Near haploid childhood acute lymphoblastic leukemia masked by hyperdiploid line

Stark, Batia; Jeison, Marta; Gobuzov, Rima; Krug, Hagit; Glaser-Gabay, Leticia; Luria, Drorit; Elhasid, Ronit; Harush, Miriam Ben; Avrahami, Gali; Fisher, Sharon; Stein, Jerry; Zaizov, Rina; Yaniv, Isaac

doi:10.1016/s0165-4608(01)00411-3

Cited by 40 publications

(35 citation statements)

References 28 publications

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“…It should not be surprising that hypodiploid cells are viable. Cancer cells do not need to be diploid: even haploid cell lines are absolutely viable (Kessous et al, 1980;Stark et al, 2001). Furthermore, most genes, which are necessary for the development of diverse human organs, are dispensable for somatic cells in culture.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of G1-like arrest by low concentrations of paclitaxel: next cell cycle p53-dependent arrest with sub G1 DNA content mediated by prolonged mitosis

Demidenko

Kalurupalle²,

Hanko³

et al. 2008

Oncogene

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Paclitaxel (PTX) and other microtubule inhibitors cause mitotic arrest. However, low concentrations of PTX (low PTX) paradoxically cause G1 arrest (without mitotic arrest). Here, we demonstrated that unexpectedly, low PTX did not cause G1 arrest in the first cell cycle and did not prevent cells from passing through S phase and entering mitosis. Mitosis was prolonged but cells still divided, producing either two or three cells (tripolar mitosis), thus explaining a sub G1 peak caused by low PTX. Importantly, sub G1 cells were viable and nonapoptotic. Some cells fused back and then progressed to mitosis, frequently producing three cells again before becoming arrested in the next cell-cycle interphase. Thus, low PTX caused postmitotic arrest in second and even the third cell cycles. By increasing concentration of PTX, tripolar mitosis was transformed to mitotic slippage, thus eliminating a sub G1 peak. Time-lapse microscopy revealed that prolonged mitosis ensured a p53-dependent postmitotic arrest. We conclude that PTX directly affects cells only in mitosis and the duration of mitosis determines cell fate, including p53-dependent G1-like arrest.

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Section: Discussionmentioning

confidence: 99%

Mechanism of G1-like arrest by low concentrations of paclitaxel: next cell cycle p53-dependent arrest with sub G1 DNA content mediated by prolonged mitosis

Demidenko

Kalurupalle²,

Hanko³

et al. 2008

Oncogene

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“…26 A common assumption has been that the widespread LOH resulting from hypodiploidy leads to the unmasking of recessive alleles. 5,23,27,28 A candidate could be TP53, since the loss of chromosome 17, and thereby 1 TP53 allele, together with a mutation in the remaining copy in low-hypodiploid ALL, could result in complete absence of a functioning protein. However, this would only explain the monosomy for this particular chromosome.…”

Section: Near-haploid and Low-hypodiploid All Harbor Distinct Mutatiomentioning

confidence: 99%

“…4,25 The leukemogenic effect of the endoreduplication may be to restore the gene copy numbers to more normal levels, increasing the fitness of the cell, and to decrease the risk of nondisjunction events resulting in nullisomy. It is notable that the doubled clones frequently are no longer seen 28,29 which may indicate that they are more sensitive to treatment than the founder hypodiploid clones (Figure 1), although it cannot be excluded that cases where the doubled clone still dominates at relapse may be misclassified as high hyperdiploid and thus remain undetected, introducing a bias.…”

Section: Near-haploid and Low-hypodiploid All Harbor Distinct Mutatiomentioning

confidence: 99%

Near-haploid and low-hypodiploid acute lymphoblastic leukemia: two distinct subtypes with consistently poor prognosis

Safavi

Paulsson

2017

Blood

116

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Hypodiploidy <40 chromosomes is an uncommon genetic feature of acute lymphoblastic leukemia (ALL) in both children and adults. It has long been clear by cytogenetic analyses, and recently confirmed by mutational profiling, that these cases may be further subdivided into 2 subtypes: near-haploid ALL with 24 to 30 chromosomes and low-hypodiploid ALL with 31 to 39 chromosomes. Both groups are associated with a very poor prognosis, and these patients are among those who could benefit most from novel treatments.

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“…Chromosomal aberrations when detected must be clonal (when present in a minimum of two cells with the same extra chromosomes or structural aberrations, or at least three cells with the same chromosome loss). Near-haploidy (<30 chromosomes) and low hypodiploidy (30-39 chromosomes) may undergo clonal evolution and double-up as hyperdiploid and near-triploid metaphases respectively [8]. Nearhaploidy and low hypodiploidy confer a poor prognosis and are assigned to high risk therapy.…”

Section: B) G-banded Karyotypingmentioning

confidence: 99%

Routine Cytogenetic Analysis of Chromosome Abnormalities in Acute Lymphoblastic Leukemia

Meng¹

2015

Int Jour of Biomed Res

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Acute lymphoblastic leukemia (ALL) is the most common cancer in children. Acquired chromosomal and genetic abnormalities have been used to define distinct biological and clinical subtypes of ALL. These aberrations have been shown to be associated with patient outcome and are used to direct therapy. Conventional cytogenetics analysis (CCA) is currently the gold standard to detect chromosome abnormalities in hematological malignancies. In this review we briefly describe the CCA methodology, advantages and limitations of CCA, the main chromosomal abnormalities and their prognostic significance in ALL.

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Near haploid childhood acute lymphoblastic leukemia masked by hyperdiploid line

Cited by 40 publications

References 28 publications

Mechanism of G1-like arrest by low concentrations of paclitaxel: next cell cycle p53-dependent arrest with sub G1 DNA content mediated by prolonged mitosis

Mechanism of G1-like arrest by low concentrations of paclitaxel: next cell cycle p53-dependent arrest with sub G1 DNA content mediated by prolonged mitosis

Near-haploid and low-hypodiploid acute lymphoblastic leukemia: two distinct subtypes with consistently poor prognosis

Routine Cytogenetic Analysis of Chromosome Abnormalities in Acute Lymphoblastic Leukemia

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