Mutational analysis differentiating sporadic carcinomas from colitis-associated colorectal carcinomas.


Journal

Cell communication and signaling : CCS
ISSN: 1478-811X
Titre abrégé: Cell Commun Signal
Pays: England
ID NLM: 101170464

Informations de publication

Date de publication:
10 Oct 2024
Historique:
received: 28 06 2024
accepted: 27 09 2024
medline: 11 10 2024
pubmed: 11 10 2024
entrez: 10 10 2024
Statut: epublish

Résumé

Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) that is associated with increased risk of developing colitis-associated carcinoma (CAC). The genetic profile of CACs is fairly similar to the sporadic colorectal carcinomas (sCRCs), although showing certain differences in the timing and sequence of alterations that contribute to carcinogenesis. Also, both cancer types typically show a strong histological resemblance, which complicates the pathologists' diagnosis. Due to the different clinical consequences, it is of utmost importance to categorize the corresponding cancer type correctly. In this study, we determined the mutation profiles of 64 CACs and sCRCs in the hotspot regions of 50 cancer-associated genes and compared them to 29 controls to identify genetic gene variants that can facilitate the pathologists' diagnosis. Pearson Chi-Square or Fisher's exact tests were used for statistical analyses. We found that sCRCs tend to mutate more frequently in APC and PIK3CA genes than CACs and that mainly males were affected. Our CAC cohort identified the KRAS G12D mutation as group-specific variant that was not detected in the sCRCs. When separating conventional from non-conventional CACs, it was discovered that the conventional type shows significantly more mutations for ATM. Taken together, our data highlights genetic differences between sCRC and CAC and enables the possibility to utilize specific gene alterations to support the pathologist's diagnosis.

Sections du résumé

BACKGROUND BACKGROUND
Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) that is associated with increased risk of developing colitis-associated carcinoma (CAC). The genetic profile of CACs is fairly similar to the sporadic colorectal carcinomas (sCRCs), although showing certain differences in the timing and sequence of alterations that contribute to carcinogenesis. Also, both cancer types typically show a strong histological resemblance, which complicates the pathologists' diagnosis. Due to the different clinical consequences, it is of utmost importance to categorize the corresponding cancer type correctly.
METHODS METHODS
In this study, we determined the mutation profiles of 64 CACs and sCRCs in the hotspot regions of 50 cancer-associated genes and compared them to 29 controls to identify genetic gene variants that can facilitate the pathologists' diagnosis. Pearson Chi-Square or Fisher's exact tests were used for statistical analyses.
RESULTS RESULTS
We found that sCRCs tend to mutate more frequently in APC and PIK3CA genes than CACs and that mainly males were affected. Our CAC cohort identified the KRAS G12D mutation as group-specific variant that was not detected in the sCRCs. When separating conventional from non-conventional CACs, it was discovered that the conventional type shows significantly more mutations for ATM.
CONCLUSIONS CONCLUSIONS
Taken together, our data highlights genetic differences between sCRC and CAC and enables the possibility to utilize specific gene alterations to support the pathologist's diagnosis.

Identifiants

pubmed: 39390564
doi: 10.1186/s12964-024-01856-8
pii: 10.1186/s12964-024-01856-8
doi:

Substances chimiques

Class I Phosphatidylinositol 3-Kinases EC 2.7.1.137
PIK3CA protein, human EC 2.7.1.137
Adenomatous Polyposis Coli Protein 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

483

Informations de copyright

© 2024. The Author(s).

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Auteurs

Theresa Dregelies (T)

Institut für Pathologie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Klinikum Bayreuth, Preuschwitzer Str. 101, 95445, Bayreuth, Germany.
Lehrstuhl für Mikrobiologie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Staudtstr. 5, 91058, Erlangen, Germany.

Franziska Haumaier (F)

Institut für Pathologie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Klinikum Bayreuth, Preuschwitzer Str. 101, 95445, Bayreuth, Germany.

William Sterlacci (W)

Institut für Pathologie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Klinikum Bayreuth, Preuschwitzer Str. 101, 95445, Bayreuth, Germany.

Steffen Backert (S)

Lehrstuhl für Mikrobiologie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Staudtstr. 5, 91058, Erlangen, Germany.

Michael Vieth (M)

Institut für Pathologie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Klinikum Bayreuth, Preuschwitzer Str. 101, 95445, Bayreuth, Germany. michael.vieth@fau.de.
Bavarian Cancer Research Center (BZKF), Erlangen, Germany. michael.vieth@fau.de.

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