Evidence map›Paper›PMID 36185232›Full record

ArticleFrontiers in oncology2022

Case report: Common clonal origin of concurrent langerhans cell histiocytosis and acute myeloid leukemia.

Shintaro Kazama, Kazuaki Yokoyama, Toshimitsu Ueki, Hiroko Kazumoto, Hidetoshi Satomi, Masahiko Sumi, Ichiro Ito, Nozomi Yusa, Rika Kasajima, Eigo Shimizu and 8 more

Abstract readCase Reports
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Langerhans cell sarcoma and myeloproliferative neoplasms: close or distant relatives?Virchows Archiv : an international journal of pathology · 2025
    Article
  4. Review
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

18 authors.

Shintaro KazamaDepartment of Hematology, Nagano Red Cross Hospital, Nagano, Japan.
Kazuaki YokoyamaDivision of Molecular Therapy, Institute of Medical Science, Advanced Clinical Research Center, The University of Tokyo, Tokyo, Japan.
Toshimitsu UekiDepartment of Hematology, Nagano Red Cross Hospital, Nagano, Japan.
Hiroko KazumotoDepartment of Hematology, Nagano Red Cross Hospital, Nagano, Japan.
Hidetoshi SatomiDepartment of Diagnostic Pathology and Cytology, Osaka International Cancer Institute, Osaka, Japan.
Masahiko SumiDepartment of Hematology, Nagano Red Cross Hospital, Nagano, Japan.
Ichiro ItoDepartment of Pathology, Nagano Red Cross Hospital, Nagano, Japan.
Nozomi YusaDepartment of Applied Genomics, Research Hospital, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Rika KasajimaMolecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, Yokohama, Japan.
Eigo ShimizuDivision of Health Medical Data Science, Health Intelligence Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Rui YamaguchiDivision of Cancer Systems Biology, Aichi Cancer Center Research Institute, Nagoya, Japan.
Seiya ImotoDivision of Health Medical Data Science, Health Intelligence Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Satoru MiyanoDepartment of Integrated Data Science, Medical and Dental Data Science Center, Tokyo Medical and Dental University, Tokyo, Japan.
Yukihisa TanakaDepartment of Diagnostic Pathology, IMSUT Hospital, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Tamami DendaDepartment of Diagnostic Pathology, IMSUT Hospital, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yasunori OtaDepartment of Diagnostic Pathology, IMSUT Hospital, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Arinobu TojoDepartment of Data Science and Faculty Affairs, Tokyo Medical and Dental University, Tokyo, Japan.
Hikaru KobayashiDepartment of Hematology, Nagano Red Cross Hospital, Nagano, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Langerhans cell histiocytosis (LCH) and acute myeloid leukemia (AML) are distinct entities of blood neoplasms, and the exact developmental origin of both neoplasms are considered be heterogenous among patients. However, reports of concurrent LCH and AML are rare. Herein we report a novel case of concurrent LCH and AML which shared same the driver mutations, strongly suggesting a common clonal origin.An 84-year-old female presented with cervical lymphadenopathy and pruritic skin rash on the face and scalp. Laboratory tests revealed pancytopenia with 13% of blasts, elevated LDH and liver enzymes, in addition to generalised lymphadenopathy and splenomegaly by computed tomography. Bone marrow specimens showed massive infiltration of MPO-positive myeloblasts, whereas S-100 and CD1a positive atypical dendritic cell-like cells accounted for 10% of the atypical cells on bone marrow pathology, suggesting a mixture of LCH and AML. A biopsy specimen from a cervical lymph node and the skin demonstrated the accumulation of atypical cells which were positive for S-100 and CD1a. LCH was found in lymph nodes, skin and bone marrow; AML was found in peripheral blood and bone marrow (AML was predominant compared with LCH in the bone marrow). Next generation sequencing revealed four somatic driver mutations (

Indexed as

acute myeloid leukemiaBRAF V600Edendritic cellshistiocytic disordersinflammatory myeloid neoplasmlangerhans cell histiocytosisMAPK pathwayNRAS

Identifiers

PMID36185232
PMCPMC9523168

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