An analysis of abnormalities of the retinoblastoma gene in human ovarian and endometrial carcinoma

Article Abstract:

While cancer-causing oncogenes have been more widely studied, there is growing interest in tumor suppressor genes. These genes act in a Mendelian recessive manner; that is, one abnormal tumor suppressor gene has little or no effect in the presence of a normal suppressor gene. However, when both tumor suppressor genes are defective, a tumor may develop. The most widely studied tumor suppressor gene is the retinoblastoma gene, which had been found to be defective in virtually all cases of retinoblastoma. The gene, which is located on the long arm of chromosome 13 at 13q14, is thought to be involved in other tumors as well. Patients with retinoblastoma have a 100-fold increased risk of osteogenic sarcoma, and abnormalities of the retinoblastoma gene are found in numerous tissue culture lines of cancer cells. For this reason, the retinoblastoma genes were studied in ovarian carcinomas and endometrial carcinomas; normal ovaries and nonmalignant endometrial hyperplasias were also studied. The authors looked for retinoblastoma genes using the Southern blot procedure, which meant that only a homozygous deletion of the retinoblastoma gene was likely to be detected. Just such a pair of deletions was identified in 1 of 24 patients with ovarian cancer. The finding is of interest due to a peculiar feature of the case history. The patient, a 73-year-old woman, had a tumor that was identified as an endometrioid tumor of ovarian origin (although the endometrium of the uterus cannot be entirely ruled out as the source). Although the tumor appeared to have low malignant potential on histological examination and the patient possessed no known adverse prognostic indicators, the disease progressed rapidly and the woman died eight months after diagnosis. It is suggested that the homozygous deletions of the retinoblastoma tumor suppressor gene may have contributed to the rapidly progressive course of her disease. (Consumer Summary produced by Reliance Medical Information, Inc.)

Physiological aspects, Ovarian cancer, Endometrial cancer, Tumor suppressor genes

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Kaposi's sarcoma in patients with acquired immune deficiency syndrome: a flow cytometric DNA analysis of 26 lesions in 21 patients

Article Abstract:

Many cancer cells have chromosome abnormalities. Unlike normal human cells, in which the chromosomes are organized in 23 pairs, cancer cells may have fewer or more than the normal 46. While the normal paired chromosome complement is referred to as diploidy, an abnormal set of chromosomes is called aneuploidy. Although it is arduous to directly analyze the chromosomes, researchers have taken to estimating the chromosome complement using a technique called flow cytometry. In this technique, separated individual cells are stained with a fluorescent dye, which binds to DNA, and dribbled on-by-one through a device which measures the individual DNA content of each cell. Using this automated technique, researchers from a number of different fields have found that aneuploidy, or an abnormal chromosome complement, correlates with a poorer prognosis for many, but not all cancers. In an investigation of cells of Kaposi's sarcoma, however, aneuploid cells were not observed. In specimens of 26 lesions from 21 patients with AIDS, all the cells appeared to be diploid. In addition, the fraction of cells which were engaged in DNA synthesis at the time the specimen was taken was between 2 and 13 percent, somewhat low for a cancer. The results indicate that Kaposi's sarcoma is actually more like a proliferative disease rather than a malignant tumor. (Consumer Summary produced by Reliance Medical Information, Inc.)

Research, Flow cytometry, AIDS (Disease), Kaposi's sarcoma, AIDS research, Ploidy

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Possible involvement of the retinoblastoma gene in undifferentiated sinonasal carcinoma

Article Abstract:

Retinoblastoma is a malignant glioma, or tumor of neuroglia cells of the retina, the layer in the eye that receives images formed by the lens. This cancer occurs in young children and appears to show a hereditary pattern. The formation of the tumor is activated by the loss of genetic material, specifically at the RB-1 gene on chromosome 13. Patients with the inherited form of neuroblastoma have a specific gene defect and are at increased risk of developing tumors at sites other than the eye (such as bone) in later life. A case is described of a 38-year-old patient with sinonasal undifferentiated carcinoma (SNUC), an undeveloped cancer of the nasal sinuses. The patient had been treated for retinoblastoma affecting both eyes, by enucleation (removal) of the tumorous left eye and by irradiation of the right eye. A defect was detected on the RB-1 gene of the SNUC cells but not in normal tissue. These results show that genetic mutations of the RB-1 gene may be involved in the formation or progression of tumors of ectodermal tissue, such as skin, mouth gland, and sensory tissue. (Consumer Summary produced by Reliance Medical Information, Inc.)

Head and neck cancer

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