ReviewRecent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer2015
Thyroid C-Cell Biology and Oncogenic Transformation.
Review in Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 60 citations in OpenAlex.
- Homeobox genes in endocrine tumorigenesis: mechanisms, tumor microenvironment interaction, and therapeutic potential.Medical oncology (Northwood, London, England) · 2026Review
- Glucagon-like peptide-1 receptor (GLP-1R) overexpression defines a distinct immunogenetic subset in primary and metastatic thyroid cancer: implications for GLP-1R agonist therapy.Frontiers in oncology · 2026Article
- Single-cell analysis reveals the cellular and transcriptional heterogeneity of the normal pediatric thyroid.Frontiers in endocrinology · 2026Article
- Proteomic Profiling of Medullary Thyroid Cancer Identifies CAPN1 as a Key Regulator of NF1 and RET Fueled Growth.Thyroid : official journal of the American Thyroid Association · 2025Article
- Gender and tumor size-specific calcitonin cutoff value for diagnosing MTC in 10,618 patients with thyroid nodule surgery.Endocrine · 2024Article
- Pregnancy influences expression of interferon-stimulated genes, progesterone receptor and progesterone-induced blocking factor in ovine thyroid.Animal bioscience · 2024Article
- The Role of Lipid Metabolism Disorders in the Development of Thyroid Cancer.International journal of molecular sciences · 2024Review
- Non-Apoptotic Programmed Cell Death in Thyroid Diseases.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Review
- The Role of Altered Mitochondrial Metabolism in Thyroid Cancer Development and Mitochondria-Targeted Thyroid Cancer Treatment.International journal of molecular sciences · 2021Review
- Development of Functional Thyroid C Cell-like Cells from Human Pluripotent Cells in 2D and in 3D Scaffolds.Cells · 2021Article
- ONC201 Shows Potent Anticancer Activity Against Medullary Thyroid Cancer via Transcriptional Inhibition ofMolecular cancer therapeutics · 2021Article
- Frequent Subgraph Mining of Functional Interaction Patterns Across Multiple Cancers.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2021Article
- Article
- A phenome-wide association study of 26 mendelian genes reveals phenotypic expressivity of common and rare variants within the general population.PLoS genetics · 2020Article
- Establishment of cumulative assessment groups of pesticides for their effects on the thyroid.EFSA journal. European Food Safety Authority · 2019Article
- Regulation of GDNF expression in Sertoli cells.Reproduction (Cambridge, England) · 2019Review
- Article
- Deconvolution of expression microarray data reveals 131I-induced responses otherwise undetected in thyroid tissue.PloS one · 2018Article
- Reduced Retinoblastoma Protein Expression Is Associated with Decreased Patient Survival in Medullary Thyroid Cancer.Thyroid : official journal of the American Thyroid Association · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The thyroid parafollicular cell, or commonly named "C-cell," functions in serum calcium homeostasis. Elevations in serum calcium trigger release of calcitonin from the C-cell, which in turn functions to inhibit absorption of calcium by the intestine, resorption of bone by the osteoclast, and reabsorption of calcium by renal tubular cells. Oncogenic transformation of the thyroid C-cell is thought to progress through a hyperplastic process prior to malignancy with increasing levels of serum calcitonin serving as a biomarker for tumor burden. The discovery that multiple endocrine neoplasia type 2 is caused by activating mutations of the RET gene serves to highlight the RET-RAS-MAPK signaling pathway in both initiation and progression of medullary thyroid carcinoma (MTC). Thyroid C-cells are known to express RET at high levels relative to most cell types; therefore, aberrant activation of this receptor is targeted primarily to the C-cell, providing one possible cause of tissue-specific oncogenesis. The role of RET signaling in normal C-cell function is unknown though calcitonin gene transcription appears to be sensitive to RET activation. Beyond RET, the modeling of oncogenesis in animals and screening of human tumors for candidate gene mutations have uncovered mutation of RAS family members and inactivation of Rb1 regulatory pathway as potential mediators of C-cell transformation. A growing understanding of how RET interacts with these pathways, both in normal C-cell function and during oncogenic transformation, will help in the development of novel molecular-targeted therapies.
Indexed as
Identifiers
What OpenQuestion holds
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.