ReviewInternational journal of molecular sciences2017
New Insights in Thyroid Cancer and p53 Family Proteins.
Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
57 citing papers in PubMed, 97 citations in OpenAlex.
- Trial
- Pathogenesis of Thyroid Cancer with Particular Emphasis on the Role of AnoikisJournal of clinical research in pediatric endocrinology · 2026Review
- CHI3L1 Is Associated With TP53 Signaling and Promotes Papillary Thyroid Carcinoma Progression.Cancer reports (Hoboken, N.J.) · 2026Article
- Cancer Stemness and Dedifferentiation in Anaplastic Thyroid Carcinoma: Insights into a Multigenic, Microenvironmental Network and the Role of CD44.Biomedicines · 2026Review
- Retroelements in thyroid cancer: epigenetic plasticity, dedifferentiation, and therapeutic opportunities.Reviews in endocrine & metabolic disorders · 2026Review
- The CHK1 inhibitor Prexasertib is effective againstFrontiers in endocrinology · 2026Article
- Molecular Diagnostics and Personalized Therapeutics in Differentiated Thyroid Carcinoma: A Clinically Oriented Review.Diagnostics (Basel, Switzerland) · 2025Review
- FTO-mediated the destabilization of RASGRF1 mRNA impedes thyroid cancer progression and suppresses macrophage M2 polarization.Cell biology and toxicology · 2025Article
- miR-7-5p and Importin-7 Regulate the p53 Dynamics and Stability in Malignant and Benign Thyroid Cells.International journal of molecular sciences · 2025Article
- PCSK9 promotes progression of anaplastic thyroid cancer through E-cadherin endocytosis.Cell death & disease · 2025Article
- TP53 gene mutation in lymphoepithelioma‑like carcinoma of the breast with thyroid cancer: A case report.Oncology letters · 2025Article
- Mutational Landmarks in Anaplastic Thyroid Cancer: A Perspective of a New Treatment Strategy.Journal of clinical medicine · 2025Review
- Integrated computational analysis of molecular mechanisms underlying perfluorooctane sulfonic acid induced thyroid toxicity.Scientific reports · 2025Article
- The intratumor microbiota and thyroid cancer: a review.Frontiers in endocrinology · 2025Review
- New Horizons of Biomarkers in Metastatic Thyroid Cancer.Journal of Cancer · 2025Review
- FOXE1 Gene is a Probable Tumor Suppressor Gene with Decreased Expression as Papillary Thyroid Cancers Grow, and is Absent in Anaplastic Thyroid Cancers.Biochemical genetics · 2024Article
- Article
- Comprehensive bioinformatics analysis unveils THEMIS2 as a carcinogenic indicator related to immune infiltration and prognosis of thyroid cancer.Scientific reports · 2024Article
- Systemic treatments for radioiodine-refractory thyroid cancers.Frontiers in endocrinology · 2024Review
- Molecular signature incorporating the immune microenvironment enhances thyroid cancer outcome prediction.Cell genomics · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thyroid cancers are common endocrine malignancies that comprise tumors with different clinical and histological features. Indeed, papillary and follicular thyroid cancers are slow-growing, well-differentiated tumors, whereas anaplastic thyroid cancers are undifferentiated neoplasias that behave much more aggressively. Well-differentiated thyroid carcinomas are efficiently cured by surgery and radioiodine, unlike undifferentiated tumors that fail to uptake radioactive iodine and are usually resistant to chemotherapy. Therefore, novel and more effective therapies for these aggressive neoplasias are urgently needed. Whereas most genetic events underlying the pathogenesis of well-differentiated thyroid cancers have been identified, the molecular mechanisms that generate undifferentiated thyroid carcinomas are still unclear. To date, one of the best-characterized genetic alterations leading to the development of poorly differentiated thyroid tumors is the loss of the p53 tumor suppressor gene. In addition, the existence of a complex network among p53 family members (p63 and p73) and their interactions with other factors that promote thyroid cancer progression has been well documented. In this review, we provide an update on the current knowledge of the role of p53 family proteins in thyroid cancer and their possible use as a therapeutic target for the treatment of the most aggressive variants of this disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.