Evidence map›Paper›PMID 25430560›Full record

ReviewBritish journal of haematology2015

Progress in understanding the pathogenesis of Langerhans cell histiocytosis: back to Histiocytosis X?

Marie-Luise Berres, Miriam Merad, Carl E Allen

Open access · greenAbstract readReview
In one paragraph

Review in British journal of haematology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 178 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Orbital histiocytosis; From A to Z.International ophthalmology · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Cholesteatoma Masquerading as Recurrent Langerhans Cell Histiocytosis.The journal of international advanced otology · 2023
    Article
  18. Article
  19. Article
  20. [Red-brown, erosive papules in an infant].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2022
    Article

7 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 2 countries.

Marie-Luise BerresDepartment of Oncological Sciences, Mount Sinai School of Medicine, New York, NY, USA; Tisch Cancer Institute, Mount Sinai School of Medicine, New York, NY, USA; Immunology Institute, Mount Sinai School of Medicine, New York, NY, USA; Department of Internal Medicine III, University Hospital, RWTH Aachen, Aachen, Germany.
Miriam Merad
Carl E Allen
Icahn School of Medicine at Mount Sinai · USChildren's Cancer Center · US

Funding

ERK control of Dendritic Cell Differentiation, Homeostasis and DiseaseR01CA154947 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CARL E ALLEN, MIRIAM MERAD · 2011 to 2026
$7.0M
Redefining Langerhans Cell Histiocytosis as a Myeloid Dysplasia and Identifying BR01CA154489 · NCI · BAYLOR COLLEGE OF MEDICINE · PI ALLEN, CARL E · 2011 to 2015
$1.6M
NCI NIH HHS CA154489NCI NIH HHS CA154947ANCI NIH HHS R01 CA154489NCI NIH HHS R01 CA154947
6 · The paper itself

Abstract

Langerhans cell histiocytosis (LCH), the most common histiocytic disorder, is characterized by the accumulation of CD1A(+) /CD207(+) mononuclear phagocytes within granulomatous lesions that can affect nearly all organ systems. Historically, LCH has been presumed to arise from transformed or pathologically activated epidermal dendritic cells called Langerhans cells. However, new evidence supports a model in which LCH occurs as a consequence of a misguided differentiation programme of myeloid dendritic cell precursors. Genetic, molecular and functional data implicate activation of the ERK signalling pathway at critical stages in myeloid differentiation as an essential and universal driver of LCH pathology. Based on these findings, we propose that LCH should be re-defined as an inflammatory myeloid neoplasia. Increased understanding of LCH pathogenesis will provide opportunities to optimize and personalize therapy through improved risk-stratification, targeted therapy and assessment of therapy response based on specific molecular features and origin of the pathological myeloid cells.

Indexed as

Cell DifferentiationHistiocytosis, Langerhans-CellLangerhans CellsModels, BiologicalMyeloid CellsNeoplasmsAntigens, CDAntigens, CD1HumansLectins, C-TypeMannose-Binding LectinsMAP Kinase Signaling SystemAntigens, CDAntigens, CD1CD1a antigenCD207 protein, humanLectins, C-TypeMannose-Binding LectinsBRAF V600Eextracellular signal-regulated kinase signalling pathwayinflammatory myeloid neoplasiaLangerhans cell histiocytosismisguided myeloid differentiation

Identifiers

PMID25430560
PMCPMC5193221
OpenAlexW2083168581

What OpenQuestion holds

Textmetadata
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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.