Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1530/ERC-15-0307 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
MIG6 loss increased RET inhibitor tolerant persister cells in RET-rearranged non-small cell lung cancer.
Cancer Lett
November 2024
Division of Experimental Chemotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo, Japan; Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo, Japan. Electronic address:
Article Synopsis
- Recent RET tyrosine kinase inhibitors (TKIs) show promise for treating RET-rearranged non-small cell lung cancer (NSCLC) and RET-mutated thyroid cancer, but resistance limits their effectiveness over time.* -
- A CRISPR/Cas9 screening identified genes related to drug-tolerant persister cells, revealing that loss of MED12 or MIG6 increases these resistant cells and activates EGFR, leading to treatment failure.* -
- Combining EGFR inhibitors with RET TKIs proved effective in overcoming resistance, and further experiments indicated that targeting either EGFR or RET enhances sensitivity to treatments in resistant cancer models.*
Medullary Thyroid Cancer - Feature Review and Update on Systemic Treatment.
Acta Clin Croat
June 2020
1Department of Oncology and Nuclear Medicine, Sestre Milosrdnice University Hospital Centre, Zagreb, Croatia; 2University of Zagreb, School of Medicine; 3University of Zagreb, School of Dental Medicine.
Medullary thyroid carcinoma (MTC) is a rare malignancy that originates from parafollicular (C cells) of the thyroid and accounts for 2-4% of all thyroid malignancies. MTC may be sporadic or inherited, the latter as part of the MEN 2 syndromes. Germline mutations in the proto-oncogene (REarranged during Transfection) are driver mutations in hereditary MTC, whereas somatic mutations and, less frequently, mutations, have been described in tumor tissues of sporadic MTC.
View Article and Find Full Text PDFGIPC2 is an endocrine-specific tumor suppressor gene for both sporadic and hereditary tumors of RET- and SDHB-, but not VHL-associated clusters of pheochromocytoma/paraganglioma.
Cell Death Dis
May 2021
Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and School of Basic Medicine, Peking Union Medical College, Beijing, China.
Pheochromocytoma/paraganglioma (PPGL) is an endocrine tumor of the chromaffin cells in the adrenal medulla or the paraganglia. Currently, about 70% of PPGLs can be explained by germline or somatic mutations in several broadly expressed susceptibility genes including RET, VHL, and SDHB, while for the remaining, mainly sporadic cases, the pathogenesis is still unclear. Even for known susceptible genes, how mutations in these mostly ubiquitous genes result in tissue-specific pathogenesis remains unanswered, and why RET-mutated tumors almost always occur in the adrenal while SDHB-mutated tumors mostly occur extra-adrenal remains a mystery.
View Article and Find Full Text PDFOctreotide and pasireotide effects on medullary thyroid carcinoma (MTC) cells growth, migration and invasion.
Mol Cell Endocrinol
January 2021
Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy.
Medullary thyroid carcinoma (MTC) is a rare neuroendocrine neoplasm of the parafollicular thyroid C cells. Although somatostatin receptors are expressed by MTCs, treatment with octreotide has shown poor efficacy, whereas recently pasireotide has demonstrated antiproliferative effects in persistent postoperative MTCs. Aim of this study was to test the effects of octreotide and pasireotide on MTC cells proliferation, cell cycle proteins expression, MAPK activation, apoptosis, calcitonin secretion, migration and invasion in TT cell line as well as in primary MTC cultured cells.
View Article and Find Full Text PDFCD133 Expression in Medullary Thyroid Cancer Cells Identifies Patients with Poor Prognosis.
J Clin Endocrinol Metab
November 2020
Hereditary Endocrine Cancer Group, Madrid, Spain.
Article Synopsis
- Researchers investigated the role of the stem cell marker CD133 in medullary thyroid cancer (MTC) to identify high-risk patients and improve treatment outcomes.
- The study analyzed 74 MTC cases, finding that increased CD133 expression was linked to worse clinical outcomes and faster disease progression, especially in RET-mutated tumors.
- Additionally, a specific microRNA (hsa-miR-30a-5p) was identified as a regulator of CD133 expression, suggesting potential avenues for targeted therapies in aggressive MTC cases.*
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!