contrast with most other posttransplant cancers where males outnumber females by more than 2:1, Thirty-eight percent of patients have in situ lesions. A worrying finding is that patients with invasive lesions are much younger (average age 42 years) than their counterparts in the general population, whose average age is usually between 50 and 80 years. Prior to the development of the malignancies 56% of transplant patients have condyloma acuminata ("genital warts"), suggesting that human papillomavirus plays an important role in the development of these tumors.

It is possible that many in situ carcinomas of the uterine cervix are missed because they are asymptomatic. Therefore all postadolescent female allograft recipients should have regular pelvic examinations and cervical smears to detect these lesions, and also carcinomas of the vulvar and anal areas.3,4

Most hepatobiliary tumors are hepatomas and a substantial number of patients have a preceding history of hepatitis B infection.3,4 Increasing numbers of patients with a history of hepatitis C infection are now being encountered.

Most sarcomas (other than KS) involve the soft tissues or visceral organs whereas cartilage or bone involvement is uncommon. The major types in descending order are fibrous histiocytoma, leiomyosarcoma, fibrosarcoma, rhabdomyosarcoma, hemangiosarcoma, and mesothelioma.3,4

Posttransplant malignancies probably arise from a complex interplay of many factors.3-5,7-9,12 Severely depressed immunity may impair the body's ability to eliminate malignant cells induced by various carcinogens.3,4 Chronic antigenic stimulation by the foreign antigens of transplanted organs, by repeated infections, or transfusions of blood or blood products may overstimulate a partially depressed immune system and lead to PTLD.3,4 Alternatively, defective feedback mechanisms may fail to control the extent of immune reactions and lead to unrestrained lymphoid proliferation and PTLD. Furthermore, once this loss of regulation occurs, the defensive ability of the immune system is weakened and other nonlymphoid malignancies may appear.3,4

Activation of oncogenic viruses probably plays an important role in the development of some tumors.3,4,8,9 Epstein-Barr virus is strongly implicated in causing PTLD, some smooth muscle tumors, and, some cases of Hodgkin's disease; various strains of papillomavirus in causing carcinomas of the vulva, perineum, uterine cervix, and anus, but there is controversy concerning the role of these virus in causing skin cancers: hepatitis B or hepatitis C virus in causing hepatomas; and herpes virus type 8 (HHV-8) appears to play an important role in the development of KS.

Some immunosuppressive agents may directly damage DNA and cause can-cers.3,4 Immunosuppressive agents may enhance the effects of other carcinogens, such as sunlight in causing carcinomas of the skin, or papilloma virus in causing carcinomas of the uterine cervix or vulva.3,4 Genetic factors may affect susceptibility to neoplasia by affecting carcinogen metabolism, level of interferon secretion, response to virus infections, or regulation of the immune response by the major histocompatibility system.3,4

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