PMID- 37400148
OWN - NLM
STAT- MEDLINE
DCOM- 20230705
LR  - 20230707
IS  - 1790-6245 (Electronic)
IS  - 1109-6535 (Print)
IS  - 1109-6535 (Linking)
VI  - 20
IP  - 4
DP  - 2023 Jul-Aug
TI  - Genetic Pathways in Peritoneal Mesothelioma Tumorigenesis.
PG  - 363-374
LID - 10.21873/cgp.20388 [doi]
AB  - BACKGROUND/AIM: Mesotheliomas are tumors similar to, and probably derived from, 
      mesothelial cells. They carry acquired chromosomal rearrangements, deletions 
      affecting CDKN2A, pathogenetic polymorphisms in NF2, and fusion genes which often 
      contain the promiscuous EWSR1, FUS, and ALK as partner genes. Here, we report the 
      cytogenomic results on two peritoneal mesotheliomas. MATERIALS AND METHODS: Both 
      tumors were examined using G-banding with karyotyping and array comparative 
      genomic hybridization (aCGH). One of them was further investigated with RNA 
      sequencing, reverse transcription polymerase chain reaction (RT-PCR), Sanger 
      sequencing, and fluorescence in situ hybridization (FISH). RESULTS: In the first 
      mesothelioma, the karyotype was 
      25 approximately 26,X,+5,+7,+20[cp4]/50 approximately 52,idemx2[cp7]/46,XX[2]. aCGH detected gains of 
      chromosomes 5, 7, and 20 with retained heterozygosity on these chromosomes. In 
      the second tumor, the karyotype was 46,XX,inv(10)(p11q25)[7]/46,XX[3]. aCGH did 
      not detect any gains or losses and showed heterozygosity for all chromosomes. RNA 
      sequencing, RT-PCR/Sanger sequencing, and FISH showed that the inv(10) fused 
      MAP3K8 from 10p11 with ABLIM1 from 10q25. The MAP3K8::ABLIM1 chimera lacked exon 
      9 of MAP3K8. CONCLUSION: Our data, together with information on previously 
      described mesotheliomas, illustrate two pathogenetic mechanisms in peritoneal 
      mesothelioma: One pathway is characterized by hyperhaploidy, but with retained 
      disomies for chromosomes 5, 7, and 20; this may be particularly prevalent in 
      biphasic mesotheliomas. The second pathway is characterized by rearrangements of 
      MAP3K8 from which exon 9 of MAP3K8 is lost. The absence of exon 9 from 
      oncogenetically rearranged MAP3K8 is a common theme in thyroid carcinoma, lung 
      cancer, and spitzoid as well as other melanoma subtypes.
CI  - Copyright (c) 2023, International Institute of Anticancer Research (Dr. George J. 
      Delinasios), All rights reserved.
FAU - Panagopoulos, Ioannis
AU  - Panagopoulos I
AD  - Section for Cancer Cytogenetics, Institute for Cancer Genetics and Informatics, 
      The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway; 
      ioannis.panagopoulos@rr-research.no.
FAU - Andersen, Kristin
AU  - Andersen K
AD  - Section for Cancer Cytogenetics, Institute for Cancer Genetics and Informatics, 
      The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
FAU - Brunetti, Marta
AU  - Brunetti M
AD  - Section for Cancer Cytogenetics, Institute for Cancer Genetics and Informatics, 
      The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
FAU - Gorunova, Ludmila
AU  - Gorunova L
AD  - Section for Cancer Cytogenetics, Institute for Cancer Genetics and Informatics, 
      The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
FAU - Davidson, Ben
AU  - Davidson B
AD  - Department of Pathology, Oslo University Hospital, Oslo, Norway.
AD  - Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, 
      Norway.
FAU - Lund-Iversen, Marius
AU  - Lund-Iversen M
AD  - Department of Pathology, Oslo University Hospital, Oslo, Norway.
FAU - Micci, Francesca
AU  - Micci F
AD  - Section for Cancer Cytogenetics, Institute for Cancer Genetics and Informatics, 
      The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
FAU - Heim, Sverre
AU  - Heim S
AD  - Section for Cancer Cytogenetics, Institute for Cancer Genetics and Informatics, 
      The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
AD  - Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, 
      Norway.
LA  - eng
PT  - Journal Article
PL  - Greece
TA  - Cancer Genomics Proteomics
JT  - Cancer genomics & proteomics
JID - 101188791
RN  - 0 (ABLIM1 protein, human)
RN  - 0 (Microfilament Proteins)
RN  - 0 (LIM Domain Proteins)
SB  - IM
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Comparative Genomic Hybridization
MH  - *Mesothelioma, Malignant
MH  - *Mesothelioma/genetics
MH  - Carcinogenesis
MH  - Cell Transformation, Neoplastic
MH  - *Peritoneal Neoplasms/genetics/metabolism
MH  - Microfilament Proteins/genetics
MH  - LIM Domain Proteins/genetics
PMC - PMC10320557
OTO - NOTNLM
OT  - MAP3K8::ABLIM1 chimeric gene
OT  - Peritoneal mesothelioma
OT  - biphasic mesothelioma
OT  - disomic chromosomes
OT  - exon 9 of MAP3K8
OT  - hyperhaploidy
OT  - inv(10)(p11q25)
COIS- The Authors declare that they have no potential conflicts of interest.
EDAT- 2023/07/04 01:05
MHDA- 2023/07/05 06:42
PMCR- 2023/07/03
CRDT- 2023/07/03 20:53
PHST- 2023/05/01 00:00 [received]
PHST- 2023/05/22 00:00 [revised]
PHST- 2023/06/15 00:00 [accepted]
PHST- 2023/07/05 06:42 [medline]
PHST- 2023/07/04 01:05 [pubmed]
PHST- 2023/07/03 20:53 [entrez]
PHST- 2023/07/03 00:00 [pmc-release]
AID - 20/4/363 [pii]
AID - 10.21873/cgp.20388 [doi]
PST - ppublish
SO  - Cancer Genomics Proteomics. 2023 Jul-Aug;20(4):363-374. doi: 10.21873/cgp.20388.