Papillary thyroid cancer and its gene polymorphism; A molecular mechanistic perspective

Abstract

Thyroid cancer stands as the predominant malignancy within the endocrine system, comprising about 1% of newly identified cancer instances. Papillary Thyroid Cancer (PTC) is the predominant form of thyroid cancer, representing 80% or more of thyroid malignancies. Thyroid carcinoma harbours assorted genetic alterations which are highly prevalent, several of these characteristics are unique to this form of cancer. The conventional oncogenic genetic modifications frequently observed in thyroid carcinoma encompass RAS mutations RET/PTC rearrangements and PAX8-peroxisome proliferator-activated receptor g (PPARg) fusion oncogene. The lately discovered activating mutation in BRAF (the gene for the B-type RAF kinase, BRAF) the most widespread genetic modification in thyroid cancer (30-83%). RKIP (RAF kinase inhibitory protein) had formerly been delineated as a phospholipid binding protein. Mammalian RKIP/PEBP differs from other identified proteins and its role is still being clarified. RKIP over-expression can inhibit MEK interaction with RAF-1 and B-RAF. It plays a role in thyroid cancer progression and lymph node metastasis. So, elucidating mutational profile and protein expression of above cell signalling molecules will be very useful in determining a proper therapeutic target for anti-cancer molecules. Given that tumors often possess numerous genetic and cell signalling abnormalities, thus inhibiting a single signalling pathway is often therapeutically inefficacious, more success could be foreseen with agents directed against multiple cellular pathways.By determining the genetic profile and protein expression of mentioned MAP Kinase pathway molecules new targets can be identified for chemotherapic drugs and novel strategies will be charted out to make modifications in the map kinase pathway with the aim to stop the occurrence and distant metastasis of thyroid cancer.