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Biomedical subjects

R R Reimer

Publications and source records attributed to R R Reimer.

At least 19 recordsLinked to original sources
PubMed1983

Treatment of advanced ovarian cancer with cisplatin, adriamycin, and cyclophosphamide: effect of treatment and incidence of intracranial metastases.

A retrospective analysis of 42 patients with stage III, IV, or recurrent epithelial ovarian carcinoma treated with monthly cisplatin, Adriamycin, and cyclophosphamide (PAC) was made. Of 36 patients with measurable disease, 18 (50%) achieved a clinical complete response (CR) and 12 (33%) achieved a partial response (PR) for an objective response rate of 83%. Six stage III patients remained without measurable disease after surgery and postoperative PAC and are included in the survival data. The median survival of all patients was 22 months (10 months for nonresponders), with a median duration of response of 15 months (19+ months for clinical complete responders). Of 16 patients who underwent second-look laparotomy while in clinical CR, 8 were pathologically free of disease. Of these 8 surgically staged CRs, 2 have suffered CNS relapses, while the rest remain free of disease. One additional patient, who had been found to have only microscopic disease at the time of second-look surgery, subsequently relapsed in the CNS, for a total of 3 patients with CNS relapse. We conclude that PAC is an effective regimen, but that prolonged survival of these patients may put them at greater risk for CNS relapse.

Adult↗
PubMed1982

Carotid body tumors in humans: genetics and epidemiology.

Genetic factors in the etiology of carotid body tumors (CBT) were sought in a medical record review of 222 histologically diagnosed cases at 12 U.S. medical centers. Patients in the series, which had a marked female predominance (146 females:76 males), usually developed tumors between the fourth and seventh decades of life (mean, 44.7 yr). In 16 patients who also had other extra-adrenal paragangliomas, suggesting a multiple primary tumor syndrome, CBT were diagnosed significantly earlier (mean, 35.4 yr; P less than 0.01). The occurrence of thyroid cancer in 5 other patients appeared to be excessive. Familial CBT was recognized in 16 patients from 13 affected families, including 9 newly ascertained kindreds. Compared with non-familial lesions, familial CBT tended to develop bilaterally (38% vs. 8% unilaterally) and at slightly earlier ages (41.6 vs. 44.9 yr). CBT was reported to occur in an autosomal dominant pattern in some families and within sibships in others; relatives were not examined for confirmation. The familial findings are generally consistent with a two-step mutation model of the development of hereditary and nonhereditary CBT; apparent deviations from the model might be clarified with additional data on this rare neoplasm.

Adolescent↗
PubMed1980

Malignant melanoma and Charcot-Marie-Tooth disease.

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.

Adult↗
PubMed1979

Immunologic abnormalities in melanoma-prone families.

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.

B-Lymphocytes↗
PubMed1979

Immune response to melanoma extracts in three melanoma-prone families.

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.

Antigens, Neoplasm↗
PubMed1978

Precursor lesions in familial melanoma. A new genetic preneoplastic syndrome.

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.

Adult↗
PubMed1978

Chemotherapy of recurrent breast cancer.

Several chemotherapeutic agents given singly or in combination are capable of producing significant tumor regression in recurrent breast cancer. Such remissions improve both the quality and duration of life. To date, the most active combinations have been variations of Cooper's CMFVP therapy or regimens containing Adriamycin. Further improvements in survival may be realized from the addition of hormonal and/or immune therapy to these active combinations as well as from the development of new drugs.

Alkylating Agents↗
PubMed1978

Second primary neoplasms following ovarian cancer.

Follow-up surveys of patients with ovarian cancer revealed an increased risk of second primary cancers of the uterine corpus, colon, bladder, breast, and hematopoietic system. The excess risk or uterine corpus cancer was independent of therapy. The risk of colon cancer was increased in all treatment groups but was especially high among patients receiving radiation or chemotherapy. The predisposition to other neoplasms was limited to certain treatment groups: bladder cancer to irradiation, leukemia to chemotherapy, and lymphoma to either modality. The pattern of second neoplasms following ovarian cancer appears to be influenced by therapy as well as by common etiologic factors.

Alkylating Agents↗
PubMed1978

Precursor lesions in familial melanoma.

Familial occurrences of malignant melanoma may be related to an inherited syndrome of precursor cutaneous lesions with distinct clinical and histologic features. Recognition of the syndrome in the relatives of melanoma patients identifies a subset of family members at high risk for melanoma, facilitating their early diagnosis and treatment. Further studies of these families may provide insight into the biology of malignant melanoma and the pathophysiology of malignant transformation in benign nevi.

Female↗
PubMed1978

Origin of familial malignant melanomas from heritable melanocytic lesions. 'The B-K mole syndrome'.

Distinctive melanocytic moles are described in 37 patients from six melanoma families. Among the family members examined by the authors, 15 of 17 patients with melanoma and 22 of 41 nonmelanoma relatives had the unique moles. The clinical and histological features of these moles have been designated the "B-K mole syndrome." The clinical features of the syndrome include the presence of less than 10 to greater than 100 moles prominent of the upper trunk and extremities, and variability of mole size (5 mm to 15 mm), outline, and color combination. Histologically, B-K moles show atypical melanocytic hyperplasia, lymphocytic infiltration, delicate fibroplasia, and new blood vessels that occur within a compound nevus or de novo. The transformation of two B-K moles into malignant melanomas was documented photographically.

Adolescent↗
PubMed1977

Acute leukemia after alkylating-agent therapy of ovarian cancer.

To estimate the leukemogenic potential of alkylating agents, we surveyed 70 institutions using these drugs for the frequency of second cancers in patients with advanced ovarian cancer. Thirteen cases of acute nonlymphocytic leukemia occurred among 5455 patients, as compared to 0.62 cases expected (relative risk = 21.0). All 13 had received alkylating agents. Nine also received radiotherapy. The relative risk for patients given chemotherapy was 36.1 and rose to 171.4 for those surviving for two years (rate = 13.75 per 1000 patients per year). To evaluate the role of therapy versus underlying disease, a historical control of 13,309 patients with ovarian cancer in the National Cancer Institute's End Results Program was analyzed. No excess of leukemia was noted in this group, even among 6596 women receiving radiation. The excess of acute nonlymphocytic leukemia, therefore, appears attribute to alkylating agents, although the effect may be enhanced by exposure to radiation, as previously suggested for Hodgkin's disease.

Acute Disease↗
PubMed1977

Breast carcinoma following radiotherapy of metastatic Wilm's tumor.

A 22-year-old women developed breast cancer 15 years after radiotherapy to the lung for metastatic Wilms tumor. Her 32-year-old mother died of bilateral breast cancer, suggesting a genetic predisposition to radiogenic cancer. Recent improvements in the survival of children with certain cancers necessitate long-term surveillance for iatrogenic neoplasia, particularly when familial susceptibility is evident.

Adult↗