By Hans G. Drexler, Jun Minowada (auth.), John R. W. Masters, Bernhard O. Palsson (eds.)
This publication describes all human leukemia-lymphoma phone traces which have been validated and that develop regularly below standardised invitro stipulations. those traces are derived from cells belonging to all of the significant hematopoietic phone lineages, i.e. B- and T-lymphocytes, ordinary killer cells, granulocytic cells and megakaryocytic cells. The scientific info, the tradition stipulations and the key phenotypic positive aspects of the cellphone strains are defined with citations. This booklet is the 1st publication describing human leukemia-lymphoma telephone strains and should be of curiosity to scientists all for the components of hematology, oncology, immunology, molecular biology and cytogenetics.
Cancer phone Lines, Volumes 1-3: those three volumes supply a accomplished textual content at the tradition of demonstrated telephone strains from all types of human melanoma. The volumes supply a uncomplicated guide and reference source for each melanoma examine scientist utilizing human melanoma cells.
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One of many major motives of failure within the therapy of breast melanoma is the intrinsic presence of, or improvement of, drug resistance via the melanoma cells. fresh experiences at the mechanisms of melanoma drug resistance have yielded very important details highlighting either how tumour cells may possibly break out those healing constraints and that drug resistance may perhaps extra impinge on tumour phone capabilities that could eventually advertise an hostile cellphone phenotype.
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Additional info for Human Cell Culture: Cancer Cell Lines Part 3: Leukemias and Lymphomas
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Translocation t(9;22)(q34;q11) occurs in 12 of the cell lines included. In most cases, the BCR-ABL fusion product has been characterized. Next most frequent was translocation t(1;19) resulting in the characteristic E2A-PBX1 fusion product. Interestingly, BCP cell line TS-2 is carrying a t(1;19) abnormality, but no evidence of the E2A-PBX1 gene rearrangement was found by RT-PCR. Cell line KMO-90 is also harboring a point mutation at codon 177 of the p53 gene as identified by SSCP analysis . Translocation t(4;11) was found in four cell lines.
E. p16/p14 and p15, on chromosome 9p21 has been facilitated by analysis of various tumor cell lines [81,82], The localization of these genes, encoding cyclin-dependent kinase inhibitor proteins, has also been established in cell lines [83,84]. The sequence of the MLL gene spanning the breakpoint at chromosome 11q23 was determined by analysis of the BCP cell line RS4;11 . The fusion of the TEL gene on chromosome 12 to the AML1 gene on chromosome 21, as it occurs in up to 30% of childhood B-lineage ALL, has also been demonstrated in tumor cell lines .