To gain insight into the real incidence of the numeric chromosomal aberrations and the cell lineage involvement of the neoplastic process in multiple myeloma (MM) , we examined 18 Chinese MM patients by May-Grunwald-Giemsa (MGG) staining and fluorescence in situ hybridization using three DNA centromeric probes specific for chromosomes 3 , 7 , and 9. In this investigation , cytogenetic abnormalities were detected in plasma cells (PCs) , myeloid cells (MCs), and lymphoid cells (LCs) in all of the MM patients studied. This is the first demonstration of the cytogenetic aberration involved in the myeloid series. Multiple myeloma (MM) has been regarded as the neoplastic disease of the terminally differentiated B cell with elusive oncogenesis. Although the majority of the tumor cells found in the bone marrow can be recognized by their typical plasma cell morphology, they are the progeny of a yet unidentified myeloma progenitor cell. Suggested possibilities of this clonogenic cell include peripheral blood B-lymphoid cell, pre-B cell, and hematopoietic stem cell.1 Thus far, knowledge on the nature and development of the clonogenic cell has been lacking. This shortcoming has been an obstacle to rational intervention and contributed to a high fatality of MM from ineffective treatment.The low proliferative rate of the tumor cells in this malignancy has hampered the conventional cytogenetic analysis. An abnormal karyotype, often a complex mixture of numeric and structural changes, is found in ϳ50% of patients.2 Recent data have revealed that 55% of MM patients had three or more trisomies involving chromosomes 3, 5, 7, 9, 11, 15, 19, and 21. 3 The significance of these chromosomal aberrations in MM pathogenesis remains obscure. As a large number of proliferating or nondividing cells can be examined, use of fluorescence in situ hybridization (FISH) has improved the detection of cytogenetic abnormalities in MM. In addition, by combination with morphological assessment of the cells studied, the lineage of cells that are involved in the neoplastic transformation can be elucidated. Using FISH and 10 ␣-satellite DNA probes, Drach et al 4 showed that 88.9% of MMs were aneuploid for at least one chromosome examined and 66% had aberrations in three or more chromosomes. In the same study, mature myeloid cells evaluated showed no abnormality. 4 After FISH procedure, cytomorphological details are so obscured that it would be very difficult to ascertain the cell types being assessed. Using combined morphological and FISH
A case of advanced leiomyosarcoma of the urinary bladder is reported in a 25-year old man who, in a short time, experienced a complete ‘spontaneous’ regression of his fatal illness. He first presented with severe haemoperitoneum resulting from an unresectable bleeding tumour of the urinary bladder. Debulking surgery was performed, followed by salvage chemotherapy. Histological and ultrastructural examinations of the tumour confirmed a poorly differentiated leiomyosarcoma. The residual disease failed to respond to salvage chemotherapy, but regressed ‘spontaneously’ 5 months after cessation of therapy. The patient is alive without evidence of disease 51 months after the diagnosis. This remarkable phenomenon and relatively long survival in a poor-risk leiomyosarcoma of the urinary bladder has never been reported previously.
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