Abstract
Our understanding of how DNA copy number changes contribute to disease, including cancer, has to a large degree been focused on the changes in gene dosage that they generate and has neglected the effects of the DNA rearrangements that lead to their formation. A new study reports an innovative analytical framework for copy number alterations that are oncogenic primarily owing to the genomic rearrangements that underlie them.
MeSH terms
-
Basic Helix-Loop-Helix Transcription Factors / genetics
-
Basic Helix-Loop-Helix Transcription Factors / metabolism
-
Chromosome Aberrations
-
Chromosomes, Human, Pair 14
-
Chromosomes, Human, Pair 6
-
Chromosomes, Human, Pair 8
-
DNA Copy Number Variations*
-
Enhancer Elements, Genetic*
-
GATA2 Transcription Factor / genetics
-
GATA2 Transcription Factor / metabolism
-
Gene Dosage
-
Gene Expression Regulation, Neoplastic*
-
Humans
-
Insulin-Like Growth Factor II / genetics
-
Insulin-Like Growth Factor II / metabolism
-
Neoplasms / genetics*
-
Neoplasms / metabolism
-
Neoplasms / pathology
-
Proto-Oncogene Proteins / genetics
-
Proto-Oncogene Proteins / metabolism
-
Proto-Oncogene Proteins c-myc / genetics
-
Proto-Oncogene Proteins c-myc / metabolism
-
T-Cell Acute Lymphocytic Leukemia Protein 1
Substances
-
Basic Helix-Loop-Helix Transcription Factors
-
GATA2 Transcription Factor
-
GATA2 protein, human
-
IGF2 protein, human
-
MYC protein, human
-
Proto-Oncogene Proteins
-
Proto-Oncogene Proteins c-myc
-
T-Cell Acute Lymphocytic Leukemia Protein 1
-
TAL1 protein, human
-
Insulin-Like Growth Factor II