Evidence map›Paper›PMID 35655404›Full record

ArticleGenes, chromosomes & cancer2022

Inflammatory leiomyosarcoma/rhabdomyoblastic tumor: A report of two cases with novel genetic findings.

Madina Sukhanova, Farres Obeidin, Lukas Streich, Borislav A Alexiev

Open access · hybridAbstract readCase Reports
In one paragraph

Article in Genes, chromosomes & cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Rhabdomyosarcoma in children and young adults.Virchows Archiv : an international journal of pathology · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. 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

4 authors at 1 institution in 1 country.

Madina SukhanovaDepartment of Pathology, Northwestern University Feinberg School of Medicine, Northwestern Memorial Hospital, Chicago, Illinois, USA.ORCID 0000-0002-1843-7038
Farres ObeidinDepartment of Pathology, Northwestern University Feinberg School of Medicine, Northwestern Memorial Hospital, Chicago, Illinois, USA.ORCID 0000-0001-8461-9238
Lukas StreichDepartment of Pathology, Northwestern University Feinberg School of Medicine, Northwestern Memorial Hospital, Chicago, Illinois, USA.
Borislav A AlexievDepartment of Pathology, Northwestern University Feinberg School of Medicine, Northwestern Memorial Hospital, Chicago, Illinois, USA.ORCID 0000-0002-0262-2263
Northwestern University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory leiomyosarcoma (ILMS) is a malignant neoplasm showing smooth muscle differentiation, a prominent inflammatory infiltrate, and near-haploidization. These tumors have significant pathologic and genetic overlap with the recently described "inflammatory rhabdomyoblastic tumor (IRT)," suggesting that ILMS and IRT may belong to one entity. Herein, we describe two cases of ILMS/IRT with attention to new cytogenetic and sequencing findings. The tumors were composed of sheets and fascicles of variably pleomorphic tumor cells showing spindled and epithelioid to rhabdoid morphology and a prominent histiocyte-rich inflammatory infiltrate typical of ILMS/IRT. In case 1, chromosomal microarray analysis showed a near-haploid pattern with loss of heterozygosity resulting from loss of one copy of all autosomes except for chromosomes 5, 20, 21, and 22. Case 2 showed areas with high-grade rhabdomyosarcomatous transformation. In this case, the low-grade tumor component revealed a hyper-diploid pattern with loss of heterozygosity for most of autosomes but with a normal diploid copy number state except for chromosomes 5, 20, and 22, which showed a relative gain. The high-grade tumor component showed a similar pattern of copy-neutral loss of heterozygosity with additional abnormalities, including mosaic segmental gains at 1p, 5p, 8q, 9p, 20q, and segmental loss at 8p. Next-generation sequencing identified sequence variants in NF1, TP53, SMARCA4, KRAS, and MSH6. MSH6 variant was confirmed as germline, consistent with the diagnosis of hereditary nonpolyposis colorectal cancer (HNPCC) syndrome in one of our study patients and suggestive that ILMS/IRT might be part of the HNPCC cancer spectrum.

Indexed as

Colorectal Neoplasms, Hereditary NonpolyposisLeiomyosarcomaChromosome AberrationsDNA-Binding ProteinsDNA HelicasesHeterozygoteHumansNuclear ProteinsTranscription FactorsDNA-Binding ProteinsDNA HelicasesNuclear ProteinsSMARCA4 protein, humanTranscription Factorsdriver mutationsinflammatory leiomyosarcoma/rhabdomyoblastic tumorinflammatory rhabdomyoblastic tumor

Identifiers

PMID35655404
PMCPMC9545443
OpenAlexW4281636486

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.