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At least 55 records · Page 3Linked to original sources
PubMed1989

Alterations in the p53 gene and the clonal evolution of the blast crisis of chronic myelocytic leukemia.

Molecular mechanisms responsible for the clinical progression of chronic myelocytic leukemia to its accelerated phase or to blast crisis have not been defined. We found alterations of the p53 gene (p53 is a 53-kDa nuclear protein) including deletions and rearrangements in 8 of 34 patients in blast crisis and 1 of 4 patients in the accelerated phase, but in only 1 of 38 patients in the chronic phase of chronic myelocytic leukemia. Only two other examples of p53 gene alterations were found among 203 patients with hematologic malignancies and solid tumors. Transcripts of the p53 gene were uniformly found in chronic-phase cells, but gene expression was variable in blast crisis, and transcripts were reduced or undetectable in 10 of 16 patients. Heterogeneous alterations in the structure and expression of the p53 gene appear to be relatively frequent in blast crisis and may be involved in the evolution of disease.

Blast Crisis↗
PubMed1985

Suppression of clonal evolution in two chronic myelogenous leukaemia patients treated with leucocyte interferon.

Two patients with Philadelphia chromosome-positive (Ph1+) chronic myelogenous leukaemia (CML) were treated with human leucocyte interferon (HuIFN-alpha). Karyotypic changes in addition to the Ph1 chromosome developed in these patients before the start of HuIFN-alpha treatment. In one patient the administration of HuIFN-alpha resulted in clinical haematological remission and stable suppression of the secondary Ph1 clone. The second patient was in myeloid blastic crisis when given HuIFN-alpha. While she was receiving HuIFN-alpha, suppression of the blast cell population in the bone marrow occurred. The subsequent cytogenetic changes included a near-complete suppression of a secondary Ph 1 clone of cells carrying a deletion in the short arm of chromosome 7 and partial population of the bone marrow with primary Ph1 clone. These observations suggest a potential role for interferons in altering the progressive course of CML.

Adult↗
PubMed1987

HLA phenotype and clinicopathological behaviour of germ cell tumours: possible evidence for clonal evolution from seminomas to nonseminomas.

Analysis of 101 patients with germ cell tumours of the testis who have been typed for HLA DR antigens has provided confirmatory evidence for an association of DR5 with the development of seminoma and demonstrated an association of DR7 with metastases. These observations taken with the suggestion of HLA linkage in the small numbers of familial cases reviewed, does suggest that there is an HLA linked gene involved in the clinicopathological behaviour of germ cell tumours. Though of only theoretical interest at present these observations may be of considerable importance in the future given the observation in mice that transfection of missing MHC genes into a malignant tumour can produce a vaccine that enables previously unexposed animals to resist the original malignant tumour (Hui et al., 1984).

Dysgerminoma↗
PubMed1988

Gene probe analysis demonstrates independent clonal evolution of co-existent chronic myeloid and chronic lymphocytic leukaemia.

We describe a case of Philadelphia-positive chronic myeloid leukaemia occurring simultaneously with B-cell chronic lymphocytic leukaemia in a 69-yr-old male. Gene probe analysis of DNA from both peripheral blood and bone marrow provided evidence for the independent evolution of 2 clones in this case, with a predominant population showing immunoglobulin heavy chain gene rearrangement and a smaller population showing a rearrangement within the breakpoint cluster region of chromosome 22.

Aged↗
PubMed1976

The clonal evolution of tumor cell populations.

It is proposed that most neoplasms arise from a single cell of origin, and tumor progression results from acquired genetic variability within the original clone allowing sequential selection of more aggressive sublines. Tumor cell populations are apparently more genetically unstable than normal cells, perhaps from activation of specific gene loci in the neoplasm, continued presence of carcinogen, or even nutritional deficiencies within the tumor. The acquired genetic insta0ility and associated selection process, most readily recognized cytogenetically, results in advanced human malignancies being highly individual karyotypically and biologically. Hence, each patient's cancer may require individual specific therapy, and even this may be thwarted by emergence of a genetically variant subline resistant to the treatment. More research should be directed toward understanding and controlling the evolutionary process in tumors before it reaches the late stage usually seen in clinical cancer.

Carcinogens↗
PubMed1979

Clonal evolution of marker chromosomes in a case of myelofibrosis with myeloid metaplasia and myeloblastic transformation.

The diverse spectrum of acquired chromosome abnormalities in a female patient with myelofibrosis and myeloid metaplasia is described. A sequence of karyotypic evolution involving a ring chromosome is postulated. The terminal clinical picture was unusual in that there was obstructive renal failure from extramedullary myeloblastic transformation and infiltration of the bladder, and this was also present in other sites. Initially neutrophils showed low alkaline phosphatases activity but latterly two distinct populations in which cells had either high activity or none.

Alkaline Phosphatase↗
PubMed1976

Unusual clonal evolution in a case of chronic myelogenous leukemia.

Several unusual cytogenetic changes have occurred during the evolution of chronic myelogenous leukemia in a 32-year-old white male with this disease for 8 years. The first appearance of a hypodiploid cell line containing a dicentric marker occurred 2 years after diagnosis and this line was eliminated by several courses of therapy with hydroxyurea. A second clone, which had a partial deletion of the long arm of one of the number 8 chromosomes (8q-) was noted a year later, but this line has been refractory to intensive combination chemotherapy.

Adult↗
PubMed1988

Transposition of the oncogene c-ets-1 in a t(11;19)(q23;p13) cell line transient during clonal evolution of blast crisis chronic myeloid leukemia.

A patient with Ph-negative chronic myeloid leukemia showed active karyotypic evolution when he entered blast crisis. One cell line, which predominated briefly in an accelerated myeloid phase, was characterized by the t(11;19)(q23;p13). Chromosome in situ hybridization demonstrated movement of the oncogene c-ets-1 from the der (11q-) to the der (19p+). The breakpoint at 19p13 was in the vicinity of the human insulin receptor gene locus (INSR). No rearrangements of the c-ets and INSR genes were found in Southern blot analyses. Myeloid lineage was indicated by cell morphology and absence of immunoglobulin JH gene rearrangement and was supported by loss of the germ line bcr-3' gene. Chromosome rearrangements involving 11q23 and movement of c-ets-1 characterize monocytic and lymphoid leukemias and have not previously been reported in myeloid blast crisis of chronic myeloid leukemia.

Cell Transformation, Neoplastic↗