Adnab-9
FERAD ratio
H. pylori
familial gastric cancer
monoclonal antibody
Journal
Current oncology (Toronto, Ont.)
ISSN: 1718-7729
Titre abrégé: Curr Oncol
Pays: Switzerland
ID NLM: 9502503
Informations de publication
Date de publication:
29 08 2023
29 08 2023
Historique:
received:
17
05
2023
revised:
09
07
2023
accepted:
02
08
2023
medline:
28
9
2023
pubmed:
27
9
2023
entrez:
27
9
2023
Statut:
epublish
Résumé
We evaluated the phenotype of sporadic gastric cancer based on HP status and binding of a tumor risk marker monoclonal, Adnab-9. We compared a familial GC kindred with an extremely aggressive phenotype to HP-positive (HP+) and -negative (HP-) sporadic gastric adenocarcinoma (GC) patients in the same community to determine if similar phenotypes exist. This might facilitate gene discovery to understand the pathogenesis of aggressive GC phenotypes, particularly with publications implicating immune-related gene-based signatures, and the development of techniques to gauge the stance of the innate immune system (InImS), such as the FERAD ratio (blood ferritin:fecal Adnab-9 binding OD-background binding). Resection specimens for the sporadic and familial group were stained for HP and examined for intestinal metaplasia (IM) and immunostaining for Adnab-9. Familial kindred specimens were also tested for the E-cadherin mutation and APC (adenomatous polyposis coli). Survival was evaluated. Of 40 GC patients, 25% were HP+ with a greater proportion of intestinal metaplasia (IM) and gastric atrophy than the HP- group. The proband of the familial GC kindred, a 32-year-old mother with fatal GC, was survived by 13-year-old identical twins. Twin #1 was HP- with IM and Twin #2 was HP+. Both twins subsequently died of GC within two years. The twins did not have APC or E-cadherin mutations. The mean overall survival in the HP+ sporadic GC group was 2.47 ± 2.58 years and was 0.57 ± 0.60 years in the HP- group ( The HP+ sporadic GC group appears to proceed through a sequence of HP infection, IM and atrophy before cancer supervenes, and the HP- phenotype appear to omit this sequence. The familial cases may represent a subset with both features, but the natural history strongly resembles that of the HP- group. Two different paths of carcinogenesis may exist locally for sporadic GC. The InImS may also be implicated in prognosis. Identifying these patients will allow for treatment stratification and early diagnosis to improve GC survival.
Sections du résumé
BACKGROUND
We evaluated the phenotype of sporadic gastric cancer based on HP status and binding of a tumor risk marker monoclonal, Adnab-9.
METHODS
We compared a familial GC kindred with an extremely aggressive phenotype to HP-positive (HP+) and -negative (HP-) sporadic gastric adenocarcinoma (GC) patients in the same community to determine if similar phenotypes exist. This might facilitate gene discovery to understand the pathogenesis of aggressive GC phenotypes, particularly with publications implicating immune-related gene-based signatures, and the development of techniques to gauge the stance of the innate immune system (InImS), such as the FERAD ratio (blood ferritin:fecal Adnab-9 binding OD-background binding). Resection specimens for the sporadic and familial group were stained for HP and examined for intestinal metaplasia (IM) and immunostaining for Adnab-9. Familial kindred specimens were also tested for the E-cadherin mutation and APC (adenomatous polyposis coli). Survival was evaluated.
RESULTS
Of 40 GC patients, 25% were HP+ with a greater proportion of intestinal metaplasia (IM) and gastric atrophy than the HP- group. The proband of the familial GC kindred, a 32-year-old mother with fatal GC, was survived by 13-year-old identical twins. Twin #1 was HP- with IM and Twin #2 was HP+. Both twins subsequently died of GC within two years. The twins did not have APC or E-cadherin mutations. The mean overall survival in the HP+ sporadic GC group was 2.47 ± 2.58 years and was 0.57 ± 0.60 years in the HP- group (
CONCLUSION
The HP+ sporadic GC group appears to proceed through a sequence of HP infection, IM and atrophy before cancer supervenes, and the HP- phenotype appear to omit this sequence. The familial cases may represent a subset with both features, but the natural history strongly resembles that of the HP- group. Two different paths of carcinogenesis may exist locally for sporadic GC. The InImS may also be implicated in prognosis. Identifying these patients will allow for treatment stratification and early diagnosis to improve GC survival.
Identifiants
pubmed: 37754493
pii: curroncol30090578
doi: 10.3390/curroncol30090578
pmc: PMC10527591
doi:
Substances chimiques
Cadherins
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
7950-7963Références
Cancer Epidemiol Biomarkers Prev. 2022 Jan;31(1):200-209
pubmed: 34728467
Cancer. 2000 Feb 15;88(4):921-32
pubmed: 10679663
Hum Pathol. 1999 Apr;30(4):467-73
pubmed: 10208470
N Engl J Med. 2002 Oct 10;347(15):1175-86
pubmed: 12374879
BMC Med Genomics. 2008 Oct 25;1:54
pubmed: 18950519
Scand J Gastroenterol. 1993 Dec;28(12):1025-34
pubmed: 8303203
Int J Mol Sci. 2023 Apr 19;24(8):
pubmed: 37108697
Orphanet J Rare Dis. 2009 Oct 12;4:22
pubmed: 19822006
Gastric Cancer. 2004;7(3):178-82
pubmed: 15449208
Cancer Res. 1993 Apr 1;53(7):1690-5
pubmed: 8453643
World J Gastrointest Oncol. 2016 Feb 15;8(2):147-58
pubmed: 26909129
Scand J Gastroenterol. 1992 Sep;27(9):737-42
pubmed: 1411278
Gastroenterology. 2021 Oct;161(4):1325-1332.e7
pubmed: 34454714
Cancer Epidemiol Biomarkers Prev. 2003 Oct;12(10):1095-9
pubmed: 14578149
Hum Mutat. 1993;2(6):425-34
pubmed: 8111410
Gastric Cancer. 2000 Dec;3(4):177-186
pubmed: 11984734
Gastric Cancer. 2005;8(2):124-31
pubmed: 15864720
Nature. 1998 Mar 26;392(6674):402-5
pubmed: 9537325
J Natl Cancer Inst. 2004 Sep 15;96(18):1383-7
pubmed: 15367571
Cancer Lett. 1992 Oct 30;67(1):61-9
pubmed: 1423246
Am J Pathol. 2012 Nov;181(5):1560-72
pubmed: 22944598
Cancer Lett. 2006 Apr 8;235(1):48-52
pubmed: 15893419
N Engl J Med. 2020 Jan 30;382(5):427-436
pubmed: 31995688
Int J Cancer. 2002 Oct 10;101(5):469-74
pubmed: 12216076
Cancer. 1978 Aug;42(2):623-5
pubmed: 354773
Gastric Cancer. 2002;5(4):228-32
pubmed: 12491081
J Gastric Cancer. 2013 Jun;13(2):79-85
pubmed: 23844321
Cancer Res. 1991 Apr 15;51(8):2185-92
pubmed: 2009537
Hepatogastroenterology. 1997 Mar-Apr;44(14):604-9
pubmed: 9164544
J Histochem Cytochem. 1981 Apr;29(4):577-80
pubmed: 6166661
J Oncol. 2019 Sep 24;2019:1079710
pubmed: 31662748
Dig Dis Sci. 2013 Mar;58(3):744-50
pubmed: 23001406
World J Gastroenterol. 2023 Jan 28;29(4):706-730
pubmed: 36742169
Br J Surg. 1995 Jun;82(6):802-5
pubmed: 7627516
Curr Opin Cell Biol. 1993 Oct;5(5):797-805
pubmed: 8240823
Dig Dis Sci. 2023 Mar;68(3):791-802
pubmed: 35624327
Digestion. 2022;103(1):45-53
pubmed: 34628409
World J Gastrointest Oncol. 2020 Aug 15;12(8):857-876
pubmed: 32879664
Appl Pathol. 1984;2(1):43-8
pubmed: 6525318
Int J Pancreatol. 2001;29(3):141-50
pubmed: 12067217
Curr Opin Gastroenterol. 2018 Nov;34(6):458-464
pubmed: 30138135
CA Cancer J Clin. 2022 May;72(3):202-229
pubmed: 35143040
Biomedicines. 2021 Oct 12;9(10):
pubmed: 34680565
Cell Death Dis. 2022 Oct 27;13(10):903
pubmed: 36302755
Onco Targets Ther. 2018 Oct 25;11:7503-7512
pubmed: 30498363
Dig Dis Sci. 2002 Jan;47(1):114-21
pubmed: 11837710