Evidence map›Paper›PMID 11423973›Full record

ArticleOncogene2001

Altered gene expression in immunogenic poorly differentiated thyroid carcinomas from RET/PTC3p53-/- mice.

D J Powell, J P Russell, G Li, B A Kuo, V Fidanza, K Huebner, J L Rothstein

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  3. Article
  4. Review
  5. Article
  6. Mouse models of thyroid cancer: A 2015 update.Molecular and cellular endocrinology · 2016
    Review
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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

7 authors at 1 institution in 1 country.

D J PowellDepartment of Microbiology/Immunology and Otolaryngology-Head & Neck Surgery, Kimmel Cancer Institute, Thomas Jefferson University, Philadelphia, Pennsylvania, PA 19107, USA.
J P Russell
G Li
B A Kuo
V Fidanza
K Huebner
J L Rothstein
Thomas Jefferson University · US

Funding

Structural Analysis of TCL-1 and MTCP-1 ProteinsP01CA076259 · NCI · THOMAS JEFFERSON UNIVERSITY · PI CROCE, CARLO M · 1999 to 2003
$6.1M
TRAINING PROGRAMS IN MOLECULAR GENETICS OF CANCERT32CA009678 · NCI · THOMAS JEFFERSON UNIVERSITY · PI BUCHBERG, ARTHUR M. · 1992 to 2008
$2.3M
TRAINING PROGRAM IN DEVELOPMENTAL IMMUNOLOGYT32AI007492 · NIAID · THOMAS JEFFERSON UNIVERSITY · PI MANSER, TIMOTHY L · 1996 to 2005
$1.3M
TRAINING PROGRAM IN CANCER PHARMACOLOGYT32CA072318 · NCI · THOMAS JEFFERSON UNIVERSITY · PI FISHEL, RICHARD · 1997 to 2001
$442k
VIROLOGY AND GENETICS OF CANCERP01CA021124 · NCI · WISTAR INSTITUTE · PI KOPROWSKI, HILARY · 1985 to 1999
–
NCI NIH HHS CA21124NCI NIH HHS CA76259NCI NIH HHS T32-CA09678NCI NIH HHS T32-CA72318NIAID NIH HHS T32-AI07492
6 · The paper itself

Abstract

Cancers develop and progress via activation of oncogenes and loss of tumor suppressor genes, a progression that can be recapitulated through cross breeding mouse strains harboring genetic mutations. To define the role of RET/PTC3, p53 and Fhit in thyroid carcinogenesis, we intercrossed RET/PTC3 transgenics with p53-/- mice. This new strain, RET/PTC3p53-/-, succumb to rapidly growing and strikingly large multilobed thyroid tumors containing mixtures of both well and poorly differentiated, highly proliferative follicular epithelial cells. Interestingly, transplanted tumors from RET/PTC3p53-/- mice grew in SCID but not syngeneic immunocompetent mice indicating that these advanced tumors were immunogenic. RET/PTC3 protein expression was reduced to undetectable levels in tumors of older mice suggesting that the continued elevated expression of RET/PTC3 may not be necessary for tumor progression. Similarly, expression of Fhit protein was reduced in early tumors and undetected in older tumors irrespective of tumor histopathology. In contrast to RET/PTC3p53-/- mice, RET/PTC3Fhit-/- mice did not develop advanced thyroid carcinomas. These studies support a model of human thyroid cancer whereby thyroid epithelium expresses RET/PTC3 protein at early stages of tumor development, followed by the reduction of RET/PTC3 and loss of p53 function with progressive reduction of Fhit protein expression coincident with malignant progression.

Indexed as

Acid Anhydride HydrolasesDrosophila ProteinsNeoplasm ProteinsOncogenesSaccharomyces cerevisiae ProteinsAnimalsAntigens, DifferentiationBis(5'-adenosyl)triphosphataseCarcinomaCell Transformation, NeoplasticMiceMice, SCIDMice, TransgenicModels, BiologicalNeoplasms, ExperimentalPhosphoprotein PhosphatasesAcid Anhydride HydrolasesAntigens, DifferentiationBis(5'-adenosyl)triphosphataseDrosophila ProteinsNeoplasm ProteinsPhosphoprotein PhosphatasesProtein Phosphatase 2Protein Phosphatase 2CProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-retPTC1 protein, S cerevisiaePTC3 protein, S cerevisiaeReceptor Protein-Tyrosine KinasesRet protein, DrosophilaRet protein, mouseSaccharomyces cerevisiae ProteinsTumor Suppressor Protein p53

Identifiers

PMID11423973
OpenAlexW2095947138

What OpenQuestion holds

Textmetadata
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.