Classic Kaposi's sarcoma as a second primary neoplasm

Although the incidence of classic Kaposi's sarcoma (CKS) has been investiga ted, its occurrence following a primary neoplasm and its association with t his first neoplasm need to be determined. We analyzed a series of 124 patie nts with a secondary CKS (8.4% of a total of 1485 incident cases) which occ urred between 1961 and 1992 in the Jewish Israeli population. Data on first neoplasms and subsequent Kaposi's sarcoma were retrieved from the Israel C ancer Registry. Acquired-immune-deficiency-syndrome-related Kaposi's sarcom as were excluded from the case series. Four controls were randomly selected for each CKS case among all Cancer Registry cases free from a second neopl asm at the time of diagnosis of the CKS in the case, and matched on gender, year of birth and year of diagnosis of the first neoplasm. The average tim e lapse between first neoplasm and secondary CKS was 4.5 years, being short er for prostate cancer and for hematopoietic malignancies. As compared with Israel-born Jews, the risk of a subsequent CKS was significantly increased in immigrants [odds ratio (OR) 3.0]; this risk was particularly high in im migrants from the former Soviet Union (OR 9.4) and Poland (OR 7.0). There w as no clear trend with age at immigration; however, low age at immigration and a short length of stay in Israel endowed a higher risk of developing a secondary CKS, markedly among patients suffering from solid tumors as the f irst primary, There was an excess of secondary CKS following a non-Hodgkin' s lymphoma (OR 5.3), a Hodgkin's lymphoma (OR 7.5), a leukemia (OR 5.3) or a breast cancer (OR 2.2), Cancer patients with a first primary in the lung, colon, stomach, larynx, liver, pancreas or kidney showed secondary CKS les s frequently. Despite the lack of control of therapy for the first neoplasm , development of secondary CKS seems to be mediated by mechanisms similar t o those for hematopoietic neoplasms and selected nonhematopoietic neoplasms , such as breast cancer. The trend toward increased risk after a short time lapse and the difference in risk among immigrants indicate that genetic su sceptibility is part of the complex interplay between cellular proliferatio n and control systems. (C) 1999 Wiley-Liss, Inc.