A druggable molecular abnormality was present in 38 patients (40%).
In addition, the outcome of patients who entered a phase I trial based on a molecular abnormality was better than the outcome of patients who entered a trial without matching.
The clinical impact of these different genetic and molecular abnormalities is 3-fold.
Among patients with a normal karyotype, a similar incidence of molecular abnormalities is observed in both primary AML and tAML (52).
A set of genetic and epigenetic molecular abnormalities is a feature of primary M+ CRCs likely conferring the ability for tumour extracolic spread and determining markers for aggressive behaviour and potential therapeutic targets.
In case of several alterations, the prioritization of the molecular abnormalities is discussed by the MBB based on the following criteria: (1) In case of expression of both AR and ER/PR in a same patient, the hormone receptor with the highest expression level is taken into account.
Risk stratification, based on cytogenetics and molecular abnormalities, was used to categorize patients into three groups: favorable-, intermediand-, and unfavorable-risk groups [4].
Recently several molecular abnormalities were reported to associate with sensitivity or resistance to EGFR inhibitors, including somatic mutations in the EGFR tyrosine kinase domain, EGFR gene amplification, KRAS mutation, and MET amplification [14], [15], [16], [17].
If one or several molecular abnormalities were identified, then patients were randomised.
The most frequent molecular abnormalities are alterations to the tumor suppressor, p53 (Ahuja et al. 1989).
