Pathology and genetics of thyroid carcinoma
Abstract
Carcinomas of the thyroid comprise a heterogeneous group of neoplasms with distinctive clinical and pathological characteristics. Over the past 15 years, the application of molecular technologies to the study of these neoplasms has elucidated critical genetic pathways associated with the development of specific thyroid tumor types. In papillary thyroid carcinoma (PTC), genetic events involve RET and TRK (rearrangements) and BRAF and RAS (mutations), although RAS mutations are uncommon except in the follicular variant of PTC. These genetic alterations, which rarely overlap in the same tumor, result in signaling abnormalities in the mitogen‐activated protein kinase pathway. In contrast, genetic alterations in follicular carcinomas include PAX8‐PPARγ translocations and RAS mutations while mutations of CTNNB1 and p53 have been implicated in the development and progression of poorly differentiated and undifferentiated (anaplastic) thyroid carcinomas. Germline mutations of RET are responsible for the development of heritable forms of medullary thyroid carcinoma (MTC) while somatic mutations of this oncogene are found in a significant proportion of sporadic MTCs. The results of these studies not only have provided additional approaches to thyroid tumor classification, but also have stimulated the development of novel approaches to tumor diagnosis and additional parameters for prognostic assessment and potential biologic therapeutic strategies. J. Surg. Oncol. 2006;94:662–669. © 2006 Wiley‐Liss, Inc.
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Less than 10% of papillary thyroid carcinomas harbor p53 mutations.
“To date, less than 10% of papillary thyroid carcinomas harbor p53 mutations [27].”
From Restoration of p53 using the novel MDM2-p53 antagonist APG115 suppresses dedifferentiated papillary thyroid cancer cells (2017) · cites this paper as [27]
p53 mutations in localized PTC are infrequent.
“In addition, p53 mutations in localized PTC are infrequent [27].”
From Restoration of p53 using the novel MDM2-p53 antagonist APG115 suppresses dedifferentiated papillary thyroid cancer cells (2017) · cites this paper as [27]
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- Authors
- DeLellis, R. A.
- Affiliations
- Brown University (US)
- Corresponding author
- DeLellis, Ronald A.
- ORCID
- DeLellis, Ronald A.
- Venue
- Journal of Surgical Oncology
- Publisher
- Wiley
- Published
- 2006-11-27
- Volume
- 94
- Issue
- 8
- Pages
- 662-669
- ISSN
- 0022-4790 (ISSN-L)
- 1096-9098
- OpenAlex
- W1508880004
- Cited by
- 181
- References
- 76
- Citations by year
- 2025: 1 · 2024: 3 · 2023: 2 · 2022: 1 · 2021: 8 · 2020: 11 · 2019: 9 · 2018: 7 · 2017: 10 · 2016: 10 · 2015: 13 · 2014: 7 · 2013: 13 · 2012: 20
- FWCI
- 8.99
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Surgical Oncology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Cancer Diagnosis and Treatment
- Health Sciences › Medicine › Surgery › Thyroid and Parathyroid Surgery
- Health Sciences › Medicine › Surgery › Head and Neck Anomalies
- Keywords
- thyroid cancer, papillary thyroid carcinoma, follicular thyroid carcinoma, medullary thyroid carcinoma, RET fusion, BRAF mutation, RAS mutations, CTNNB1 mutation, TP53 mutation, anaplastic thyroid carcinoma, familial medullary thyroid carcinoma, RET germline mutation, MAPK signaling, prognostic assessment, molecular diagnosis
- MeSH terms
- Adenocarcinoma, Papillary, Carcinoma, Humans, Molecular Biology, Mutation, Multiple Endocrine Neoplasia, Genes, ras, Thyroid Neoplasms, Point Mutation, Adenoma, Oxyphilic, Adenocarcinoma, Follicular, Receptor, trkA, Proto-Oncogene Proteins B-raf, PTEN Phosphohydrolase, Proto-Oncogene Proteins c-ret
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