Carcinoma of the human uterine cervix has been associated with several infectious agents including papillomavirus. Papillomavirus group-specific antigen (GSA) and viral particles have been demonstrated in human condylomata acuminata (CA) and flat warts of the uterine cervix. Cell alterations consisting of nuclear enlargement, hyperchromasia, irregularity, binucleation and cytoplasmic clearing (koilocytosis) are often interpreted as mild to moderate dysplasia. Present evidence that human papillomavirus (HPV) is responsible for the development of these lesions relies on the association of GSA and virus particles in the affected tissue, fulfilling the first two of Koch's postulates. Direct proof of an aetiological relationship, however, requires induction of the CA change in normal, human uterine cervix after exposure to papillomavirus. Infecting human subjects with HPV is ethically unacceptable and no satisfactory alternative systems have been defined. Also, human cell cultures do not support growth or transformation by HPV. Here we report the first demonstration of the morphological transformation of human tissues with a human papillomavirus under controlled, experimental conditions. 'Transformation' is used here in its literal sense to refer to a heritable morphological alteration in the appearance of the cells. The use of this term does not indicate that the changes described are neoplastic, but they are identical to the dysplastic changes found in biopsies of uterine cervical CA. Our results demonstrate the direct involvement of CA virus in dysplastic change of human cervical tissue and indicate that the experimental system described may be useful in elucidating the contribution of human papillomaviruses to the pathogenesis of human cervical cancer.

Cell Transformation, Neoplastic↗

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The use of percent volume analysis in Coulter sizing of cells in gynecologic cytopathologic cell suspensions.

The Coulter Counter model TA II was evaluated as a gynecologic cytodiagnostic tool. The instrument produces particle size histograms as plots of percent volume versus particle volume in 16 channels with each channel corresponding to twice the volume of the next lower channel. Cell volume distributions were obtained using cell suspensions from patients with cervicitis, inflammation, dysplasia or carcinoma and were compared with those from normal subjects. Although this method is superior to other methods of volume distribution analysis, it does not satisfy the stringent requirements of a cervical cancer mass screening method.

Cell Count↗

PubMedDate not supplied

Endometrial cancer risk in relation to serum lipids and lipoprotein levels.

Blood lipids are useful biochemical indicators for assessing the risk of a number of chronic diseases, particularly those associated with obesity. In a multicenter case-control study that included 256 cases and 185 controls less than 75 years old, we studied the risk of endometrial cancer in relation to serum cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol, and triglycerides. Contrary to expectation, blood lipids were, in general, lower among cases compared with controls. The effects of low blood lipids, specifically cholesterol and low density lipoprotein cholesterol, were limited to older women (> or = 55 years). Risk of the disease in this subgroup of 177 cases and 110 controls was increased 3-4-fold among those with the lowest cholesterol or low density lipoprotein cholesterol values. For example, after adjustment for age, education, smoking status, obesity, and body fat distribution, the relative risks of endometrial cancer across decreasing quartiles of serum cholesterol were 1.0, 2.5, 2.4, and 4.2 (P for trend < 0.01). We examined blood lipid levels by disease stage. The low lipid values of older cases did not appear to be a consequence of the disease. While we cannot rule out the possibility that hypocholesterolemia is a predisposing factor for endometrial cancer, there is no obvious biological explanation for the inverse association.

Adult↗

PubMedDate not supplied

Relation of endometrial cancer risk to past and contemporary body size and body fat distribution.

In a multicenter case-control study that included 403 cases and 297 controls, we examined the relation of past and contemporary body size, including body fat distribution, to the risk of endometrial cancer. The relative contributions of past and contemporary body size were assessed by examining weight and height histories provided by the subjects. Anthropometric indicators thought to reflect early environmental influences (e.g., height and sitting height), current weight, and fat distribution patterns were measured directly. Height was not a risk factor for endometrial cancer, but inexplicably, sitting height was inversely associated with risk. Weight during early adulthood appeared to be directly related to disease risk, but the association was explained by contemporary weight and thus weight gain during adulthood. While contemporary weight was associated with risk of endometrial cancer, the effect was restricted to those in the top quartile. Women whose measured weight at interview exceeded 78 kg had 2.3 times the risk of those weighing less than 58 kg (95% confidence interval, 1.4 to 3.7). Upper-body obesity (waist-to-thigh circumference ratio) was a risk factor independent of body weight. After adjustment for weight, the relative risks of endometrial cancer across increasing quartiles of upper-body obesity were 1.0, 1.5, 1.8, and 2.6 (P for trend < 0.001). These data indicate that both obesity and the distribution of adipose tissue accumulated during adult life increase endometrial cancer risk substantially.

Adipose Tissue↗