Evidence map›Paper›PMID 39287419›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2024

Multiomics Profiling Distinguishes Sebaceous Carcinoma from Benign Sebaceous Neoplasms and Provides Insight into the Genetic Evolution of Sebaceous Carcinogenesis.

Gabriel J Starrett, Brittany C Baikie, Benjamin K Stoff, Hans E Grossniklaus, Inga Van Buren, Elizabeth G Berry, Roberto A Novoa, Kerri E Rieger, Kavita Y Sarin, Charles F Lynch and 10 more

Abstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

20 authors.

Gabriel J Starrett *Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.ORCID 0000-0001-5871-5306
Brittany C BaikieLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.ORCID 0000-0002-9844-1589
Benjamin K StoffDepartment of Dermatology, Emory University School of Medicine, Atlanta, Georgia.ORCID 0000-0003-4344-9767
Hans E GrossniklausDepartment of Ophthalmology, Emory University School of Medicine, Emory University, Atlanta, Georgia.ORCID 0000-0003-0178-9712
Inga Van BurenDignity Health St. Joseph's Medical Center, Stockton, California.ORCID 0009-0006-7635-5766
Elizabeth G BerryDepartment of Dermatology and Knight Cancer Institute, Oregon Health & Science University, Portland, Oregon.ORCID 0000-0002-7574-6718
Roberto A NovoaDepartment of Dermatology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0002-7955-0536
Kerri E RiegerDepartment of Dermatology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0002-4436-2471
Kavita Y SarinDepartment of Dermatology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0001-5363-3053
Charles F LynchIowa Cancer Registry, Department of Epidemiology, The University of Iowa, Iowa City, Iowa.ORCID 0000-0002-9542-6439
Michael C RoyerDivision of Dermatopathology, The Joint Pathology Center, Silver Spring, Maryland.ORCID 0009-0002-5063-0476
Mary L PiaskowskiLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.ORCID 0000-0001-8453-6416
Isaac BrownellDermatology Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland.ORCID 0000-0002-0090-9914
Emily Y ChuDepartment of Dermatology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.ORCID 0000-0001-5625-2782
Rama GodseDepartment of Internal Medicine, Pennsylvania Hospital, Philadelphia, Pennsylvania.ORCID 0000-0001-9717-3300
Suephy C ChenDuke Dermatology, Duke University School of Medicine, Durham, North Carolina.ORCID 0000-0002-0678-7380
Kelly J YuDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland.ORCID 0000-0003-3832-6586
Alisa M GoldsteinDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland.ORCID 0000-0002-7538-3582
Eric A EngelsDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland.ORCID 0000-0003-0203-6958
Michael R Sargen *Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland.ORCID 0000-0003-1039-2522

Funding

Viral VectorP30CA086862 · NCI · UNIVERSITY OF IOWA · PI Jon C.D. Houtman · 2000 to 2026
$70.0M
Center for Cancer Research (CCR)Division of Cancer Epidemiology and Genetics (DCEG)Intramural NIH HHS Z99 CA999999
6 · The paper itself

Abstract

purposeSebaceous carcinoma is the third most common nonkeratinocyte skin cancer in the United States with 1,000 cases per year. The clinicopathologic features of sebaceous carcinoma and benign sebaceous neoplasms (adenomas, sebaceomas) can overlap, highlighting the need for molecular biomarkers to improve classification. This study describes the genomic and transcriptomic landscape of sebaceous neoplasms in order to understand tumor etiology and biomarkers relevant for diagnosis and treatment. EXPERIMENTAL

designWe performed whole-genome sequencing (WGS) and whole-transcriptome sequencing (WTS) of sebaceous neoplasms from six academic and two federal healthcare facilities in the United States diagnosed between January 1, 1999, and December 31, 2021.

resultsWe evaluated 98 sebaceous neoplasms: 64 tumors (32 adenomas, 2 sebaceomas, 5 atypical sebaceous neoplasms, 25 carcinomas) had sufficient material for WGS, 96 tumors (42 adenomas, 11 sebaceomas, 8 atypical sebaceous neoplasms, 35 carcinomas) had sufficient material for WTS, and 62 tumors (31 adenomas, 2 sebaceomas, 5 atypical sebaceous neoplasms, 24 carcinomas) had sufficient material for combined WGS and WTS. Overall, we found decreased cholesterol biosynthesis and increased TP53 mutations, copy number gains (chromosome 6, 8q, and/or 18), and tumor mutation burden-high (>10 mutations/MB) in carcinomas compared to adenomas. Although diminished compared to adenomas, most carcinomas still had higher cholesterol biosynthesis than nonmalignant skin. Multiomics profiling also supported a precancerous model of tumor evolution with sebaceomas and atypical sebaceous neoplasms being likely intermediate lesions.

conclusionsThe study findings highlight key diagnostic biomarkers for sebaceous carcinoma and suggest that immunotherapy and modulation of cholesterol biosynthesis could be effective treatment strategies.

Indexed as

Sebaceous Gland NeoplasmsAdenocarcinoma, SebaceousAdenomaAdultAgedAged, 80 and overBiomarkers, TumorCarcinogenesisFemaleGene Expression ProfilingHumansMaleMiddle AgedMultiomicsMutationTranscriptomeBiomarkers, Tumor

Identifiers

PMID39287419
PMCPMC11530307

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Registered trials

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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.