Biomedical subjects
Publications and source records attributed to M H Greene.
Increasing reports of fractured hamate hooks have provided a sharper focus on causes, diagnosis, treatment, and associated anomalies such as ulnar neuropathy, bipartition, and accessory ossicles. This case report, presenting ulnar tunnel syndrome with bilateral hamulus bipartition, illustrates the relation between these anomalies.
Epidemiologic studies show that non-Hodgkin's lymphomas tend to develop after prolonged antigenic stimulation, after loss of normal regulation of lymphoid proliferation, or especially after both processes. Study of these tumors in vitro has greatly increased understanding of their pathophysiology and has provided a conceptual framework for their morphologic diversity. Lymphomas are now understood to be expanded clones of their normal counterparts. The anatomic location, phenotypic characteristics, proliferative capacity, and functional capabilities of the neoplasm often reflect those of the equivalent normal cells. If neoplastic transformation can occur at any stage of lymphoid differentiation, then it is theoretically possible that neoplastic lymphocytes may respond, or could be induced, to normal regulatory influences. Further study of selective cytotoxicity may reveal exploitable differences among lymphocytic subpopulations and permit more rational choices of therapy. Of major aid to future clinical trials should be the recent consensus on nomenclature by an international panel of experts.
A therapeutic response to topical fluorouracil in a patient with the large atypical nevus syndrome is presented. Six of the patients' dysplastic melanocytic nevi were treated with topical fluorouracil. Four common acquired melanocytic nevi from normal individuals were also treated. All six dysplastic nevi responded with inflammation, ulceration, and subsequent disappearance of the lesion, while the four control melanocytic nevi remained unchanged. Although we do not presently advocate the therapeutic use of fluorouracil for large atypical nevi until its safety and efficacy have been established, the response reported herein may herald an important advance in the therapy of these troublesome lesions that are known to be histogenetic precursors of malignant melanoma.
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Clinical photographs of 79 prospectively studied cases of non-familial cutaneous malignant melanoma were reviewed; special attention was directed to the distribution pattern of coexistent melanocytic lesions. A group of 15 patients had moles on the covered buttock area. Seven of these patients had large clinically atypical nevi, and biopsies of these nevi showed severe melanocytic dysplasia. Residual elements of melanocytic dysplasia were identified in five of the primary melanomas in this group of patients. It is suggested that these patients represent a distinctive syndrome, the Dysplastic Nevus Syndrome (DNS) and that they are at increased risk for development of primary cutaneous malignant melanoma. The clinically and histologically distinctive dysplastic nevi of these patients are identical to the precursor lesion for melanoma that we have previously described in a familial context, the B-K mole syndrome. This paper represents the first description of this form of dysplasia in non-familial melanoma.
Two patients with Charco-Marie-Tooth disease subsequently developed cutaneous malignant melanoma. This constellation of diseases may be due to chance, but raises the possibility of a shared neural crest defect or genetic linkage.
An outbreak of varicella-zoster infection occurred among patients of the Medicine Branch, National Cancer Institute, National Institutes of Health. Epidemiologic investigation suggested that the outbreak was due to two distinct types of disease. One type was acquired without previous exposure to other diseased patients and invariably associated with dermatomal lesions. The other, an a typical form, was associated with person-to-person transmission and equivocal initial dermatomal distribution and had an incubation period of approximately 11 to 25 days. Despite the diagnosis of zoster, the latter probably was varicella, occurring in patients who were immunodeficient because of disease, debility, and chemotherapy.
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As part of a systematic program to evaluate the late effects of antineoplastic therapy in randomized clinical trials, patients enrolled in the low-dose thio-TEPA (TSPA) and 5-fluoro-2'-deoxyuridine (FdUrd) adjuvant colorectal cancer protocols of the Veterans Administration (VA) Surgical Oncology Group between 1958 and 1964 were studied. All patients received surgery with curative intent; 470 also received TSPA, 176 received FdUrd, and 867 received surgery only. The unique VA system permitted complete follow-up through 1977, with 10,902 person-years of observation accrued among 1,613 male patients (mean survival = 6.8 yr). Expected mortality and cancer incidence were computed by applying U.S. Mortality Statistics and Connecticut Tumor Registry age-, race-, sex-, and calendar time-specific rates to the person-years of observation. The mortality experience of the 3 groups was similar. Overall, there was a significant excess in total mortality (observed/expected = 1,359/553) attributable mainly to colorectal cancer (584/14), arteriosclerotic heart disease (258/215.9), pneumonia (41/17), gastric and duodenal ulcers (15/4), and cirrhosis (14/6). No excess mortality from noncolorectal cancers was apparent, nor were there significant differences by treatment: TSPA (22/22), FdUrd (9/12), and surgery only (50/42). Among 1,402 white patients, no significant excess of incident noncolorectal cancers were observed among patients treated with TSPA (30/31, FdUrd (14/15), or surgery only (63/58). Seven incident cases of leukemia developed (4.1 expected) among all patients of various groups: TSPA (3/1.3), FdUrd (1/0.6), and surgery only (3/2.2). No excess of new primary cancers was observed among 211 nonwhite patients. An inverse relationship between the occurrence of second primary cancer and age at diagnosis, irrespective of therapy, was suggested. The results demonstrated the feasibility of this approach for assessment of late complications of anticancer therapy and suggested no measurable carcinogenic effect following very low doses of TSPA and FdUrd in a population of this size.
In a study of 13 families prone to Hodgkin's disease, the probands showed significant excesses of the HLA antigens Bw35 (7 cases) and Bw37 (3 cases). Although based on a small number of patients, the results suggest that immunogenetic mechanisms account at least partly for the familial predisposition to Hodgkin's disease.
Spontaneous sister chromatid exchanges and banded karyotypes were studied in blood lymphocytes from 96 individuals: seven patients with chronic myelogenous leukemia, 15 normal controls, and five "cancer families" comprising 12 cancer patients, 40 tumor-free blood relatives and 22 spouses. The families had: malignant melanoma; Epstein-Barr virus-associated malignancies and a birth defect syndrome; non-Hodgkin lymphoma and diverse carcinomas; Hodgkin's lymphoma and adenocarcinomas; and acute myelogenous leukemia. In addition to the Philadelphia chromosome in chronic myelogenous leukemia patients, karyotypic abnormalities, especially breaks and fragments, were found in 29% of cancer family members, but were inconsistent and usually attributable to radiotherapy. Mean sister chromatid exchange values were normal in chronic myelogenous leukemia, but low (by t-test) in tumor patients and their blood relatives in cancer-prone families. In tumor patients, mean sister chromatid exchange levels fell as age increased. After adjusting for this age effect, no significant differences remained among groups. In patients at high risk of cancer (because they have chronic myelogenous leukemia or a strong family history of cancer), spontaneous sister chromatid exchange rates were not a marker of cancer risk.
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Sixty members of 4 families prone to cutaneous malignant melanoma (CMM) and a genetically determined precursor nevus syndrome underwent extensive immunologic evaluation. The most consistent finding was a diminished in vitro response to pooled alloantigens in the one-way mixed leukocyte culture (MLC) and a tendency to low T-lymphocyte and B-lymphocyte levels. When compared to controls, low B-lymphocyte levels and reduced MLC responses were found not only in family members with CMM and/or precursor nevi but also in unaffected blood relatives and spouses. The genesis of the immune dysfunction and its possible relationship to melanoma pathogenesis remain to be clarified.
Immune reactivity to melanoma extracts was measured by the leukocyte adherence inhibition (LAI) test in 40 members of 3 melanoma-prone families. The melanoma patients had a wide range of responsiveness to the extract, the highest responder being a 10-year survivor. As a group, family members (including spouses) without disease had significantly elevated LAI responses compared to those of unrelated controls (P less than 0.01). Within the families, members with close exposure to melanoma patients for 10 years or more had a significantly higher response to melanoma antigen than did members with 0-5 years of close exposure (P less than 0.05). Responses of spouses and members at high risk of developing melanoma (B-K mole syndrome) also correlated with length of exposure to patients, which suggests that the elevated LAI response was not genetically determined. The high frequency of positive responses to melanoma antigens in these families, particularly in spouses, suggests the presence of transmissible melanoma-associated material capable of immunizing persons in contact with melanoma patients.
An analysis of cases from a multi-hospital, pathologically verified clinical series and of deaths from US mortality statistics available at the county level for 1950--1975 (excluding 1972) was made in order to obtain information on the etiology of mycosis fungoides (MF). Despite the absence of an appropriate comparison group, the cases seemed to have a high frequency of antecedent allergies, fungal and viral skin infections, sun sensitivity, familial aggregation of lymphoma and leukemia, and employment in a manufacturing occupation (especially petrochemical, textile, metal, and machinery industries). The mortality survey revealed a predominance among males, nonwhites, and residents of the northeastern US, the latter due partly to an association between MF mortality and population size. The influence of occupational exposures was suggested by the excessive MF mortality rates in counties where petroleum, rubber, primary and fabricated metal, machinery, and printing industries were located.
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In seven consecutive melanoma-prone families, pigmented lesions with distinctive clinical and histologic characteristics occurred in 18 of 20 melanoma patients (90%) and 24 of 43 first-degree relatives (56%). Recognition of these lesions led to the detection of early-stage melanoma in six family members. This syndrome appears to represent an autosomal dominant trait and may serve as a cutaneous marker to identify persons at high risk for melanoma.