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Molecular abnormalities have also been identified in tumors other than adenocarcinoma (squamous and small cell carcinoma).
Within the CN group, several molecular abnormalities have been associated with prognosis.
Although it is well-established that the pathogenesis of PDAs follows stepwise stages that display increasing cellular atypia and accumulate clonal mutations or aberrant expression of oncogenes or tumor suppressor genes such as K-Ras, p16, p53, and DPC4/SMAD4 [2], drugs that target these molecular abnormalities have not yet translated into improved clinical responses [3].
The etiology of PPB remains unknown, but pathogenetic molecular abnormalities have been reported[ 37 ].
Genetic alterations and molecular abnormalities have been identified in oral premalignant lesions.
Targeted therapies that specifically inhibit pivotal molecular abnormalities have emerged as a promising approach for various cancers, including HCC [ 5].
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With the advent of next generation sequencing (NGS) technologies the discovery of novel molecular abnormalities has accelerated.
Successive inclusion of novel molecular abnormalities has substantially modified the classification and understanding of AML in the past decade.
Moreover, targeted therapy, which specifically inhibits molecular abnormalities, has recently emerged as a novel approach for the effective medical treatment of malignancies, including HCC [ 114, 115].
There is a constant evolution in the classification of neoplasia, and the identification of specific molecular abnormalities has the potential to enhance diagnostic accuracy and, ultimately, provide a rational approach to the development of novel treatment strategies (Bisogno et al, 2012).
Unlike myxomatous degeneration in Marfan syndrome, which has been reported to result from a mutation in the gene that codes for the extracellular structural protein fibrillin, no specific molecular abnormality has been documented to be the underlying cause of myxomatous degeneration in mitral valve prolapse syndrome (MVPS).
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