Background. Thin melanomas can metastasize and be lethal. The predictive importance of tumor thickness in thin melanomas and the specific features identifying the patients at risk have not been investigated fully. Methods. Prognostic factors were analyzed in 585 patients with clinical Stage I invasive cutaneous malignant melanoma with a thickness of less than or equal to 0.8 mm. The patients were included in a population‐based cancer registry in Stockholm county during 1976–1987. They constituted about 64% of all patients with thin melanomas who were diagnosed in the region during the study period. Information was available on age, sex, anatomic site of the tumor, histologic type of melanoma, level of invasion, tumor thickness, and tumor regression. In a Cox regression analysis, the prognostic importance of each factor was studied. By a case‐control technique with individual matching for the identified independent predictors of recurrence, the additional prognostic information given by type and grade of inflammatory response, presence of vertical growth phase, mitotic rate/mm2, and histologic ulceration of the tumor was assessed. Results. After a median follow‐up time of 50 months, recurrent disease developed in 26 patients (4%). There was no difference in recurrence rate between patients treated with narrow (1–2 cm) or wide (5 cm) excision. Anatomic site, tumor thickness, level of invasion, and tumor regression were found to be independent prognostic factors in the multivariate analysis. In the case‐control study, only grade of inflammatory reaction added significant prognostic information. No subgroup could be identified that was without risk of recurrent disease. Conclusions. Thin melanomas do not seem to constitute a separate form of melanoma, but compose one end of a continuous spectrum of biologic behavior.
Specimens from 47 cases of anal squamous-cell carcinoma were examined in Stockholm county (1978 to 1981) with respect to clinical stage (43 cases), histologic grade (41 cases), and DNA content of the tumor cells (31 cases). Follow-up ranged from four to seven years (median, 5.5 years). The increased mortality in advanced stage and high-grade lesions was significant. Analysis of DNA content showed that most tumors were aneuploid. No statistically significant effect of DNA content on survival could be demonstrated. Thus, histologic grade and clinical stage seem to be the best predictors of patient outcome in squamous-cell carcinoma of the anus.
Forty-two so-called interval cancers of the breast were studied. The mammograms were reviewed and the tumors were classified as 14 'unrecognized', 9 'observer error', 1 'technical error' and 18 'true' interval cancers. By using a scoring system based upon histologic differentiation, axillary nodal status, estrogen receptor level, and nuclear DNA content, eight ductal carcinomas with high malignancy potential were identified. All of these tumors belonged to the group 'true' interval cancer. The data indicate that the mammographic subgroup 'true' interval cancer identifies the highly malignant tumors. However, even this strictly selected subgroup is heterogeneous since it also includes some tumors with low malignancy potential.
In 18 breast cancer patients the DNA histograms observed in the primary tumor at the date of diagnosis were compared with those found in the corresponding local and distant metastases at autopsy up to more than 12 yr later. All patients, except one, exhibited the same type of DNA histogram in both the primary tumor and its metastases. In one patient the DNA histogram changed from an euploid type in the primary breast carcinoma to an aneuploid type in the metastases.The results are interpreted as indicating that mammary adenocarcinoma in general exhibit a high degree of stability of the nuclear DNA content during the history of the disease. It is suggested that in breast cancer progression of the tumor disease is more likely due to a net increase andlor dissemination of tumor cells exhibiting similar genetic properties and malignancy potential than to a progressive dedifferentiation and increase of malignancy of the tumor cells.
Case histories of 5 tumor patients treated with natural leukocyte interferon-alpha (IFN-alpha) are presented. One patient with juvenile laryngeal papillomatosis responded well to interferon treatment, but the disease recurred when therapy was withdrawn. Upon reinstitution of treatment, the patient once again responded well. Another patient with myelomatosis also responded well to interferon therapy and in this case, too, the tumor recurred when interferon treatment was withdrawn. Reinstitution of interferon therapy was, however, unsuccessful. One patient with generalized giant cell tumor of bone responded with regression after more than 5 years of interferon treatment. Another patient with pulmonary osteosarcoma metastases, having received irradiation and interferon combination therapy followed by sole interferon treatment, responded well with a lasting stationary radiogram after 6 years of interferon treatment. One patient with malignant glioma, showing signs of tumor growth during the first few months of interferon therapy, eventually responded, and became disease-free after 6 years. The latter 3 patients are continuously receiving interferon therapy although more than 5 years have elapsed since their interferon therapy was initiated. It is suggested that interferon therapy for malignant tumors be given for life (or to progression of disease) in responding patients. Such a concept entails biological implications for interferon therapy in general and for antitumor action of interferons in particular. Other possible clinical schedules should only be constructed within the framework of controlled clinical trials.
The DNA distribution pattern was determined retrospectively in 25 rectal carcinomas and the possible correlation to clinical outcome evaluated. The DNA content in individual cells was measured according to a cytophotometric method based on light transmission measurement of Feulgen-stained nuclei. Tumor cells with DNA content exceeding an upper limit, i.e., the 90 percentile of the control cells, were considered to be nondiploid (aneuploid). Virtually all long-term survivors had less than 50 per cent of the tumor cells exceeding the upper diploid level, whereas those developing only a local recurrence had 50 to 70 per cent. Patients with disseminated disease and short survival time had all of their tumor cells exceeding the upper diploid level. There was a highly significant correlation between Dukes' stage and aneuploidy and probably a significant correlation between histologic grading and aneuploidy. The clinical significance of these results lies in the fact that DNA can be measured in biopsy specimens. It might thus be possible to "tailor" the operation according to the future clinical course to be expected. It could be hypothetically argued that patients with a DNA profile heralding disseminated disease and short life expectancy should have surgery that preserves quality of life, whereas those tending to develop a local recurrence should have more aggressive surgery. It may also be possible to define groups of patients thought to prosper from a more intense postoperative surveillance. The scientific basis for these suggestions is still lacking, and further studies on a prospective basis are currently in progress.
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