal metaplasia was significantly more severe and the muscularis mucosae were thicker in cancer cases with SMC in comparison with cases without SMC and control cases of gastrointestinal stromal tumor (GIST). Atrophy was also significantly more severe in cancer cases with and without SMC than in cases of GIST. The Brinkman index was also significantly higher. Cases of gastric cancer with SMC show characteristic clinicopathologic features, and SMC formation may be caused by gastritis and influenced by smoking.
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PMID:Background submucosal cysts in early gastric cancer cases have unique clinicopathologic features suggestive of postgastritis and significant smoking association. 1795 Nov 95

Breast cancer is the most common invasive cancer in women globally, and it affects more than 1 million women worldwide each year. It is a preventable disease in part, and primary care providers and public health programs play a key role in providing cancer preventive care. There are several health behaviors that may reduce the risk of breast cancer, including prolonged lactation; regular physical activity; avoiding overweight, obesity, and lifetime weight gain; avoiding excess alcohol intake; avoiding prolonged use of exogenous hormone therapy; and avoiding excessive radiation. These behaviors, although they have not been proven in clinical trials to reduce risk, are likely to be beneficial; information on them can be provided as a prevention strategy in countries of diverse means, although the methods of information delivery and follow-up will depend on financial and personnel resources. Many of these health behaviors can reduce the risk for other chronic diseases and, thus, may be of great interest for general public health. In high resource level countries, additional prevention methods are available for high-risk women, including selective estrogen response modulators and, for women at very high risk, bilateral prophylactic mastectomy and bilateral oophorectomy. Most women can benefit from advice and preventive care for reducing their risk for breast cancer.
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PMID:Breast cancer prevention in countries with diverse resources. 1883 24


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