Genomic landscape of hepatocellular carcinoma in Egyptian patients by whole exome sequencing.

Hepatocelleular carcinoma (HCC) Living Donor Liver Transplantation (LDLT) Mutational signature Whole exome sequencing

Journal

BMC medical genomics
ISSN: 1755-8794
Titre abrégé: BMC Med Genomics
Pays: England
ID NLM: 101319628

Informations de publication

Date de publication:
09 Aug 2024
Historique:
received: 02 02 2024
accepted: 17 07 2024
medline: 10 8 2024
pubmed: 10 8 2024
entrez: 9 8 2024
Statut: epublish

Résumé

Hepatocellular carcinoma (HCC) is the most common primary liver cancer. Chronic hepatitis and liver cirrhosis lead to accumulation of genetic alterations driving HCC pathogenesis. This study is designed to explore genomic landscape of HCC in Egyptian patients by whole exome sequencing. Whole exome sequencing using Ion Torrent was done on 13 HCC patients, who underwent surgical intervention (7 patients underwent living donor liver transplantation (LDLT) and 6 patients had surgical resection}. Mutational signature was mostly S1, S5, S6, and S12 in HCC. Analysis of highly mutated genes in both HCC and Non-HCC revealed the presence of highly mutated genes in HCC (AHNAK2, MUC6, MUC16, TTN, ZNF17, FLG, MUC12, OBSCN, PDE4DIP, MUC5b, and HYDIN). Among the 26 significantly mutated HCC genes-identified across 10 genome sequencing studies-in addition to TCGA, APOB and RP1L1 showed the highest number of mutations in both HCC and Non-HCC tissues. Tier 1, Tier 2 variants in TCGA SMGs in HCC and Non-HCC (TP53, PIK3CA, CDKN2A, and BAP1). Cancer Genome Landscape analysis revealed Tier 1 and Tier 2 variants in HCC (MSH2) and in Non-HCC (KMT2D and ATM). For KEGG analysis, the significantly annotated clusters in HCC were Notch signaling, Wnt signaling, PI3K-AKT pathway, Hippo signaling, Apelin signaling, Hedgehog (Hh) signaling, and MAPK signaling, in addition to ECM-receptor interaction, focal adhesion, and calcium signaling. Tier 1 and Tier 2 variants KIT, KMT2D, NOTCH1, KMT2C, PIK3CA, KIT, SMARCA4, ATM, PTEN, MSH2, and PTCH1 were low frequency variants in both HCC and Non-HCC. Our results are in accordance with previous studies in HCC regarding highly mutated genes, TCGA and specifically enriched pathways in HCC. Analysis for clinical interpretation of variants revealed the presence of Tier 1 and Tier 2 variants that represent potential clinically actionable targets. The use of sequencing techniques to detect structural variants and novel techniques as single cell sequencing together with multiomics transcriptomics, metagenomics will integrate the molecular pathogenesis of HCC in Egyptian patients.

Sections du résumé

BACKGROUND BACKGROUND
Hepatocellular carcinoma (HCC) is the most common primary liver cancer. Chronic hepatitis and liver cirrhosis lead to accumulation of genetic alterations driving HCC pathogenesis. This study is designed to explore genomic landscape of HCC in Egyptian patients by whole exome sequencing.
METHODS METHODS
Whole exome sequencing using Ion Torrent was done on 13 HCC patients, who underwent surgical intervention (7 patients underwent living donor liver transplantation (LDLT) and 6 patients had surgical resection}.
RESULTS RESULTS
Mutational signature was mostly S1, S5, S6, and S12 in HCC. Analysis of highly mutated genes in both HCC and Non-HCC revealed the presence of highly mutated genes in HCC (AHNAK2, MUC6, MUC16, TTN, ZNF17, FLG, MUC12, OBSCN, PDE4DIP, MUC5b, and HYDIN). Among the 26 significantly mutated HCC genes-identified across 10 genome sequencing studies-in addition to TCGA, APOB and RP1L1 showed the highest number of mutations in both HCC and Non-HCC tissues. Tier 1, Tier 2 variants in TCGA SMGs in HCC and Non-HCC (TP53, PIK3CA, CDKN2A, and BAP1). Cancer Genome Landscape analysis revealed Tier 1 and Tier 2 variants in HCC (MSH2) and in Non-HCC (KMT2D and ATM). For KEGG analysis, the significantly annotated clusters in HCC were Notch signaling, Wnt signaling, PI3K-AKT pathway, Hippo signaling, Apelin signaling, Hedgehog (Hh) signaling, and MAPK signaling, in addition to ECM-receptor interaction, focal adhesion, and calcium signaling. Tier 1 and Tier 2 variants KIT, KMT2D, NOTCH1, KMT2C, PIK3CA, KIT, SMARCA4, ATM, PTEN, MSH2, and PTCH1 were low frequency variants in both HCC and Non-HCC.
CONCLUSION CONCLUSIONS
Our results are in accordance with previous studies in HCC regarding highly mutated genes, TCGA and specifically enriched pathways in HCC. Analysis for clinical interpretation of variants revealed the presence of Tier 1 and Tier 2 variants that represent potential clinically actionable targets. The use of sequencing techniques to detect structural variants and novel techniques as single cell sequencing together with multiomics transcriptomics, metagenomics will integrate the molecular pathogenesis of HCC in Egyptian patients.

Identifiants

pubmed: 39123171
doi: 10.1186/s12920-024-01965-w
pii: 10.1186/s12920-024-01965-w
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

202

Subventions

Organisme : Science and Technology Development Fund
ID : Basic and Applied Research Grant Call 7 (BARG Call 7, Project ID:38229).
Organisme : Science and Technology Development Fund
ID : Basic and Applied Research Grant Call 7 (BARG Call 7, Project ID:38229).
Organisme : Science and Technology Development Fund
ID : Basic and Applied Research Grant Call 7 (BARG Call 7, Project ID:38229).
Organisme : Science and Technology Development Fund
ID : Basic and Applied Research Grant Call 7 (BARG Call 7, Project ID:38229).
Organisme : Science and Technology Development Fund
ID : Basic and Applied Research Grant Call 7 (BARG Call 7, Project ID:38229).

Informations de copyright

© 2024. The Author(s).

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Auteurs

Perihan Hamdy Kassem (PH)

Clinical Pathology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt.

Iman Fawzy Montasser (IF)

Tropical Medicine Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt. imanfawzy2@gmail.com.

Ramy Mohamed Mahmoud (RM)

Clinical Pathology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt.

Rasha Ahmed Ghorab (RA)

Clinical Pathology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt.

Dina A AbdelHakam (DA)

Clinical Pathology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt.

Marium El Sayed Ahmad Fathi (MESA)

Clinical Pathology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt.

Marwa A Abdel Wahed (MAA)

Clinical Pathology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt.

Khaled Mohey (K)

Clinical Pathology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt.

Mariam Ibrahim (M)

Pathology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt.

Mohamed El Hadidi (ME)

Institute of Cancer and Genomic Sciences, College of Medical and Dental Sciences, University of Birmingham Dubai Campus, Dubai, United Arab Emirates.
Bioinformatics Group, Center for Informatics Science(CIS), School of Information Technology and Computer Science(ITCS), Nile University, Giza, Egypt.

Yasmine M Masssoud (YM)

Tropical Medicine Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt.

Manar Salah (M)

Tropical Medicine Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt.

Arwa Abugable (A)

School of Biosciences, University of Sheffield, Sheffield, UK.

Mohamad Bahaa (M)

Hepato-Pancreatico-Biliary Surgery Department and liver Transplantation, Faculty of Medicine, Ain Shams University, Cairo, Egypt.

Sherif El Khamisy (SE)

School of Biosciences, University of Sheffield, Sheffield, UK.

Mahmoud El Meteini (ME)

Hepato-Pancreatico-Biliary Surgery Department and liver Transplantation, Faculty of Medicine, Ain Shams University, Cairo, Egypt.

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