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At least 775 records · Page 43Linked to original sources
PubMed2006

The role of SV40 in malignant mesothelioma and other human malignancies.

SV40 is a DNA tumor virus thrust upon human populations primarily as a contaminant in various vaccine preparations. Some estimates suggest that millions of people are currently infected with the virus. The virus causes primary brain tumors, bone tumors, lymphomas, and mesotheliomas when injected into some rodent models. It has also been detected in a similar spectrum of human tumors. However, epidemiological studies have failed to conclusively demonstrate a higher incidence of disease in affected populations. To date, over 60 reports from 49 different laboratories have shown SV40 sequences in tissues from human cancer patients. Six studies, however, have failed to detect evidence of virus in similar tissues. Some have suggested that SV40 may act as a cocarcinogen with asbestos to cause mesothelioma formation, or that it may be responsible for the 10-20% of mesotheliomas with no reported history of asbestos exposure. This report briefly covers the historical evidence for SV40 carcinogenesis and then covers experiments now underway to better understand the role of SV40 in human mesotheliomas.

Animals↗
PubMed1986

Are there differences in the cell cycle of normal and malignant cells? An approach to the analysis of the clonal expansion of cells in malignant epithelial proliferations in situ.

The Williams-Bjerknes model for clonal expansion of transformed cells in epithelia was used to examine a series of related questions about the growth of in situ proliferations in epidermis. Bowens disease, actinic keratosis and lentigo maligna lesions were reconstructed on a three-dimensional basis, and all were found to behave differently: the evidence supported the proposal that the 'carcinogenic advantage' enjoyed by transformed cells was proliferative in nature, and indeed varied between the three lesions. We conclude that the clonal expansion of a single cell, with different proliferative carcinogenic advantage, can explain the three-dimensional appearances of these in situ proliferations; furthermore, the well-known 'multifocality' of in situ epidermal proliferations can also be explained by the clonal expansion of a single transformed cell.

Animals↗
PubMed1997

Acinar differentiation by non-malignant immortalized human prostatic epithelial cells and its loss by malignant cells.

Invasive prostatic carcinomas and prostatic intraepithelial neoplasia (PIN) are characterized by a loss of normal cell organization, cell polarity, and cell:cell and cell:basement membrane adhesion. The objective of this study was to establish in vitro three-dimensional (3-D) cell models which can be used to investigate mechanisms involved in acinar morphogenesis and differentiation in normal prostatic epithelium and their abnormalities in cancer cells. The process of acinar morphogenesis, including structural and functional differentiation, was investigated by culture on basement membrane gels (Matrigel). The human papillomavirus 18 immortalized, non-tumorigenic cell line RWPE-1, the v-Ki-ras transformed, tumorigenic RWPE-2 cell line derived from RWPE-1 cells (see previous paper pp. 1221-1229) and the human prostatic carcinoma cell line DU-145 were used. When cultured on Matrigel, RWPE-2 cells remain as single cells or form small aggregates and DU-145 cells form large amorphous cell aggregates without any organization or lumen. In contrast, RWPE-1 cells form acini of polarized epithelium with a distinct lumen, show a distinct laminin basement membrane, and express alpha6beta1 integrins at their basal end. Exposure to conditioned medium from NIH 3T3 cultures accelerates glandular morphogenesis. Parallel cultures maintained as monolayers on plastic remain as monolayers. In the presence of the synthetic androgen mibolerone, acinar cells express prostate specific antigen (PSA) as determined by immunostaining. We conclude that normal prostate cells can undergo acinar morphogenesis while tumorigenic cells have lost this ability. The 3-D cultures provide physiologically relevant in vitro models for elucidating regulation of growth, morphogenesis and differentiation in the normal human prostate, for defining heterotypic interactions in benign prostatic hyperplasia and for establishing the basis for the loss of normal cell organization in early neoplastic lesions such as PIN as well as during tumor progression in prostate cancer.

3T3 Cells↗
PubMed1995

Malignant lymphoma of soft tissue in an HIV-1+ patient. A rare site for primary malignant lymphoma with implications for treatment. Military Medical Consortium for the Advancement of Retroviral Research.

Soft tissue lymphomas are rare; however, the only large reported series has indicated that soft tissue lymphomas may have a better prognosis than similar-grade tumors found at other sites, and even high-grade lesions may respond to local therapies. We present a human immunodeficiency virus type 1 (HIV-1)-positive, Walter Reed stage VI black male with a documented high-grade soft tissue non-Hodgkin's lymphoma with no other evidence of tumor on complete systemic evaluation. Although extranodal lymphomas are common in HIV-1 disease, we are aware of no other reports of a soft tissue lymphoma in an HIV-1-positive patient. A significant percentage of soft tissue lymphomas in the general population, even when they are high grade, responds to local therapies including surgical excision and radiation. Thus, confirmation of this diagnosis in HIV-1 disease may be important, because these patients frequently develop fatal opportunistic infections and tolerate chemotherapy poorly, especially in late stages of disease.

AIDS-Related Opportunistic Infections↗
PubMed1992

The role of occupational exposure and immunodeficiency in B-cell malignancies. Working Group on the Epidemiology of Hematolymphopoietic Malignancies in Italy.

Excesses of non-Hodgkin's lymphoma have been observed among farmers exposed to phenoxyacetic acid herbicides and, less persuasively, among workers exposed to insecticides. Exposure to organic solvents (particularly chlorinated hydrocarbons) has also been associated with an increased risk of NHL. TCDD (which is a contaminant of phenoxy herbicides), DDT, and chlorinated solvents have all been reported to induce impairment or suppression of cell-mediated immunity. We hypothesize that NHL is caused by common viruses, such as the Epstein-Barr virus, that induce proliferation and immortalization of B-cells, followed by T-cell impairment entailing cell-mediated immunodeficiency. The increased risk of NHL with HIV infection and heart or kidney transplantation, in which immunodeficiency also occurs, is consistent with this hypothesis.

Animals↗