“…This is almost certainly related to the mutagenic effect of radiotherapy and chemotherapy [1,4,8,13,15], often used in combination in the modern therapeutic procedures.…”
Acute lymphoblastic leukaemia, defined by immunological markers as a non-T, non-B, which occurred in a patient with breast cancer 2 years after the end of radiotherapy and CMF adjuvant chemotherapy, is reported.
“…This is almost certainly related to the mutagenic effect of radiotherapy and chemotherapy [1,4,8,13,15], often used in combination in the modern therapeutic procedures.…”
Acute lymphoblastic leukaemia, defined by immunological markers as a non-T, non-B, which occurred in a patient with breast cancer 2 years after the end of radiotherapy and CMF adjuvant chemotherapy, is reported.
“…Secondary neoplasias are the most hazardous consequence of intensive combined treatment modalities (radio-chemo-therapy) at the moment and amount up to 5-10 per cent of all initially diagnosed Hodgkin patients (Borum, 1980;Coltman and Dixon, 1982;Valagussa et al, 1980). The incidence of acute myeloid or myelo-monocytoid leukemia is 130 times higher in Hodgkin's patients than in normal individuals (Glicksman et al, 1982).…”
In the last four years we established five long term cultures from tumor material of Hodgkin's disease. The in vitro cells have malignant characteristics and represent the in vivo H‐ and SR‐cells. Common immunological, functional and morphological assays did not characterize the in vitro cells to be a known cell type of lymphoid, myeloid or monocytoid tissue. The in vitro Hodgkin cells are biologically active by producing factors involved in regulation and promotion of immunological response and granulopoiesis.
The relevance of the findings for pathogenesis and clinical appearance of Hodgkin's disease is discussed.
“…In fact, Valagussa et a1 found no second malignancies in 104 patients they treated for Hodgkin disease on the ABVD program [7]. Zarrabi and Rosner do cite one of acute myeloblastic leukemia in a patient with melanoma receiving dacarbazine, but the short latency period of 6 to 12 months makes it unlikely that dacarbazine was the causative factor [8].…”
ANLL followed a brief period of aplastic anemia in a man treated intensively 4 years and 3 months previously with dacarbazine as "adjuvant" therapy for malignant melanoma. This is the first reported instance in which the latency between drug exposure and onset of leukemia strongly implicates dacarbazine as a leukemogenic agent.
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