Jan 2024 DOI 10.14302/issn.2574-4496.jtc-23-4835
Hussein Saleh Hussein AbbasCorresponding author
The prevalence of thyroid cancer is rapidly increasing worldwide, majorly due to overdiagnosis and overtreatment methods of differentiated thyroid cancer. The emergent and potent preclinical models, high-throughput molecular techniques, and genetic expression microarrays have delivered deeper insights into understanding the molecular features in oncogenesis. Thus, molecular markers have become a promising tool in managing thyroid cancer for differentiating benign and malignant tumors, prognosis, recurrence, and determination of novel therapeutic targets. In differentiated thyroid cancer, molecular markers are majorly utilized for guiding the development of indeterminate thyroid nodules on fine needle aspiration (FNA) histologies. Dissimilar to this, in advanced thyroid cancer, molecular markers permit targeted treatment of a modified signaling cascade. Determining causal mutation of targeted kinase receptors in advanced thyroid cancer can depict a promising treatment strategy with mutation-targeted tyrosine kinase inhibitors to reduce progression and eradicate mutation effects when conventional methods fail to manage. This review will focus on the molecular landscape and discuss the impact of molecular markers on the prognosis, treatment, and surveillance of differentiated and anaplastic thyroid cancer.
May 2021 DOI 10.14302/issn.2689-4602.jes-21-3837
O. Henderson JeffreyCorresponding author
Department of Science and Mathematics, Judson University, Elgin, IL 60123, USA
The coronavirus infectious disease (20)19 (COVID-19) pandemic is caused by a newly identified virus (2019) SARS-CoV-2, a beta coronavirus that shares similarities with other human-infecting coronaviruses. Genomic analysis suggests that SARS-CoV-2 is closely related to SARS-CoV, a bat-related coronavirus, RaTG13, and to other pangolin-associated coronaviruses. The spike protein of coronaviruses are glycoproteins and are responsible for attaching the virus to the host cell and entering. Amino acid changes within the spike protein-encoding gene from SARS-CoV to SARS-CoV-2 enable SARS-CoV-2 to form a stable spike protein, to form a stable complex between the S protein and the receptor ACE2, to increase binding points between the S protein and ACE2, and to survive at higher temperatures. SARS-CoV-2 is zoonotic, with genomic analysis implicating bats as the original host and pangolins as the most likely intermediate host to infect humans. As SARS-CoV-2 infects humans, viral point mutations will continually occur and cause the emergence of new competitive SARS-CoV-2 strains. Two major strains include D614G and N501Y and have increased infectivity and transmission, further complicating the scope of the current COVID-19 pandemic. Vigilant monitoring of viral development and evolution is necessary for developing proper treatment methods and vaccine targets.