Evidence map›Paper›PMID 11914470›Full record

ReviewEndocrine pathology2001

C-cell hyperplasia and medullary thyroid microcarcinoma.

J A Albores-Saavedra, J E Krueger

Abstract readReview
PubMed Publisher
In one paragraph

Review in Endocrine pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 14% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. Histopathology of C Cells and Medullary Thyroid Carcinoma.Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Hyperplasia in glands with hormone excess.Endocrine-related cancer · 2016
    Review
  8. Article
  9. Article
  10. Glucagon like peptide-1 receptor expression in the human thyroid gland.The Journal of clinical endocrinology and metabolism · 2012
    Article
  11. Absence of RET gene point mutations in sporadic thyroid C-cell hyperplasia.The Journal of molecular diagnostics : JMD · 2007
    Article
  12. Review
  13. Article
  14. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

J A Albores-SaavedraDepartment of Pathology, UT Southwestern Medical Center, 5323 Harry Hines Blvd. Dallas, TX 75390-9073, USA.
J E Krueger
Southwestern Medical CenterThe University of Texas Southwestern Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since the discovery of the thyroid C-cell, considerable progress has been made regarding its origin, function, and pathology. In this article an attempt is made to summarize and update our knowledge about physiologic or reactive C-cell hyperplasia, neoplastic C-cell hyperplasia (medullary carcinoma in situ), and medullary microcarcinoma. Seldom recognized preoperatively, physiologic C-cell hyperplasia is associated with inflammatory, metabolic, and neoplastic thyroid disorders as well as with hypercalcemia. However, the pathogenesis is still unclear. Although physiologic C-cell hyperplasia may progress to medullary carcinoma, the full malignant potential is unknown. Problems related to the definition of physiologic C-cell hyperplasia are discussed. Immunohistochemistry and quantitative analysis are required for the diagnosis. By contrast, C-cell hyperplasia associated with MEN II syndromes or familial medullary carcinoma can be diagnosed preoperatively in asymptomatic children or adolescents by the detection of germline mutations of the RET protooncogene. Morphologic and genetic abnormalities support the idea that C-cells in the familial form of C-cell hyperplasia are neoplastic and can be recognized with conventional stains. Therefore, the number of C-cells is irrelevant for the diagnosis. Medullary microcarcinoma is a neoplasm that measures < 1 cm. The sporadic variant is usually an incidental microscopic finding, whereas the familial form can be diagnosed by genetic testing. Its morphologic features and biologic behavior differ from those of larger medullary carcinomas. The frequency of medullary microcarcinoma will probably increase with the use of genetic testing.

Indexed as

AdolescentBiomarkers, TumorCarcinoma in SituCarcinoma, MedullaryChildChild, PreschoolHumansHyperplasiaImmunohistochemistryMultiple Endocrine Neoplasia Type 2aThyroid GlandThyroid NeoplasmsBiomarkers, Tumor

Identifiers

PMID11914470
OpenAlexW2022341261

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.