The investigation of late cytogenetic effects in children with acute leukaemia in long remission and off all chemotherapy

Schüler, D.; Szollár, J; Koós, R; Szakmáry, E; Bogáthy, B.

doi:10.1007/bf00274689

Cited by 11 publications

(5 citation statements)

References 17 publications

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“…In our previous study, abnormal cells were seen in both synchronized and nonsynchronized cultures, and only 0.5% of cells from control synchronized cultures were abnormal. Our study confirms that nonclonal chromosome abnormalities are commonly present in the peripheral blood lymphocytes of long-term survivors of ALL [4, 6,7,9] and demonstrates a remarkable constancy in their frequency over a long period of time. No evidence for the development of cytogenetically abnormal clones was found.…”

Section: Discussionsupporting

confidence: 86%

“…Therefore, these pa-0 1986 Alan R. Liss, Inc. tients are well suited for investigation of late effects of therapy. Previous banded cytogenetic studies of peripheral blood lymphocytes from long-term survivors of childhood ALL have demonstrated nonclonal chromosome abnormalities in a small subpopulation of cells at mean frequenceis of 2.4-5.9% [4, 6,7,9]. Since aberrant cells were not found at this frequency in childhood cancer patients prior to therapy or in healthy controls [4-91, it has been suggested that the abnormalities were treatment induced.…”

Section: Introductionmentioning

confidence: 99%

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Cytogenetic studies of long‐term survivors of childhood acute lymphoblastic leukemia: A follow‐up report

Rubin

Robison

Nesbit

et al. 1986

Med. Pediatr. Oncol.

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Previous series including our earlier study of survivors of childhood acute lymphoblastic leukemia have documented the presence of nonclonal chromosome abnormalities in peripheral blood lymphocytes. To investigate whether or not these abnormalities persist, we restudied nine patients, all of whom had received radiotherapy and a minimum of 3 years of systemic chemotherapy. Therapy had been discontinued a median of 3.9 years prior to study in our first report and a median of 7.2 years prior to study in this follow-up report. Thirty metaphases from short-term cultures of phytohemagglutinin-stimulated peripheral blood from each of nine patients and nine matched controls were analyzed using G-banding. Nonclonal chromosome abnormalities were present in cells from six of the nine patients and 3.0% of patients' cells overall, as compared to seven of ten patients and 3.5% of patients' cells in the earlier study. All patients studied twice had abnormalities on one or both occasions. No evidence for the development of cytogenetically abnormal clones was found. Combined data from the two evaluations indicate that all of the patients have a small population of long-lived lymphocytes with nonclonal chromosome abnormalities, the frequency of these cells appears to remain remarkably constant over time, and the proportion of cells with chromosome abnormalities is approximately threefold greater in patients than in controls. It has become apparent that survivors of acute lymphoblastic leukemia are at increased risk for development of second malignant neoplasms. The relationship between therapy-induced chromosome damage and the development of second malignant neoplasms is currently unknown. We speculate that some cells, possibly in tissues other than peripheral blood, are preneoplastic by virtue of therapy-induced chromosome rearrangements involving critical genes and, following a long latent period, may undergo subsequent genetic or cellular changes that result in malignant transformation. Unfortunately, however, estimation of genetic damage through cytogenetic studies of peripheral blood T-lymphocytes does not appear to be a useful method for prediction of second malignant neoplasms following acute lymphoblastic leukemia, since most or all of the patients have a low level of abnormal cells.

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Section: Discussionsupporting

confidence: 86%

Section: Introductionmentioning

confidence: 99%

Cytogenetic studies of long‐term survivors of childhood acute lymphoblastic leukemia: A follow‐up report

Rubin

Robison

Nesbit

et al. 1986

Med. Pediatr. Oncol.

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“…The presence of chromosomal aberrations in stimulated lymphocytes from cancer patients without S-ANLL treated with either chemotherapy or radiotherapy, or both, has been reported by several investigators (Einhom, 1978;Miller et al, 1978;Gebhart et al, 1980;Haglund et al, 1980;Schuler et al, 1981;Lawler et al, 1982;Robinson etal., 1982;Rauscher and Bauchinger, 1983;Lambert et al. 1984).…”

Section: Discussionmentioning

confidence: 80%

Specific chromosomal mutagenesis observed in stimulated lymphocytes from patients with S‐ANLL

Mamuris

Dumont²,

Dutrillaux

et al. 1990

Intl Journal of Cancer

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An analysis of R-banded PHA-stimulated lymphocytes from 13 patients with secondary acute non-lymphocytic leukemia (S-ANLL) following breast cancer or lymphoma, and treatment by alkylating agents and/or radiotherapy, is reported. We found that chromosomes 5, 7, 11 and 17 are over-involved in structural rearrangements. These anomalies are similar to those observed in the same categories of patients without S-ANLL, and after in vitro treatment of normal lymphocytes by the alkylating agent melphalan. These anomalies are thus likely to be induced by treatment, independently of S-ANLL. However, the same chromosomes (5, 7, 11 and 17) are recurrently deficient in leukemic S-ANLL clones. In spite of these similarities, it remains unlikely that the deficiencies observed in leukemic clones were directly induced at the time of treatment. Probably, treatment of primary cancers induces nonrandom mutations of recessive genes located on these chromosomes as also indicated by chromosomal lesions. Various rearrangements including deletions of the homologous normal counterparts may then occur, unmasking mutated recessive genes. The latter stage would be concomitant with the leukemogenic process.

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“…The exis tence of rapidly and slowly growing cell clones among the lymphocytes stimulated with PHA was reported [8,13]. It appears less likely that T and B cells con stitute these tentative subpopulations [8], From the finding that the cell-cycle time of 'normal' lym phocytes of ALL children in long-lasting remission is shorter from the control cell-cycle data [12] arises the question whether this phenomenon could also be re vealed at the beginning of the illness, and what its prognostic significance may be.…”

Section: Discussionmentioning

confidence: 97%

Some Aspects of the Lymphocytes Kinetics during Treatment of Childhood Acute Lymphoblastic Leukemia

Dębiec‐Rychter¹

1983

Oncology

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The proliferative capacities of the PHA-stimulated bone marrow and peripheral blood lymphocytes were studied in children with newly diagnosed acute lymphoblastic leukemia by means of BrdU-Hoechst-Giemsa technique. The investigations were carried out at the following times: before treatment; during the first 72 h of the therapy, and after the remission induction. In patients with large amount of blasts, subpopulations of lymphocytes reacting either quickly or slowly could be distinguished. Some of the latter showed the recovery of proliferative capacities during the therapy. The problem whether the entire failure in proliferation of lymphocytes was due to the dilution of lymphocyte population by non-PHA-responsive blasts, due to the proliferation of long-lived leukemic cells or other factors, is discussed.

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The investigation of late cytogenetic effects in children with acute leukaemia in long remission and off all chemotherapy

Cited by 11 publications

References 17 publications

Cytogenetic studies of long‐term survivors of childhood acute lymphoblastic leukemia: A follow‐up report

Cytogenetic studies of long‐term survivors of childhood acute lymphoblastic leukemia: A follow‐up report

Specific chromosomal mutagenesis observed in stimulated lymphocytes from patients with S‐ANLL

Some Aspects of the Lymphocytes Kinetics during Treatment of Childhood Acute Lymphoblastic Leukemia

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