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The impact of translocations and gene fusions on cancer causation
An analysis of available data shows that gene fusions occur in all malignancies, and that they account for 20% of human cancer morbidity, with the advent of new and powerful investigative tools that enable the detection of cytogenetically cryptic rearrangements.
The emerging complexity of gene fusions in cancer
The spectrum of gene fusions in cancer and how the methods to identify them have evolved are described, and the conceptual implications of current, sequencing-based approaches for detection are discussed.
Cytogenetic and Molecular Genetic Evolution of Chronic Myeloid Leukemia
It is suggested that all these aberrations, occurring in >5% of CML with secondary changes, should be denoted major route abnormalities, except for slightly lower frequencies of the most common changes in the latter group.
A breakpoint map of recurrent chromosomal rearrangements in human neoplasia
A computer program is developed to ascertain, for the first time, all recurrent structural abnormalities in all haematological malignancies and solid tumours published up to June 19, which should help in directing future efforts aimed at identifying the molecular mechanisms involved in tumorigenesis.
Distinct patterns of hematopoietic stem cell involvement in acute lymphoblastic leukemia
It is shown that clinically and genetically different subtypes of acute lymphoblastic leukemia (ALL) originate and transform at distinct stages of hematopoietic development.
Identification of ETV6-RUNX1-like and DUX4-rearranged subtypes in paediatric B-cell precursor acute lymphoblastic leukaemia
This study delineates the fusion gene landscape in a consecutive series of 195 paediatric B-cell precursor acute lymphoblastic leukaemia (BCP ALL) and identifies a subtype characterized by an ETV6-RUNX1-like gene-expression profile and coexisting ETV 6 and IKZF1 alterations.
Fusion genes and rearranged genes as a linear function of chromosome aberrations in cancer
In every tumor type, the numbers of recurrent balanced chromosome abnormalities, fusion genes and genes rearranged as a consequence of balanced aberrations are simply a function of the number of cases with an abnormal karyotype, suggesting that there may not be any fundamental tissue-specific differences in the genetic mechanisms by which neoplasia is initiated.
Chromosomal imbalance maps of malignant solid tumors: a cytogenetic survey of 3185 neoplasms.
The relative distribution of losses indicated that different bands/regions are affected in different tumor types and that, often, several distinct candidate tumor suppressor gene loci can be discerned within the same chromosome arm, e.g., 1p12-13, 1 p22, 1p34, and 1p36 on the short arm of chromosome 1 and 7q22, 7q32, and 7Q32 on the long arm of chromosomes 7.
High hyperdiploid childhood acute lymphoblastic leukemia
Despite the high frequency of this karyotypic subgroup, many questions remain regarding the epidemiology, etiology, presence of other genetic changes, the time and cell of origin, and the formation and pathogenetic consequences of high hyperdiploidy.