Evidence map›Paper›PMID 24662765›Full record

ArticleThe Journal of investigative dermatology2014

DMBA/TPA treatment is necessary for BCC formation from patched deficient epidermal cells in Ptch(flox/flox)CD4Cre(+/-) mice.

Anja Uhmann, Ina Heß, Anke Frommhold, Simone König, Sebastian Zabel, Frauke Nitzki, Kai Dittmann, Fred Lühder, Hans Christiansen, Julia Reifenberger and 2 more

Abstract read
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In one paragraph

Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Spreading of IsolatedInternational journal of molecular sciences · 2020
    Article
  4. Article
  5. Article
  6. Cells of origin in skin cancer.The Journal of investigative dermatology · 2014
    Article
  7. Cells to surgery quiz: October 2014.The Journal of investigative dermatology · 2014
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Anja UhmannInstitute of Human Genetics, University of Göttingen, Göttingen, Germany. Electronic address: auhmann@gwdg.de.
Ina HeßInstitute of Human Genetics, University of Göttingen, Göttingen, Germany.
Anke FrommholdInstitute of Human Genetics, University of Göttingen, Göttingen, Germany.
Simone KönigInstitute of Human Genetics, University of Göttingen, Göttingen, Germany.
Sebastian ZabelInstitute of Human Genetics, University of Göttingen, Göttingen, Germany.
Frauke NitzkiInstitute of Human Genetics, University of Göttingen, Göttingen, Germany.
Kai DittmannDepartment of Cellular and Molecular Immunology, University of Göttingen, Göttingen, Germany.
Fred LühderInstitute for Multiple Sclerosis Research, University of Göttingen, Göttingen, Germany.
Hans ChristiansenDepartment of Radiation Therapy and Radiation Oncology, University of Göttingen, Göttingen, Germany.
Julia ReifenbergerDepartment of Neuropathology, University of Düsseldorf, Düsseldorf Germany.
Walter Schulz-SchaefferDepartment of Neuropathology, University of Göttingen, Göttingen, Germany.
Heidi HahnInstitute of Human Genetics, University of Göttingen, Göttingen, Germany.
University of Göttingen · DEHeinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of basal cell carcinoma (BCC), the most frequently diagnosed tumor among persons with European ancestry, is closely linked to mutations in the Hedgehog (Hh) receptor and tumor suppressor Patched1 (Ptch). Using Ptch(flox/flox)CD4Cre(+/-) mice, in which Ptch was ablated in CD4Cre-expressing cells, we demonstrate that the targeted cells can give rise to BCC after treatment with DMBA (7,12-dimethylbenz(a)anthracene)/TPA (12-O-tetradecanoylphorbol-13-acetate), but not after wounding of the skin. In addition, in this model, BCC are not caused by malfunctioning of Ptch-deficient T cells, as BCC did not develop when bone marrow (BM) of Ptch(flox/flox)CD4Cre(+/-) mice was transplanted into Ptch wild-type mice. Instead, lineage-tracing experiments and flow cytometric analyses suggest that the tumors are initiated from rare Ptch-deficient stem cell-like cells of the epidermis that express CD4. As DMBA/TPA is a prerequisite for BCC development in this model, the initiated cells need a second stimulus for expansion and tumor formation. However, in contrast to papilloma, this stimulus seems to be unrelated to alterations in the Ras signaling cascade. Together, these data suggest that biallelic loss of Ptch in CD4(+) cells does not suffice for BCC formation and that BCC formation requires a second so far unknown event, at least in the Ptch(flox/flox)CD4Cre(+/-) BCC mouse model.

Indexed as

9,10-Dimethyl-1,2-benzanthraceneAllelesAnimalsBasal Cell CarcinomaCarcinogenesisCarcinogensCD4-Positive T-LymphocytesDisease Models, AnimalEpidermisMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMutationPatched-1 ReceptorPatched Receptors9,10-Dimethyl-1,2-benzanthraceneCarcinogensHras protein, mousePatched-1 ReceptorPatched ReceptorsProto-Oncogene Proteins p21(ras)PTCH1 protein, humanPtch1 protein, mouseReceptors, Cell SurfaceTetradecanoylphorbol Acetate

Identifiers

PMID24662765
OpenAlexW2044103347

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.