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Biomedical subjects

M H Greene

Publications and source records attributed to M H Greene.

At least 55 records · Page 3Linked to original sources
PubMed1985

Hereditary malignant melanoma is not linked to the HLA complex on chromosome 6.

Detailed HLA typing was performed in 11 families with hereditary cutaneous malignant melanoma (CMM) and dysplastic nevi to determine if the melanoma susceptibility locus was genetically linked to the major histocompatibility complex. Previously published data from 19 other families were re-analyzed in the same manner. When data from all 30 families were pooled and CMM was defined as the disease trait, the hypothesis of linkage was rejected for all values of recombination (theta) less than 40%. Data on family members' status regarding dysplastic nevi (DN), a well-characterized precursor of hereditary CMM, were available for our 11 families and 7 previously-reported families. Linkage analysis between the combined CMM/DN trait and HLA provided strong evidence against this hypothesis. Significant heterogeneity was observed when various sub-groups of families were compared; these data suggested that preferential reporting of positive linkage findings and misclassification of study subjects' CMM susceptibility status may have contributed to previous beliefs that the hereditary melanoma gene was linked to HLA. When our data are combined with previously-published information, we conclude that there is strong evidence against linkage of a CMM/DN gene with the major histocompatibility complex.

Chromosomes, Human, 6-12 and X↗
PubMed1985

High risk of malignant melanoma in melanoma-prone families with dysplastic nevi.

The risk of hereditary cutaneous malignant melanoma was evaluated in 401 members of 14 families with an autosomal dominant form of melanoma. We documented 127 primary melanomas in 69 family members, including 39 new melanomas diagnosed in 22 study participants from the time of first examination through a maximum of 8 years of follow-up. The 39 newly diagnosed melanomas occurred only in family members with dysplastic nevi, a known precursor of familial melanoma. Of 77 patients with dysplastic nevus syndrome without prior melanomas, 4 developed their first melanoma during prospective follow-up, as compared with 0.03 cases expected. The prospective age-adjusted incidence for melanoma was 14.3/1000 patients with dysplastic nevus per year, with a cumulative melanoma risk (+/- SE) of 7.2% (+/- 3.6) at 8 years. The actuarial probability of melanoma developing in family members with dysplastic nevi was 56.0% (+/- 10.1) from age 20 to age 59. This study confirms that dysplastic nevi are clinical markers of high risk for, and precursors of, hereditary melanoma.

Adolescent↗
PubMed1985

Dysplastic nevus syndrome. Familial and sporadic precursors of cutaneous melanoma.

Familial dysplastic nevus syndrome is an autosomal-dominant precursor of hereditary melanoma in which individuals have clinically and histologically distinctive nevi and a markedly increased risk for development of melanoma. Dysplastic nevi also are found in sporadic forms. Classification of the condition of the patient and proper management including regular examination of nevi can help to determine the risk of melanoma and minimize the potential for neoplastic progression.

Female↗
PubMed1985

Cancer trends in a population at risk of acquired immunodeficiency syndrome.

Recent case reports have suggested that the acquired immunodeficiency syndrome (AIDS) may be associated with cancers other than Kaposi's sarcoma (KS). We have used the population-based registries of the Surveillance, Epidemiology, and End Results (SEER) Program to examine these relationships on a statistical basis by comparing the morbidity odds ratio (OR) and 95% confidence interval (CI) for specific cancer sites in pre- and post-AIDS time periods. Among never-married 20- to 49-year-old men, a surrogate group representing homosexual men, significant increases in the morbidity OR's for KS between 1973-80 and 1981-82 were apparent in the San Francisco standard metropolitan statistical area (OR: 51.8; CI: 18.6-143.6) and in other areas covered by the SEER Program (OR: 18.6; CI: 2.2-154.5). Furthermore, a significant increase was found in the morbidity OR for Burkitt-like lymphoma in the San Francisco metropolitan area (OR: 9.1; CI: 1.8-45.6). In San Francisco County (which includes the City of San Francisco), there was a 2,043-fold increase in the morbidity OR for KS and a fivefold increase for Burkitt-like lymphomas, but there were no significant changes for other cancers between 1973-79 and 1982. Similarly, no significant changes in morbidity OR's were observed for other cancers in the remaining SEER registries. These findings provided statistical support for the excess risk of Burkitt-like lymphoma in a group at risk of AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Second cancer following lymphatic and hematopoietic cancers in Connecticut, 1935-82.

The risk of developing a second primary cancer was evaluated in approximately 19,000 persons with initial cancers of the lymphatic and hematopoietic system in Connecticut between 1935 and 1982. Significant excesses for all second cancers were observed among patients with leukemia (34%), Hodgkin's disease (70%), non-Hodgkin's lymphoma (25%), and multiple myeloma (24%). In general, the risk of second cancers was greater in males than in females, even for cohorts not showing an excess of surveillance-related prostate cancer. Among patients with leukemia, significant excesses of cancers of the lung, kidney/ureter, and prostate were noted; cutaneous melanoma was elevated only in males. These excesses did not persist in the small number of long-term survivors. Possible etiologic factors included tobacco smoking for lung and kidney cancers, medical surveillance artifact for prostate cancer, and immunosuppression for malignant melanoma and lung cancer. The large number and good prognoses of patients with chronic lymphocytic leukemia strongly influenced the pattern of second cancers when all leukemias were analyzed together; no evidence was found for an increased risk of second cancer in patients with acute lymphocytic leukemia. A disproportionate number of subsequent cancers, particularly those of the kidney and ureter, were diagnosed incidentally at autopsy. Patients with Hodgkin's disease displayed significant excesses of cancers of the buccal cavity and pharynx, lung, female breast, and thyroid. The latter 3 sites remained significantly elevated in long-term survivors (10 yr or more postdiagnosis), so that radiation therapy may have contributed to their development. Among persons with non-Hodgkin's lymphoma, cancers of the stomach, lung, brain, and connective tissue occurred excessively. The first 3 sites, plus cancers of the urinary bladder, remained elevated among long-term survivors. The brain cancer excess, not previously reported, may represent misclassification of central nervous system lymphoma. The risk of gastric cancer is reminiscent of similar findings in patients with both acquired and genetically determined immunodeficiency disorders. The alkylating agent, cyclophosphamide, used extensively in the treatment of non-Hodgkin's lymphoma, is known to cause bladder cancer in man.(ABSTRACT TRUNCATED AT 400 WORDS)

Connecticut↗
PubMed1984

Determinants of retrovirus (HTLV-III) antibody and immunodeficiency conditions in homosexual men.

A cohort of homosexual men at high risk of the acquired immunodeficiency syndrome (AIDS) was monitored to examine the relation between lifestyle, clinical conditions, T-lymphocyte subsets, and antibody to the AIDS-associated human retrovirus, human T-cell leukaemia virus III (HTLV-III). HTLV-III antibodies were present in 35 (53%) of the 66 subjects tested in June, 1982. 4 of the seronegative subjects had HTLV-III antibodies when re-tested one year later, a seroconversion rate of 1.2% per month. In the HTLV-III seropositive subjects, AIDS developed at a rate of 6.9% per year (minimum incidence of AIDS = 4.6% per year) and other clinical signs of immunodeficiency (lesser AIDS) at 13.1% per year. All 6 of the AIDS cases and at least 8 of the 10 lesser AIDS cases had detectable HTLV-III antibodies 1 week to 21 months before diagnosis. Of 24 other subjects with stable lymphadenopathy, 19 (79%) had or acquired HTLV-III antibodies. Lower helper T-cell counts were very closely related to HTLV-III seropositivity (r = -0.53, p = 0.0001), even in the 26 healthy subjects with no clinical abnormalities (r = -0.37, p = 0.07). In both univariate and multivariate analyses, the lifestyle risk factors for HTLV-III seropositivity were large number of homosexual partners (p less than or equal to 0.03) and receptive anal intercourse (p less than or equal to 0.03), with an apparent synergistic interaction between these two activities (chi 2 = 8.71, p = 0.003). These data suggest that frequent receptive anal intercourse with many homosexual partners predisposes to HTLV-III infection with the consequent emergence of lymphadenopathy and the various manifestations of lesser and fully fledged AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Prognostic significance of histologic classification and grading of epithelial malignancies of the ovary.

Overall survival in 1938 women with epithelial ovarian cancer receiving primary treatment at Mayo Clinic was 35% at 5 years, 28% at 10 years, and 15% at 25 years. For most histologic cell types, observed differences in survival were more apparent than real since the behavior of different cell types was similar when compared stage for stage and grade for grade. Mucinous cystadenocarcinomas tended to be low grade and low stage, while serous cystadenocarcinomas tended to be high grade and high stage. For Stage I disease, factors other than cell type seemed to be more important in determining survival; specifically, Stage IA1 patients did significantly better than all other Stage I patients. In Stage III disease, the amount of residual tumor made a significant difference in survival for all grades. In Stage IV disease, the amount of residual made a highly significant difference in survival for grade 1 disease.

Adenocarcinoma↗
PubMed1984

A study of tumor progression: the precursor lesions of superficial spreading and nodular melanoma.

Six evident lesional steps of tumor progression form the neoplastic system that affects the human epidermal melanocyte: 1) the common acquired melanocytic nevus; 2) a melanocytic nevus with lentiginous melanocytic hyperplasia, i.e., aberrant differentiation; 3) a melanocytic nevus with aberrant differentiation and melanocytic nuclear atypia, i.e., melanocytic dysplasia; 4) the radial growth phase of primary melanoma; 5) the vertical growth phase of primary melanoma; and 6) metastatic melanoma. The common acquired melanocytic nevus is viewed as a focal proliferation of melanocytes, destined in most instances to follow a programmed pathway of differentiation that leads to disappearance of the nevus. If the pathway of differentiation is not followed, characteristic lesions result, and such lesions are regarded as the formal histogenetic precursors of melanoma. Such a developmental flaw is termed aberrant differentiation, and the resultant precursor lesion is designated melanocytic dysplasia. The vast majority of melanocytic nevi showing melanocytic dysplasia are terminal lesions that do not progress to melanoma. If melanoma is to develop via a precursor lesion, however, the nevus with melanocytic dysplasia is that precursor. When melanomas do develop, they develop focally within the precursor. The resultant primary melanoma itself does not follow a pathway of inexorable expansion of a population of melanoma cells in space and time. Rather, primary melanomas, with the exception of nodular melanoma, also evolve in a stepwise fashion. The first step, termed the radial growth phase, is characterized by the net enlargement of the tumor at its periphery, along the radii of an imperfect circle. Tumors in this stage of development show a characteristic pattern of growth within the epidermis and a distinctive form of invasion of the papillary dermis. Such melanomas are not associated with metastasis, and it is hypothesized that such tumors do not have competence for metastasis. For a melanoma to acquire competence for metastasis it must progress to the next step of tumor progression--the vertical growth phase. This lesional step is characterized by the appearance of a new population of cells within the melanoma, not an expansion of the cells forming the pre-existing radial growth phase. The net growth of the cells of the vertical growth phase is perpendicular to the directional growth of the radial growth phase. As a rule, the cells of the vertical growth phase grow in an expansile fashion, expansile as a balloon expands: a growth form characteristic of metastases.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1984

Fibroblasts from patients with hereditary cutaneous malignant melanoma are abnormally sensitive to the mutagenic effect of simulated sunlight and 4-nitroquinoline 1-oxide.

Because of a possible etiologic link between mutations and carcinogenesis, we compared fibroblasts derived from skin biopsies of several patients with hereditary cutaneous malignant melanoma and the dysplastic nevus syndrome for sensitivity to the mutagenic and/or cytotoxic effect of broad-spectrum simulated sunlight and of a UV mimetic carcinogen, 4-nitroquinoline 1-oxide (4NQO). The genetic marker was resistance to 6-thioguanine; loss of colony-forming ability was the assay for cytotoxicity. All five strains tested were more sensitive than normal to the killing effect of 4NQO (slopes of survival curves were 2- to 3-fold steeper), but only one strain was hypersensitive to killing by Sun Lamp radiation. Two strains were tested for mutagenicity. The response of each to the mutagenic action of these agents corresponded to its response to cell killing. Both strains were hypermutable after exposure to 4NQO, but only one showed a higher than normal frequency of mutants induced by simulated sunlight. The finding that nonmalignant fibroblasts from patients with a hereditary variant of malignant melanoma are abnormally susceptible to carcinogen-induced mutations suggests that hypersensitivity to mutagens contributes to risk of melanoma in patients. It also supports the somatic cell mutation hypothesis for the origin of cancer.

4-Nitroquinoline-1-oxide↗
PubMed1984

The epidemiology of ovarian cancer.

Although no unequivocally effective ovarian cancer prevention strategies have emerged, epidemiologic studies have identified high-risk populations. The striking international variation (apparently a fivefold difference) can probably be explained on the basis of differential parity, differing classification measures, and differences in the underlying population age distribution. United States age-adjusted mortality has increased slightly in the past 30 years, and the cancer remains predominantly a disease of older adult white women of northern European extraction. The increases in age-specific mortality and age-adjusted mortality over time may be related to a decrease in average family size. Pregnancy, especially pregnancy before age 25 years, and use of oral contraceptives are protective; the risk of ovarian cancer increases with increasing years of ovulation. A positive family history is also associated with a substantial increase in ovarian cancer risk. Survivors of ovarian cancer are more susceptible to cancers of the breast, endometrium, and colon than are similarly-aged normal women, most probably because all four cancers share some common risk factor(s). Various alkylating agents are clearly leukemogenic in survivors of ovarian cancer, an observation that suggests caution in the use of adjuvant chemotherapy in women at relatively low risk of relapse.

Adolescent↗
PubMed1984

Incidence of Kaposi's sarcoma and mycosis fungoides in the United States including Puerto Rico, 1973-81.

The incidence of Kaposi's sarcoma (KS) was examined with the use of data from the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute. KS is a manifestation of the recent epidemic of acquired immunodeficiency syndrome (AIDS) that has occurred particularly among homosexual men. The incidence of KS in 1973-79 was found to be higher (0.29 male and 0.07 female cases/100,000/yr) than is usually cited for the pre-AIDS KS incidence rates. Collectively, the 9 SEER registries in the United States showed only a slight increase in the incidence of KS between 1973-79 and 1980-81. However, the SEER registry covering San Francisco, which is a high-risk area for AIDS, showed a marked excess of KS in 1981. The KS case rate among never-married men younger than 50 years old, a surrogate index of homosexuality, was found to be markedly elevated in the post-AIDS period, compared with the case rate of a reference disease, mycosis fungoides. Never-married men younger than 50 years old, therefore, constitute a SEER-identifiable population who can be monitored for risk of KS and other neoplasms that might be related to AIDS. In addition, the incidence rate of KS in the SEER registry of Puerto Rico was generally higher than that in the U.S. SEER registries, despite data that suggested that KS may be underreported. The demographic characteristics of patients diagnosed as having KS in Puerto Rico suggested the classical rather than the AIDS-related form of KS.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Colorectal cancer in rural Nebraska.

A case-control interview study of colorectal cancer was conducted in two rural counties of eastern Nebraska to determine reasons for the elevated colon cancer mortality rates during 1950 to 1969. Comparison of the information provided by 86 colorectal cancer cases and 176 matched controls (or their next of kin) revealed an increased risk among persons of Czech background, with persons of Bohemian and Moravian extraction predominating in this area. The data suggest an interaction between Bohemian ancestry and certain dietary patterns in the pathogenesis of colon cancer in this region. Colon cancer risk was elevated among commercial beer drinkers regardless of their ethnic background, although Bohemians reported heavier consumption. An excess risk was also associated with intestinal polyps, reported more often by Moravians, and with familial occurrence of gastrointestinal and other cancers. Since 1969, the mortality and incidence rates for colon cancer in this area have declined, possibly as a consequence of acculturation of the American-born descendants of Czech immigrants.

Age Factors↗