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Advances in genome-sequencing technologies and powerful analytics are increasingly being used to pinpoint errant genes and other molecular abnormalities that drive cancer's growth.
Both TDP-43 pathology and failure of RNA editing of AMPA receptor subunit GluA2, are etiology-linked molecular abnormalities that concomitantly occur in the motor neurons of the majority of patients with amyotrophic lateral sclerosis (ALS).
After standard induction chemotherapy, patients are assigned to different post-remission strategies on the basis of cytogenetic and molecular abnormalities that broadly define adverse, intermediate and favourable risk categories2,3.
Being different with classical diagnostic imaging, molecular imaging sets forth to probe the molecular abnormalities that are the basis of disease rather than to image the end effects of these molecular alterations [1, 2].
A powerful novel discovery approach should recapitulate previous findings, as well as identify novel molecular abnormalities that offer advantages relative to what is known.
Concerning these aspects, gene expression profiling of MM is a challenge promise, not only to identify prognostic indicators of clinical outcome, but as a means of characterizing specific molecular abnormalities that may underlie all the time-related poor signs of MM.
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A professor of biology, Dr. Ingram was best known for his discovery, in the early 1950's, that a single amino acid substitution is responsible for the molecular abnormality that leads to sickle cell anemia.
Of particular interest, EGFR mutation is the first molecular abnormality that is more frequent in nonsmoking patients with non-small cell lung cancer (NSCLC).
Recent advances in CML research have highlighted the role of the Bcr-Abl oncoprotein as a molecular abnormality that leads to phenotypic changes in Bcr-Abl expressing cells, and contributes to malignant transformation of cells.
Recent large-scale analyses of gene mutations in MDS and related diseases have identified molecular abnormalities (genotypes) that are specific for each MDS subtype (phenotype).
This idea is reinforced by the anomalous response of H292, which suggests these cells are driven by very different molecular abnormalities, and that their TKI-induced cell cycle arrest is mechanistically distinct from that seen in the other lines.
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Justyna Jupowicz-Kozak
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