ReviewMolecular and cellular endocrinology2010
The PI3K-Akt-mTOR pathway in initiation and progression of thyroid tumors.
Review in Molecular and cellular endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.
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
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 184 citations in OpenAlex.
- miR-451a is underexpressed and targets AKT/mTOR pathway in papillary thyroid carcinoma.Oncotarget · 2016Pooled it
- Targeting the Warburg Effect in Anaplastic Thyroid Carcinoma: Metabolic Vulnerabilities and Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Glucose Metabolic Reprogramming in Thyroid Cancer: Underlying Molecular Mechanisms and Links to Progression and Treatment.Current medical science · 2026Review
- Somatic genomic profiling reveals clinically relevant heterogeneity inJournal of clinical & translational endocrinology · 2026Article
- Article
- Integrated bulk and single-cell transcriptomic profiling reveals NECTIN-TIGIT interaction underlies T cell exhaustion in papillary thyroid carcinoma.Clinical and experimental medicine · 2025Article
- Exploring the molecular mechanisms of comorbidity between thyroid cancer and breast cancer through multi-omics data.Scientific reports · 2025Article
- Association between depressive symptoms and thyroid nodule incidence in women: a prospective observational study.BMC public health · 2025Observational
- Atypical thyroid manifestation in Cowden disease: a case report and literature review.Frontiers in pediatrics · 2025Article
- YTHDC2 Retards Cell Proliferation and Triggers Apoptosis in Papillary Thyroid Cancer by Regulating CYLD-Mediated Inactivation of Akt Signaling.Applied biochemistry and biotechnology · 2024Article
- Mechanism of action of Taohong Siwu decoction in the alleviation of primary dysmenorrhea.Frontiers in medicine · 2024Article
- The Evolving Genomic Landscape of Pediatric Papillary Thyroid Cancer.Current opinion in endocrine and metabolic research · 2023Article
- The potential role of reprogrammed glucose metabolism: an emerging actionable codependent target in thyroid cancer.Journal of translational medicine · 2023Review
- Mechanistic Insights of Thyroid Cancer Progression.Endocrinology · 2023Review
- Multi-Omics and Management of Follicular Carcinoma of the Thyroid.Biomedicines · 2023Review
- Antitumor Activity of Berberine by Activating Autophagy and Apoptosis in CAL-62 and BHT-101 Anaplastic Thyroid Carcinoma Cell Lines.Drug design, development and therapy · 2023Article
- Metformin Decreases Serum Thyroglobulin Concentration in Nonmedullary Thyroid Carcinoma.Journal of the Endocrine Society · 2022Article
- Posttranslational Modifications in Thyroid Cancer: Implications for Pathogenesis, Diagnosis, Classification, and Treatment.Cancers · 2022Review
- Rab22a Promotes Epithelial-Mesenchymal Transition in Papillary Thyroid Carcinoma by Activating PI3K/AKT/mTOR Signaling Pathway.BioMed research international · 2022Article
- Fasting serum glucose and lymph node metastasis in non-diabetic PTC patients: a 10-Year multicenter retrospective study.Journal of Cancer · 2022Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The phosphoinositide-3 (OH) kinase (PI3K) signaling cascade is involved in regulating glucose uptake and metabolism, growth, motility, and other essential functions for cell survival. Unregulated activation of this pathway commonly occurs in cancer through a variety of mechanisms, including genetic mutations of kinases and regulatory proteins, epigenetic alterations that alter gene expression and translation, and posttranslational modifications. In thyroid cancer, constitutive activation of PI3K signaling has been shown to play a role in the genetic predisposition for thyroid neoplasia in Cowden's syndrome, and is recognized to be frequently overactivated in sporadic forms of thyroid cancer including those with aggressive clinical behaviors. In this review, the key signaling molecules in the PI3K signaling cascade, the abnormalities known to occur in thyroid cancer, and the potential for therapeutic targeting of PI3K pathway members will be discussed.
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.