Treatment-related chronic myeloid leukaemia (CML) is a less commonly recognised entity. It differs from treatment-related acute leukaemias in frequency, clinical course, and prognosis. Previously two cases of CML have been described following treatment of myasthenia gravis associated with thymoma treated by thymectomy. We report a 25-yr-old man with myasthenia gravis without thymoma who developed CML, 68 months after thymectomy. Cytogenetic study showed translocation (9,22)(q34;q11) with 10% showing double Ph chromosome. Reverse-transcriptase polymerase chain reaction (RT-PCR) of peripheral blood demonstrated the presence of p210(BCR/ABL) with b3a2 transcripts. He was treated with hydroxyurea, and still remained in the chronic phase during the last 6 months of follow up. His myasthenic symptoms remained stable.
Pedigree analysis of the oral cancer (OC) patients registered at our Centre had disclosed familial aggregation of oral cancer which hitherto has not been largely reported. There is a paucity of information on the genetic determinism for familial oral cancer predisposition. Therefore, we investigated constitutional chromosome abnormalities and bleomycin-induced chromosome sensitivity of 7 familial and 10 sporadic oral cancer patients and 14 unaffected family members (first-degree relatives) to determine whether these factors could give any clues regarding cancer-predisposing factors. Neither the oral cancer patients nor the unaffected family members showed any constitutional chromosomal abnormalities. However, with regard to bleomycin sensitivity, there was significant difference between the oral-cancer patients and unaffected relatives. The mean b/c value was I .68 f 0.48 for familial OC patients, I. I 2 f 0.36 for sporadic OC patients and 0.52 f 0. I 8 for the unaffected family members (p < 0.00 I). A noteworthy observation was that one unaffected family member also showed bleomycin hypersensitivity and expressed a mean b/c value of I .32, at the initiation of the study. That patient later developed oral carcinoma. This clearly demonstrates that mutagen hypersensitivity among unaffected relatives in OC families may be related to cancer predisposition. The mutagen sensitivity study is being continued in a larger series of subjects, for the development of a cytogenetic marker for prediction of cancer susceptibility.8 1996 Wiley-Liss, Inc.
Cardiovascular autonomic neuropathy (CAN) is one of the most clinically significant complications of diabetes mellitus. Even though many ethological factors have been attributed for the pathogenesis of this disease no attempts were made to correlate DNA damage as a causative factor. Hence the present study was undertaken to asses the extent of somatic DNA damages by cytokinesisblock micronuclei assay (CBMN). An attempt is also being made to correlate the habits and/or risk factors and socioeconomic status with CAN. The CBMN frequency of 46 patients suffering from autonomic neuropathy was compared with that of 25 healthy age and sex matched controls. All the subjects were suffering from type 2 diabetes for at least 8 years and have varying degrees of coronary artery diseases. The mean CBMN frequency of the patients was statistically higher than that of the healthy control subjects (P \ 0.05). The CBMN frequency was found to be significantly altered in CAN patients who where physical inactivity and smoking. A significant correlation could also be observed between CAN and smoking, diabetes mellitus, hypertension, dyslipidemia, abdominal obesity, and physical activity.
Pedigree analysis of the oral cancer (OC) patients registered at our Centre had disclosed familial aggregation of oral cancer which hitherto has not been largely reported. There is a paucity of information on the genetic determinism for familial oral cancer predisposition. Therefore, we investigated constitutional chromosome abnormalities and bleomycin-induced chromosome sensitivity of 7 familial and 10 sporadic oral cancer patients and 14 unaffected family members (first-degree relatives) to determine whether these factors could give any clues regarding cancer-predisposing factors. Neither the oral cancer patients nor the unaffected family members showed any constitutional chromosomal abnormalities. However, with regard to bleomycin sensitivity, there was significant difference between the oral-cancer patients and unaffected relatives. The mean b/c value was I .68 f 0.48 for familial OC patients, I. I 2 f 0.36 for sporadic OC patients and 0.52 f 0. I 8 for the unaffected family members (p < 0.00 I). A noteworthy observation was that one unaffected family member also showed bleomycin hypersensitivity and expressed a mean b/c value of I .32, at the initiation of the study. That patient later developed oral carcinoma. This clearly demonstrates that mutagen hypersensitivity among unaffected relatives in OC families may be related to cancer predisposition. The mutagen sensitivity study is being continued in a larger series of subjects, for the development of a cytogenetic marker for prediction of cancer susceptibility.8 1996 Wiley-Liss, Inc.
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