Advances in molecular pathogenesis thyroid cancer: therapeutic implications

2014 ◽  
Author(s):  
Pilar Santisteban ◽  
Ana Sastre-Perona ◽  
Leon Wert-Lamas ◽  
Garcilaso Riesco-Eizaguirre
Keyword(s):  
Thyroid Cancer ◽  
Molecular Pathogenesis ◽  
Therapeutic Implications

scholarly journals ENDOCRINE TUMOURS: Advances in the molecular pathogenesis of thyroid cancer: lessons from the cancer genome

2016 ◽  
Vol 175 (5) ◽  
pp. R203-R217 ◽  
Author(s):  
Garcilaso Riesco-Eizaguirre ◽  
Pilar Santisteban
Keyword(s):  
Thyroid Cancer ◽  
Cancer Genomics ◽  
Treatment Strategies ◽  
Genetic Alterations ◽  
Cancer Genome ◽  
Molecular Pathogenesis ◽  
Cancer Genes ◽  
New Information ◽  
Novel Treatment Strategies ◽  
And Behavior

Thyroid cancer is the most common endocrine malignancy giving rise to one of the most indolent solid cancers, but also one of the most lethal. In recent years, systematic studies of the cancer genome, most importantly those derived from The Cancer Genome Altas (TCGA), have catalogued aberrations in the DNA, chromatin, and RNA of the genomes of thousands of tumors relative to matched normal cellular genomes and have analyzed their epigenetic and protein consequences. Cancer genomics is therefore providing new information on cancer development and behavior, as well as new insights into genetic alterations and molecular pathways. From this genomic perspective, we will review the main advances concerning some essential aspects of the molecular pathogenesis of thyroid cancer such as mutational mechanisms, new cancer genes implicated in tumor initiation and progression, the role of non-coding RNA, and the advent of new susceptibility genes in thyroid cancer predisposition. This look across these genomic and cellular alterations results in the reshaping of the multistep development of thyroid tumors and offers new tools and opportunities for further research and clinical development of novel treatment strategies.

Driving toward precision medicine for B cell lymphomas: Targeting the molecular pathogenesis at the gene level

2020 ◽  
Vol 26 (4) ◽  
pp. 943-966 ◽  
Author(s):  
Clement Chung
Keyword(s):  
B Cell ◽  
Killer Cell ◽  
Treatment Resistance ◽  
Molecular Pathogenesis ◽  
Janus Kinase ◽  
Molecular Heterogeneity ◽  
B Cell Lymphomas ◽  
Regulatory Pathways ◽  
Therapeutic Implications ◽  
Molecular Abnormalities

Lymphomas are a diverse group of hematologic malignancies that arise from either T cell, B cell or the natural killer cell lineage. B cell lymphomas arise from gene mutations with critical functions during normal B cell development. Recent advances in the understanding of molecular pathogenesis demonstrate that many different recurrent genomic and molecular abnormalities and dysregulated oncogenic regulatory pathways exist for many subtypes of B cell lymphomas, both across and within histological subtypes. Pathogenetic processes such as (1) chromosomal aberrations, for example, t(14;18) in follicular lymphoma, t(11;14) in mantle cell lymphoma, t(8;14) in Burkitt lymphoma; dysregulations in signaling pathways of (2) nuclear factor- κB (NF-κB); (3) B cell receptor (BCR); (4) Janus kinase/signal transducers and transcription activators (JAK-STAT); (5) impaired apoptosis/cell cycle regulation due to mutated, rearranged or amplified MYC, BCL-2, BCL-6 proto-oncogenes; (6) epigenetic aberrations may contribute to pathogenesis. More studies are under way to elucidate the molecular heterogeneity underlying many types of lymphomas that account for variable responses to treatment, generation of subclones and treatment resistance. Although significant research is still needed, targeted therapy promises to provide new options for the treatment of patients with lymphomas. This article provides a non-exhaustive overview on the current understanding on the genetics of pathogenesis of B cell lymphomas and their therapeutic implications.

scholarly journals Ameloblastoma: A Review of Recent Molecular Pathogenetic Discoveries

2015 ◽  
Vol 7s2 ◽  
pp. BIC.S29329 ◽  
Author(s):  
Noah A. Brown ◽  
Bryan L. Betz
Keyword(s):  
Sonic Hedgehog ◽  
Mapk Pathway ◽  
Molecular Pathogenesis ◽  
Large Majority ◽  
Pathogenetic Mechanism ◽  
Therapeutic Implications ◽  
Activating Mutations ◽  
Shh Pathway ◽  
Odontogenic Neoplasm

Ameloblastoma is an odontogenic neoplasm whose molecular pathogenesis has only recently been elucidated. The discovery of recurrent activating mutations in FGFR2, BRAF, and RAS in a large majority of ameloblastomas has implicated dysregulation of MAPK pathway signaling as a critical step in the pathogenesis of this tumor. Some degree of controversy exists regarding the role of mutations affecting the sonic hedgehog (SHH) pathway, specifically Smoothened (SMO), which have been postulated to serve as either an alternative pathogenetic mechanism or secondary mutations. Here, we review recent advances in our understanding of the molecular pathogenesis of ameloblastoma as well as the diagnostic, prognostic, and therapeutic implications of these discoveries.

scholarly journals Clinical and therapeutic implications of Sprouty2 feedback dysregulation in BRAF V600E-mutation-positive papillary thyroid cancer

Surgery ◽  
2013 ◽  
Vol 154 (6) ◽  
pp. 1239-1245 ◽  
Author(s):  
Linda A. Dultz ◽  
Shumon Dhar ◽  
Jennifer B. Ogilvie ◽  
Keith S. Heller ◽  
Dafna Bar-Sagi ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Papillary Thyroid Cancer ◽  
Braf V600e Mutation ◽  
Braf V600e ◽  
Papillary Thyroid ◽  
Therapeutic Implications
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