Relation between 99mTc-tetrofosmin thyroid scintigraphy and mitogen-activated protein kinase in papillary thyroid cancer patients

2011 ◽  
Vol 29 (8) ◽  
pp. 533-539 ◽  
Author(s):  
Kenkichi Baba ◽  
Masatoshi Ishibashi ◽  
Hayato Kaida ◽  
Teruhiko Fujii ◽  
Yuji Hiromatsu ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Protein Kinase ◽  
Cancer Patients ◽  
Papillary Thyroid Cancer ◽  
Mitogen Activated Protein Kinase ◽  
Papillary Thyroid ◽  
Thyroid Scintigraphy ◽  
99Mtc Tetrofosmin ◽  
Mitogen Activated Protein

scholarly journals Recurrent Somatic MAP2K1 Mutations in Papillary Thyroid Cancer and Colorectal Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Rong Bu ◽  
Abdul K. Siraj ◽  
Tariq Masoodi ◽  
Sandeep Kumar Parvathareddy ◽  
Kaleem Iqbal ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Thyroid Cancer ◽  
Protein Kinase ◽  
Papillary Thyroid Cancer ◽  
Middle Eastern ◽  
Mitogen Activated Protein Kinase ◽  
Papillary Thyroid ◽  
Dual Specificity ◽  
Mitogen Activated Protein ◽  
Specificity Protein

Mitogen-activated protein kinase kinase 1 (MAP2K1) is a dual specificity protein kinase that phosphorylates both threonine and tyrosine residues in ERK. MAP2K1 mutations have been identified in several cancers. However, their role in Middle Eastern papillary thyroid cancer (PTC) and colorectal cancer (CRC) is lacking. In this study, we evaluated the prevalence of MAP2K1 mutations in a large cohort of Middle Eastern PTC and CRC using whole-exome and Sanger sequencing technology. In the discovery cohort of 100 PTC and 100 CRC cases (comprising 50 MAPK mutant and 50 MAPK wildtype cases each), we found one MAP2K1 mutation each in PTC and CRC, both of which were MAPK wildtype. We further analyzed 286 PTC and 289 CRC MAPK wildtype cases and found three MAP2K1 mutant PTC cases and two MAP2K1 mutant CRC cases. Thus, the overall prevalence of MAP2K1 mutation in MAPK wildtype cases was 1.1% (4/336) in PTC and 0.9% (3/339) in CRC. Histopathologically, three of the four MAP2K1 mutant PTC cases were follicular variant and all four tumors were unifocal with absence of extra-thyroidal extension. All the three CRC cases harboring MAP2K1 mutation were of older age (> 50 years) and had moderately differentiated stage II/III tumors located in the left colon. In conclusion, this is the first comprehensive report of MAP2K1 somatic mutations prevalence in PTC and CRC from this ethnicity. The mutually exclusive nature of MAP2K1 and MAPK mutations suggests that each of these mutation may function as an initiating mutation driving tumorigenesis through MAPK signaling pathway.

scholarly journals Radiation-related genomic profile of papillary thyroid cancer after the Chernobyl accident

Science ◽  
2021 ◽  
pp. eabg2538 ◽  
Author(s):  
Lindsay M. Morton ◽  
Danielle M. Karyadi ◽  
Chip Stewart ◽  
Tetiana I. Bogdanova ◽  
Eric T. Dawson ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Radiation Dose ◽  
Papillary Thyroid Cancer ◽  
Nuclear Power ◽  
Mitogen Activated Protein Kinase ◽  
Papillary Thyroid ◽  
Dna Double Strand Breaks ◽  
Environmental Radiation ◽  
Mitogen Activated Protein ◽  
Non Homologous End Joining

The 1986 Chernobyl nuclear power plant accident increased papillary thyroid cancer (PTC) incidence in surrounding regions, particularly for 131I-exposed children. We analyzed genomic, transcriptomic, and epigenomic characteristics of 440 PTCs from Ukraine (359 with estimated childhood 131I exposure and 81 unexposed children born after 1986). PTCs displayed radiation dose-dependent enrichment of fusion drivers, nearly all in the mitogen-activated protein kinase pathway, and increases in small deletions and simple/balanced structural variants that were clonal and bore hallmarks of non-homologous end-joining repair. Radiation-related genomic alterations were more pronounced for those younger at exposure. Transcriptomic and epigenomic features were strongly associated with driver events but not radiation dose. Our results point to DNA double-strand breaks as early carcinogenic events that subsequently enable PTC growth following environmental radiation exposure.

scholarly journals RNA-sequencing investigation identifies an effective risk score generated by three novel lncRNAs for the survival of papillary thyroid cancer patients

Oncotarget ◽  
2017 ◽  
Vol 8 (43) ◽  
pp. 74139-74158 ◽  
Author(s):  
Yi-Huan Luo ◽  
Liang Liang ◽  
Rong-Quan He ◽  
Dong-Yue Wen ◽  
Guo-Fei Deng ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cancer Patients ◽  
Rna Sequencing ◽  
Papillary Thyroid Cancer ◽  
Risk Score ◽  
Papillary Thyroid

scholarly journals Radioiodine-Refractory Thyroid Cancer: Molecular Basis of Redifferentiation Therapies, Management, and Novel Therapies

Cancers ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1382 ◽  
Author(s):  
Mohamed Aashiq ◽  
Deborah A. Silverman ◽  
Shorook Na’ara ◽  
Hideaki Takahashi ◽  
Moran Amit
Keyword(s):  
Thyroid Cancer ◽  
Protein Kinase ◽  
Tyrosine Kinase ◽  
Mitogen Activated Protein Kinase ◽  
Sodium Iodide Symporter ◽  
Tumor Resistance ◽  
Loss Of Function ◽  
Iodide Uptake ◽  
Mitogen Activated Protein ◽  
Recurrent Thyroid Cancer

Recurrent, metastatic disease represents the most frequent cause of death for patients with thyroid cancer, and radioactive iodine (RAI) remains a mainstay of therapy for these patients. Unfortunately, many thyroid cancer patients have tumors that no longer trap iodine, and hence are refractory to RAI, heralding a poor prognosis. RAI-refractory (RAI-R) cancer cells result from the loss of thyroid differentiation features, such as iodide uptake and organification. This loss of differentiation features correlates with the degree of mitogen-activated protein kinase (MAPK) activation, which is higher in tumors with BRAF (B-Raf proto-oncogene) mutations than in those with RTK (receptor tyrosine kinase) or RAS (rat sarcoma) mutations. Hence, inhibition of the mitogen-activated protein kinase kinase-1 and -2 (MEK-1 and -2) downstream of RAF (rapidly accelerated fibrosarcoma) could sensitize RAI refractivity in thyroid cancer. However, a significant hurdle is the development of secondary tumor resistance (escape mechanisms) to these drugs through upregulation of tyrosine kinase receptors or another alternative signaling pathway. The sodium iodide symporter (NIS) is a plasma membrane glycoprotein, a member of solute carrier family 5A (SLC5A5), located on the basolateral surfaces of the thyroid follicular epithelial cells, which mediates active iodide transport into thyroid follicular cells. The mechanisms responsible for NIS loss of function in RAI-R thyroid cancer remains unclear. In a study of patients with recurrent thyroid cancer, expression levels of specific ribosomal machinery—namely PIGU (phosphatidylinositol glycan anchor biosynthesis class U), a subunit of the GPI (glycosylphosphatidylinositol transamidase complex—correlated with RAI avidity in radioiodine scanning, NIS levels, and biochemical response to RAI treatment. Here, we review the proposed mechanisms for RAI refractivity and the management of RAI-refractive metastatic, recurrent thyroid cancer. We also describe novel targeted systemic agents that are in use or under investigation for RAI-refractory disease, their mechanisms of action, and their adverse events.

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