t(5;6;12) associated with resistance to imatinib mesylate in chronic myeloid leukemia

Denčić‐Fekete, Marija; Đorđević, Vesna; Storlazzi, Clelia Tiziana; Janković, Gradimir; Bogdanović, Andrija; Jovanović, Jovan; Rocchi, Mariano; Todoric-Zivanovic, Biljana; Strnad, Milica; Gotić, Mirjana

doi:10.1007/s12185-009-0275-8

Cited by 2 publications

(2 citation statements)

References 23 publications

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“…Karyotype changes in Ph+ clone emerged 40 months after the imatinib therapy was started, as the only sign of disease relapse. This distinctive karyotype included complex translocation and the rare event of centromere fission which were previously published [10,11]. Negative search for mutations by Sanger sequencing in the kinase domain further contributed to the complexity of the case.…”

Section: Discussionmentioning

confidence: 89%

Several different cytogenetic clones arising during treatment of Philadelphia positive chronic myeloid leukemia with tyrosine kinase inhibitors lead to the progression into Philadelphia negative acute myeloid leukemia

et al. 2021

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When the final article is assigned to volumes/issues of the Journal, the Article in Press version will be removed and the final version appear in the associated published volumes/issues of the Journal. The date the article was made available online first will be carried over. primenom TKI terapije TKI ne treba da isključi regularno testiranje kostne srži bolesnika sa CML citogenetskom analizom. Otkrivanje kariotipskih abnormalnosti sa lošom prognozom je od velikog značaja zbog mogućnosti razvoja sekundarnih malignitetamijelodisplastičnog sindroma i AML. Ključne reči: hronična mijeloidna leukemija, tirozin kinazni inhibitori, filadelfija hromozom, rezistencija na terapiju, abnormalnosti hromozoma 7.

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Section: Discussionmentioning

confidence: 89%

Several different cytogenetic clones arising during treatment of Philadelphia positive chronic myeloid leukemia with tyrosine kinase inhibitors lead to the progression into Philadelphia negative acute myeloid leukemia

et al. 2021

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“…CIN is responsible for pre-treatment existance or acquisition during treatment of multiple mechanisms contributing to (multi)drug resistance. It is well documented that CIN significantly correlates with inherent and acquired (multi)drug resistance [68][69][70][71][72][73][74][75][76][77][78][79][80][81][82][83][84] and (multi)drug/chemoresistance acquisition is accompanied by new evolved chromosome imbalances [74,76,80,81,[168][169][170][171][172][173][174][175][176][177][178][179][180]. In support, RNA and protein expression profiles after drug-resistance acquisition differ from parental drug-sensitive cells in expression of tens to thousands genes [174,179,[181][182][183][184][185][186][187][188][189].…”

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confidence: 99%

Evolutionary karyotypic theory of cancer versus conventional cancer gene mutation theory

Stepanenko

Kavsan

2012

Biopolym. Cell

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For decades the conventional gene mutation cancer theory has been postulating that cancer is a genetic disease considered as a result of deterministic sequential accumulation of mutations in the handful of «driver» cancer genes occurring in a continuous linear pattern of cancer progression. However, in contrast to this postulate, recent whole genome and exome sequencing studies of primary tumor bulk and metastases or separate regions withing the same sample have revealed a large number of stochastic gene mutations for each individual with the same cancer type and significant intratumoral genetic heterogeneity with «branched evolutionary tumor growth» or «punctuated clonal evolution without observable intermediate branching» or «no dominant clones in the cancer tissue». Meanwhile, the stochastic karyotypic variation and intratumor heterogeneity are recognized to be the driving force of tumor evolution and major factors in determining relapse with acquired drug resistance. The karyotype evolution/chromosome instability and the resulting magnitude of intratumor heterogeneity significantly correlate with tumorigenic potential of cells, tumor disease progression from precancerous lesions to malignant tumors and metastases, correlate with patient survival, treatment sensitivity, and the risk of acquired resistance. Here, we discuss importance of the evolutionary karyotypic theory in understanding the cancer biology and mechanisms of tumor drug resistance

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t(5;6;12) associated with resistance to imatinib mesylate in chronic myeloid leukemia

Cited by 2 publications

References 23 publications

Several different cytogenetic clones arising during treatment of Philadelphia positive chronic myeloid leukemia with tyrosine kinase inhibitors lead to the progression into Philadelphia negative acute myeloid leukemia

Several different cytogenetic clones arising during treatment of Philadelphia positive chronic myeloid leukemia with tyrosine kinase inhibitors lead to the progression into Philadelphia negative acute myeloid leukemia

Evolutionary karyotypic theory of cancer versus conventional cancer gene mutation theory

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