Hepatocellular carcinoma after direct‐acting antivirals for hepatitis C is associated with KIR‐HLA types predicting weak NK cell‐mediated immunity

Background and aims Second‐generation direct‐acting antivirals (2G DAA) to cure HCV have led to dramatic clinical improvements. HCV‐associated hepatocellular carcinoma (HCC), however, remains common. Impaired immune tumor surveillance may play a role in HCC development. Our cohort evaluated the effe...

Full description

Saved in:
Bibliographic Details
Published inEuropean journal of immunology Vol. 54; no. 8; pp. e2350678 - n/a
Main Authors Ryan, James C., Haight, Christina, Niemi, Erene C., Grab, Joshua D., Dodge, Jennifer L., Lanier, Lewis L., Monto, Alexander
Format Journal Article
LanguageEnglish
Published Germany Wiley Subscription Services, Inc 01.08.2024
Subjects
Online AccessGet full text

Cover

Loading…
Abstract Background and aims Second‐generation direct‐acting antivirals (2G DAA) to cure HCV have led to dramatic clinical improvements. HCV‐associated hepatocellular carcinoma (HCC), however, remains common. Impaired immune tumor surveillance may play a role in HCC development. Our cohort evaluated the effects of innate immune types and clinical variables on outcomes including HCC. Methods Participants underwent full HLA class I/KIR typing and long‐term HCV follow‐up. Results A total of 353 HCV+ participants were followed for a mean of 7 years. Cirrhosis: 25% at baseline, developed in 12% during follow‐up. 158 participants received 2G DAA therapy. HCC developed without HCV therapy in 20 subjects, 24 HCC after HCV therapy, and 10 of these after 2G DAA. Two predictors of HCC among 2G DAA‐treated patients: cirrhosis (OR, 10.0, p = 0.002) and HLA/KIR profiles predicting weak natural killer (NK) cell‐mediated immunity (NK cell complementation groups 6, 9, 11, 12, OR of 5.1, p = 0.02). Without 2G DAA therapy: cirrhosis was the main clinical predictor of HCC (OR, 30.8, p < 0.0001), and weak NK‐cell‐mediated immunity did not predict HCC. Conclusion Cirrhosis is the main risk state predisposing to HCC, but weak NK‐cell‐mediated immunity may predispose to post‐2G DAA HCC more than intermediate or strong NK‐cell‐mediated immunity. In patients with hepatitis C cirrhosis who are treated with 2G DAA, predicted weak NK‐cell‐mediated immunity may predispose to HCC development more than predicted intermediate or strong NK‐cell‐mediated immunity.
AbstractList Background and aims Second‐generation direct‐acting antivirals (2G DAA) to cure HCV have led to dramatic clinical improvements. HCV‐associated hepatocellular carcinoma (HCC), however, remains common. Impaired immune tumor surveillance may play a role in HCC development. Our cohort evaluated the effects of innate immune types and clinical variables on outcomes including HCC. Methods Participants underwent full HLA class I/KIR typing and long‐term HCV follow‐up. Results A total of 353 HCV+ participants were followed for a mean of 7 years. Cirrhosis: 25% at baseline, developed in 12% during follow‐up. 158 participants received 2G DAA therapy. HCC developed without HCV therapy in 20 subjects, 24 HCC after HCV therapy, and 10 of these after 2G DAA. Two predictors of HCC among 2G DAA‐treated patients: cirrhosis (OR, 10.0, p = 0.002) and HLA/KIR profiles predicting weak natural killer (NK) cell‐mediated immunity (NK cell complementation groups 6, 9, 11, 12, OR of 5.1, p = 0.02). Without 2G DAA therapy: cirrhosis was the main clinical predictor of HCC (OR, 30.8, p < 0.0001), and weak NK‐cell‐mediated immunity did not predict HCC. Conclusion Cirrhosis is the main risk state predisposing to HCC, but weak NK‐cell‐mediated immunity may predispose to post‐2G DAA HCC more than intermediate or strong NK‐cell‐mediated immunity. In patients with hepatitis C cirrhosis who are treated with 2G DAA, predicted weak NK‐cell‐mediated immunity may predispose to HCC development more than predicted intermediate or strong NK‐cell‐mediated immunity.
Second-generation direct-acting antivirals (2G DAA) to cure HCV have led to dramatic clinical improvements. HCV-associated hepatocellular carcinoma (HCC), however, remains common. Impaired immune tumor surveillance may play a role in HCC development. Our cohort evaluated the effects of innate immune types and clinical variables on outcomes including HCC.BACKGROUND AND AIMSSecond-generation direct-acting antivirals (2G DAA) to cure HCV have led to dramatic clinical improvements. HCV-associated hepatocellular carcinoma (HCC), however, remains common. Impaired immune tumor surveillance may play a role in HCC development. Our cohort evaluated the effects of innate immune types and clinical variables on outcomes including HCC.Participants underwent full HLA class I/KIR typing and long-term HCV follow-up.METHODSParticipants underwent full HLA class I/KIR typing and long-term HCV follow-up.A total of 353 HCV+ participants were followed for a mean of 7 years. Cirrhosis: 25% at baseline, developed in 12% during follow-up. 158 participants received 2G DAA therapy. HCC developed without HCV therapy in 20 subjects, 24 HCC after HCV therapy, and 10 of these after 2G DAA. Two predictors of HCC among 2G DAA-treated patients: cirrhosis (OR, 10.0, p = 0.002) and HLA/KIR profiles predicting weak natural killer (NK) cell-mediated immunity (NK cell complementation groups 6, 9, 11, 12, OR of 5.1, p = 0.02). Without 2G DAA therapy: cirrhosis was the main clinical predictor of HCC (OR, 30.8, p < 0.0001), and weak NK-cell-mediated immunity did not predict HCC.RESULTSA total of 353 HCV+ participants were followed for a mean of 7 years. Cirrhosis: 25% at baseline, developed in 12% during follow-up. 158 participants received 2G DAA therapy. HCC developed without HCV therapy in 20 subjects, 24 HCC after HCV therapy, and 10 of these after 2G DAA. Two predictors of HCC among 2G DAA-treated patients: cirrhosis (OR, 10.0, p = 0.002) and HLA/KIR profiles predicting weak natural killer (NK) cell-mediated immunity (NK cell complementation groups 6, 9, 11, 12, OR of 5.1, p = 0.02). Without 2G DAA therapy: cirrhosis was the main clinical predictor of HCC (OR, 30.8, p < 0.0001), and weak NK-cell-mediated immunity did not predict HCC.Cirrhosis is the main risk state predisposing to HCC, but weak NK-cell-mediated immunity may predispose to post-2G DAA HCC more than intermediate or strong NK-cell-mediated immunity.CONCLUSIONCirrhosis is the main risk state predisposing to HCC, but weak NK-cell-mediated immunity may predispose to post-2G DAA HCC more than intermediate or strong NK-cell-mediated immunity.
Background and aimsSecond‐generation direct‐acting antivirals (2G DAA) to cure HCV have led to dramatic clinical improvements. HCV‐associated hepatocellular carcinoma (HCC), however, remains common. Impaired immune tumor surveillance may play a role in HCC development. Our cohort evaluated the effects of innate immune types and clinical variables on outcomes including HCC.MethodsParticipants underwent full HLA class I/KIR typing and long‐term HCV follow‐up.ResultsA total of 353 HCV+ participants were followed for a mean of 7 years. Cirrhosis: 25% at baseline, developed in 12% during follow‐up. 158 participants received 2G DAA therapy. HCC developed without HCV therapy in 20 subjects, 24 HCC after HCV therapy, and 10 of these after 2G DAA. Two predictors of HCC among 2G DAA‐treated patients: cirrhosis (OR, 10.0, p = 0.002) and HLA/KIR profiles predicting weak natural killer (NK) cell‐mediated immunity (NK cell complementation groups 6, 9, 11, 12, OR of 5.1, p = 0.02). Without 2G DAA therapy: cirrhosis was the main clinical predictor of HCC (OR, 30.8, p < 0.0001), and weak NK‐cell‐mediated immunity did not predict HCC.ConclusionCirrhosis is the main risk state predisposing to HCC, but weak NK‐cell‐mediated immunity may predispose to post‐2G DAA HCC more than intermediate or strong NK‐cell‐mediated immunity.
Second-generation direct-acting antivirals (2G DAA) to cure HCV have led to dramatic clinical improvements. HCV-associated hepatocellular carcinoma (HCC), however, remains common. Impaired immune tumor surveillance may play a role in HCC development. Our cohort evaluated the effects of innate immune types and clinical variables on outcomes including HCC. Participants underwent full HLA class I/KIR typing and long-term HCV follow-up. A total of 353 HCV+ participants were followed for a mean of 7 years. Cirrhosis: 25% at baseline, developed in 12% during follow-up. 158 participants received 2G DAA therapy. HCC developed without HCV therapy in 20 subjects, 24 HCC after HCV therapy, and 10 of these after 2G DAA. Two predictors of HCC among 2G DAA-treated patients: cirrhosis (OR, 10.0, p = 0.002) and HLA/KIR profiles predicting weak natural killer (NK) cell-mediated immunity (NK cell complementation groups 6, 9, 11, 12, OR of 5.1, p = 0.02). Without 2G DAA therapy: cirrhosis was the main clinical predictor of HCC (OR, 30.8, p < 0.0001), and weak NK-cell-mediated immunity did not predict HCC. Cirrhosis is the main risk state predisposing to HCC, but weak NK-cell-mediated immunity may predispose to post-2G DAA HCC more than intermediate or strong NK-cell-mediated immunity.
In patients with hepatitis C cirrhosis who are treated with 2G DAA, predicted weak NK cell-mediated immunity may predispose to HCC development more than predicted intermediate or strong NK cell-mediated immunity
Author Dodge, Jennifer L.
Haight, Christina
Niemi, Erene C.
Lanier, Lewis L.
Grab, Joshua D.
Ryan, James C.
Monto, Alexander
AuthorAffiliation 1 Department of Medicine, San Francisco Veterans Affairs Medical Center, San Francisco, CA
5 Department of Microbiology and Immunology, University of California, San Francisco, CA
3 Department of Medicine, University of California, San Francisco, CA
2 Division of Gastroenterology, University of California, San Francisco, CA
4 Population and Public Health Sciences, Keck School of Medicine, University of Southern California, Los Angeles, CA
AuthorAffiliation_xml – name: 2 Division of Gastroenterology, University of California, San Francisco, CA
– name: 1 Department of Medicine, San Francisco Veterans Affairs Medical Center, San Francisco, CA
– name: 5 Department of Microbiology and Immunology, University of California, San Francisco, CA
– name: 3 Department of Medicine, University of California, San Francisco, CA
– name: 4 Population and Public Health Sciences, Keck School of Medicine, University of Southern California, Los Angeles, CA
Author_xml – sequence: 1
  givenname: James C.
  surname: Ryan
  fullname: Ryan, James C.
  organization: University of California
– sequence: 2
  givenname: Christina
  surname: Haight
  fullname: Haight, Christina
  organization: San Francisco Veterans Affairs Medical Center
– sequence: 3
  givenname: Erene C.
  surname: Niemi
  fullname: Niemi, Erene C.
  organization: San Francisco Veterans Affairs Medical Center
– sequence: 4
  givenname: Joshua D.
  surname: Grab
  fullname: Grab, Joshua D.
  organization: University of California
– sequence: 5
  givenname: Jennifer L.
  surname: Dodge
  fullname: Dodge, Jennifer L.
  organization: University of Southern California
– sequence: 6
  givenname: Lewis L.
  surname: Lanier
  fullname: Lanier, Lewis L.
  organization: University of California
– sequence: 7
  givenname: Alexander
  orcidid: 0000-0002-2710-6871
  surname: Monto
  fullname: Monto, Alexander
  email: alexander.monto@va.gov
  organization: University of California
BackLink https://www.ncbi.nlm.nih.gov/pubmed/38700055$$D View this record in MEDLINE/PubMed
BookMark eNp9ksFu1DAQhi1URLeFI1dkiQuXFDu24-SEqlVhl65AQnC2HGfS9ZLEi-10tTceocc-H0-Cw5YVcODi0Wi--f8Zec7QyeAGQOg5JReUkPw1bOxFTnImSCHLR2hGRU4zTjk9QTNCKM_yqiSn6CyEDSGkKkT1BJ2yUqZEiBm6X8BWR2eg68ZOe2y0N3Zwvca6jeBxYz2Y-OP7nTbRDjdYD9HeWq-7gFvn8XrqttEGPMfp0SE4Y3WEBu9sXOPr5afUulhd4rjfQsBbD409CO1Af8UfrvHknJg-FX712b4fBxv3T9HjNrnAs4d4jr68vfo8X2Srj--W88tVZpgsZCYrUxSsbVta1gZEDkaA5AUHU-USSl4LBsAaJnjdmLqlKTVSCN6mYDSr2Dl6c9DdjnUawsAQ03Zq622v_V45bdXflcGu1Y27VZRKLkjJk8KrBwXvvo0QouptmNbSA7gxKEYEqVjJ-GT28h9040Y_pP0SVVYlz2lJE_Xiz5GOs_z-tQRkB8B4F4KH9ohQoqarUOkq1PEqEp8f-J3tYP9_WF29XwqZS_YTY6u_ng
Cites_doi 10.1016/j.jhep.2016.04.008
10.1016/j.jhep.2016.01.029
10.1002/hep.30823
10.1002/hep.29855
10.4049/jimmunol.1501358
10.1111/tan.13754
10.1016/j.coi.2004.07.010
10.1182/blood-2008-02-137521
10.1084/jem.182.2.605
10.1111/j.1600-065X.1997.tb00935.x
10.1001/jamaoncol.2017.3055
10.1111/j.1399-0039.1995.tb02408.x
10.1038/ng2077
10.1002/hep.29086
10.1093/infdis/jit801
10.1002/hep.29811
10.1016/j.humimm.2008.05.001
10.1016/j.humimm.2017.10.008
10.1002/(SICI)1097-0142(19970701)80:1<22::AID-CNCR4>3.0.CO;2-H
10.1053/j.gastro.2019.07.033
10.4049/jimmunol.168.5.2307
10.1016/j.cell.2020.11.041
10.1111/j.1399-0039.2007.00923.x
10.1016/j.jhep.2016.06.009
10.1111/tan.12299
10.3390/cancers13133267
10.1053/j.gastro.2019.07.040
10.1371/journal.pone.0167934
10.1002/1097-0142(19940501)73:9<2253::AID-CNCR2820730904>3.0.CO;2-9
10.1016/j.jceh.2018.06.009
10.1093/nar/gkq1128
ContentType Journal Article
Copyright ([0‐9]+) Wiley‐VCH GmbH
([0‐9]+) Wiley‐VCH GmbH.
2024. This article is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Copyright_xml – notice: ([0‐9]+) Wiley‐VCH GmbH
– notice: ([0‐9]+) Wiley‐VCH GmbH.
– notice: 2024. This article is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
DBID 24P
AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
7QP
7T5
7TK
7TM
8FD
FR3
H94
K9.
M7N
P64
RC3
7X8
5PM
DOI 10.1002/eji.202350678
DatabaseName Wiley Online Library Journals (Open Access)
CrossRef
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
Calcium & Calcified Tissue Abstracts
Immunology Abstracts
Neurosciences Abstracts
Nucleic Acids Abstracts
Technology Research Database
Engineering Research Database
AIDS and Cancer Research Abstracts
ProQuest Health & Medical Complete (Alumni)
Algology Mycology and Protozoology Abstracts (Microbiology C)
Biotechnology and BioEngineering Abstracts
Genetics Abstracts
MEDLINE - Academic
PubMed Central (Full Participant titles)
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
Genetics Abstracts
Technology Research Database
Algology Mycology and Protozoology Abstracts (Microbiology C)
Nucleic Acids Abstracts
AIDS and Cancer Research Abstracts
ProQuest Health & Medical Complete (Alumni)
Immunology Abstracts
Engineering Research Database
Calcium & Calcified Tissue Abstracts
Neurosciences Abstracts
Biotechnology and BioEngineering Abstracts
MEDLINE - Academic
DatabaseTitleList
MEDLINE - Academic
Genetics Abstracts
MEDLINE

Database_xml – sequence: 1
  dbid: 24P
  name: Wiley Online Library Open Access
  url: https://authorservices.wiley.com/open-science/open-access/browse-journals.html
  sourceTypes: Publisher
– sequence: 2
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 3
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
Biology
EISSN 1521-4141
EndPage n/a
ExternalDocumentID PMC11745084
38700055
10_1002_eji_202350678
EJI5727
Genre article
Journal Article
GrantInformation_xml – fundername: Dr. Ryan in addition to the University of California, San Francisco Liver Center
  funderid: P30 DK026743
– fundername: Department of Veterans Affairs Merit
  funderid: CX000295‐05A2
– fundername: Dr. Monto and the National Institute of Allergy and Infectious Diseases (NIAID) R01
  funderid: AI083113‐01A1
– fundername: Department of Veterans Affairs Merit
  grantid: CX000295-05A2
– fundername: Dr. Monto and the National Institute of Allergy and Infectious Diseases (NIAID) R01
  grantid: AI083113-01A1
– fundername: CSRD VA
  grantid: I01 CX000295
– fundername: NIAID NIH HHS
  grantid: R01 AI083113
– fundername: NIDDK NIH HHS
  grantid: P30 DK026743
GroupedDBID ---
.3N
.55
.GA
.GJ
.HR
.Y3
05W
0R~
10A
1L6
1OB
1OC
1ZS
24P
31~
33P
3O-
3SF
3WU
4.4
4ZD
50Y
50Z
51W
51X
52M
52N
52O
52P
52S
52T
52U
52W
52X
53G
5GY
5RE
5VS
66C
702
7PT
8-0
8-1
8-3
8-4
8-5
8UM
930
A03
AAESR
AAEVG
AAHHS
AAHQN
AAIPD
AAMNL
AANHP
AANLZ
AAONW
AASGY
AAXRX
AAYCA
AAZKR
ABCQN
ABCUV
ABEFU
ABEML
ABIJN
ABJNI
ABLJU
ABPVW
ABQWH
ACAHQ
ACBWZ
ACCFJ
ACCZN
ACFBH
ACGFS
ACPOU
ACPRK
ACRPL
ACSCC
ACXBN
ACXQS
ACYXJ
ADBBV
ADEOM
ADIZJ
ADKYN
ADMGS
ADNMO
ADOZA
ADXAS
ADZMN
ADZOD
AEEZP
AEIGN
AEIMD
AENEX
AEQDE
AEUQT
AEUYR
AFBPY
AFFNX
AFFPM
AFGKR
AFPWT
AFRAH
AFWVQ
AFZJQ
AHBTC
AHMBA
AI.
AITYG
AIURR
AIWBW
AJBDE
AJXKR
ALAGY
ALMA_UNASSIGNED_HOLDINGS
ALUQN
ALVPJ
AMBMR
AMYDB
AOETA
ASPBG
ATUGU
AUFTA
AVWKF
AZBYB
AZFZN
AZVAB
BAFTC
BDRZF
BFHJK
BHBCM
BMNLL
BMXJE
BNHUX
BROTX
BRXPI
BY8
CS3
D-E
D-F
DCZOG
DPXWK
DR2
DRFUL
DRSTM
DU5
EBD
EBS
EJD
EMOBN
F00
F01
F04
F5P
FEDTE
G-S
G.N
GNP
GODZA
H.T
H.X
HBH
HF~
HGLYW
HHY
HHZ
HVGLF
HZ~
IX1
J0M
J5H
JPC
KQQ
L7B
LATKE
LAW
LC2
LC3
LEEKS
LH4
LITHE
LOXES
LP6
LP7
LUTES
LW6
LYRES
M65
MEWTI
MK4
MRFUL
MRSTM
MSFUL
MSSTM
MXFUL
MXSTM
N04
N05
N9A
NF~
NNB
O66
O9-
OHT
OIG
OK1
OVD
P2P
P2W
P2X
P4D
PALCI
PQQKQ
Q.N
Q11
QB0
QRW
R.K
RGB
RIWAO
RJQFR
ROL
RWI
RX1
SAMSI
SUPJJ
SV3
TEORI
UB1
UPT
V2E
VH1
W8V
W99
WBKPD
WHWMO
WIB
WIH
WIK
WIN
WJL
WOHZO
WQJ
WRC
WUP
WVDHM
WXSBR
X7M
XG1
XPP
XV2
Y6R
ZGI
ZXP
ZZTAW
~IA
~KM
~WT
AAYXX
AEYWJ
AGHNM
AGQPQ
AGYGG
CITATION
AAMMB
AEFGJ
AGXDD
AIDQK
AIDYY
CGR
CUY
CVF
ECM
EIF
NPM
7QP
7T5
7TK
7TM
8FD
FR3
H94
K9.
M7N
P64
RC3
7X8
5PM
ID FETCH-LOGICAL-c3767-79c663fff18bce52ec5e7464ec927e84b53ee3d354bdcbf153ec7554fec7ca393
IEDL.DBID DR2
ISSN 0014-2980
1521-4141
IngestDate Thu Aug 21 18:33:28 EDT 2025
Fri Jul 11 04:17:03 EDT 2025
Wed Aug 13 09:47:51 EDT 2025
Sun Aug 03 01:52:42 EDT 2025
Tue Jul 01 03:51:42 EDT 2025
Wed Jan 22 17:17:14 EST 2025
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 8
Keywords Hepatocellular
Carcinoma
Killer Cells
Antiviral Agents
Innate
Hepatitis C
Natural
Immunity
Language English
License Attribution-NonCommercial-NoDerivs
([0‐9]+) Wiley‐VCH GmbH.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c3767-79c663fff18bce52ec5e7464ec927e84b53ee3d354bdcbf153ec7554fec7ca393
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
Author contributions: JCR and AM: study concept and design; JCR, CH, ECN, LLL, AM: acquisition of data and performance of immunological studies; JDG, JLD, AM: statistical analysis; JCR, JDG, JLD, LLL, AM: interpretation of analyses; JCR and AM: drafting of manuscript; JCR, JDG, JLD, LLL, AM: critical revision of the manuscript for important intellectual content; JCR and AM: obtained funding and provided study supervision.
ORCID 0000-0002-2710-6871
OpenAccessLink https://proxy.k.utb.cz/login?url=https://onlinelibrary.wiley.com/doi/abs/10.1002%2Feji.202350678
PMID 38700055
PQID 3089842181
PQPubID 986365
PageCount 10
ParticipantIDs pubmedcentral_primary_oai_pubmedcentral_nih_gov_11745084
proquest_miscellaneous_3050938349
proquest_journals_3089842181
pubmed_primary_38700055
crossref_primary_10_1002_eji_202350678
wiley_primary_10_1002_eji_202350678_EJI5727
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate August 2024
PublicationDateYYYYMMDD 2024-08-01
PublicationDate_xml – month: 08
  year: 2024
  text: August 2024
PublicationDecade 2020
PublicationPlace Germany
PublicationPlace_xml – name: Germany
– name: Weinheim
PublicationTitle European journal of immunology
PublicationTitleAlternate Eur J Immunol
PublicationYear 2024
Publisher Wiley Subscription Services, Inc
Publisher_xml – name: Wiley Subscription Services, Inc
References 1997; 80
2007; 39
2019; 9
2017; 3
1997; 155
2021; 184
2007; 70
2018; 67
2011; 39
2014; 83
2018; 68
2016; 11
2015; 195
2021; 13
2014; 209
2004; 16
2020; 95
2020; 71
2002; 168
1995; 45
2016; 65
2008; 69
2016; 64
2019; 157
2008; 112
1995; 182
1994; 73
2018; 79
e_1_2_9_30_1
e_1_2_9_31_1
e_1_2_9_11_1
e_1_2_9_10_1
e_1_2_9_13_1
e_1_2_9_32_1
e_1_2_9_12_1
e_1_2_9_33_1
e_1_2_9_15_1
e_1_2_9_14_1
e_1_2_9_17_1
e_1_2_9_16_1
e_1_2_9_19_1
e_1_2_9_18_1
e_1_2_9_20_1
e_1_2_9_22_1
e_1_2_9_21_1
e_1_2_9_24_1
e_1_2_9_23_1
e_1_2_9_8_1
e_1_2_9_7_1
e_1_2_9_6_1
e_1_2_9_5_1
e_1_2_9_4_1
e_1_2_9_3_1
e_1_2_9_2_1
e_1_2_9_9_1
e_1_2_9_26_1
e_1_2_9_25_1
e_1_2_9_28_1
e_1_2_9_27_1
e_1_2_9_29_1
References_xml – volume: 69
  start-page: 443
  year: 2008
  end-page: 464
  article-title: Balancing selection and heterogeneity across the classical human leukocyte antigen loci: a meta‐analytic review of 497 population studies
  publication-title: Hum. Immunol.
– volume: 157
  start-page: 1264
  year: 2019
  end-page: 1278.e4
  article-title: Increased risk for hepatocellular carcinoma persists up to 10 years after HCV eradication in patients with baseline cirrhosis or high FIB‐4 scores
  publication-title: Gastroenterology
– volume: 16
  start-page: 626
  year: 2004
  end-page: 633
  article-title: Killer immunoglobulin‐like receptors
  publication-title: Curr. Opin. Immunol.
– volume: 79
  start-page: 5
  year: 2018
  end-page: 12
  article-title: An historical approach to the genetic distribution of KIR and HLA ligands in Eastern Sicilians compared to modern descendants of their invaders
  publication-title: Hum. Immunol.
– volume: 70
  start-page: 415
  year: 2007
  end-page: 422
  article-title: Facilitation of KIR genotyping by a PCR‐SSP method that amplifies short DNA fragments
  publication-title: Tissue Antigens
– volume: 68
  start-page: 449
  year: 2018
  end-page: 461
  article-title: Direct‐acting antivirals do not increase the risk of hepatocellular carcinoma recurrence after local‐regional therapy or liver transplant waitlist dropout
  publication-title: Hepatology
– volume: 39
  start-page: 1114
  year: 2007
  end-page: 1119
  article-title: Global diversity and evidence for coevolution of KIR and HLA
  publication-title: Nat. Genet.
– volume: 168
  start-page: 2307
  year: 2002
  article-title: Allelic polymorphism synergizes with variable gene content to individualize human KIR genotype
  publication-title: J. Immunol.
– volume: 65
  start-page: 856
  year: 2016
  end-page: 858
  article-title: Unexpected high incidence of hepatocellular carcinoma in cirrhotic patients with sustained virologic response following interferon‐free direct‐acting antiviral treatment
  publication-title: J. Hepatol.
– volume: 39
  start-page: D913
  year: 2011
  end-page: D919
  article-title: Allele frequency net: a database and online repository for immune gene frequencies in worldwide populations
  publication-title: Nucleic Acids Res.
– volume: 73
  start-page: 2253
  year: 1994
  end-page: 2258
  article-title: Expression of hepatitis C virus in hepatocellular carcinoma
  publication-title: Cancer
– volume: 112
  start-page: 708
  year: 2008
  end-page: 710
  article-title: Human leukocyte antigens A23, A24, and A32 but not A25 are ligands for KIR3DL1
  publication-title: Blood
– volume: 155
  start-page: 5
  year: 1997
  end-page: 9
  article-title: How to recognize a foreign submarine
  publication-title: Immunol. Rev.
– volume: 95
  start-page: 179
  year: 2020
  end-page: 188
  article-title: Distribution of human killer cell immunoglobulin‐like receptors and ligands among blood donors of Catalonia
  publication-title: HLA
– volume: 195
  start-page: 3160
  year: 2015
  end-page: 3170
  article-title: Polymorphic HLA‐C receptors balance the functional characteristics of KIR haplotypes
  publication-title: J. Immunol.
– volume: 209
  start-page: 1602
  year: 2014
  end-page: 1612
  article-title: Monocyte activation by interferon alpha is associated with failure to achieve a sustained virologic response after treatment for hepatitis C virus infection
  publication-title: J. Infect. Dis.
– volume: 182
  start-page: 605
  year: 1995
  end-page: 609
  article-title: Amino acid substitutions can influence the natural killer (NK)‐mediated recognition of HLA‐C molecules. Role of serine‐77 and lysine‐80 in the target cell protection from lysis mediated by “group 2” or “group 1” NK clones
  publication-title: J. Exp. Med.
– volume: 45
  start-page: 1
  year: 1995
  end-page: 11
  article-title: Locus‐specific amplification of HLA class I genes from genomic DNA: locus‐specific sequences in the first and third introns of HLA‐A, ‐B, and ‐C alleles
  publication-title: Tissue Antigens
– volume: 64
  start-page: 1224
  year: 2016
  end-page: 1231
  article-title: Impact of direct acting antiviral therapy in patients with chronic hepatitis C and decompensated cirrhosis
  publication-title: J. Hepatol.
– volume: 3
  start-page: 1683
  year: 2017
  end-page: 16913
  article-title: The burden of primary liver cancer and underlying etiologies from 1990 to 2015 at the global, regional, and national level: results from the global burden of disease study 2015
  publication-title: JAMA Oncol.
– volume: 65
  start-page: 719
  year: 2016
  end-page: 726
  article-title: Unexpected high rate of early tumor recurrence in patients with HCV‐related HCC undergoing interferon‐free therapy
  publication-title: J. Hepatol.
– volume: 11
  year: 2016
  article-title: DAAs rapidly reduce inflammation but increase serum VEGF level: a rationale for tumor risk during anti‐HCV treatment
  publication-title: PLoS One
– volume: 184
  start-page: 404
  year: 2021
  end-page: 421.e16
  article-title: Single‐cell landscape of the ecosystem in early‐relapse hepatocellular carcinoma
  publication-title: Cell
– volume: 68
  start-page: 827
  year: 2018
  end-page: 838
  article-title: Direct‐acting antiviral sustained virologic response: impact on mortality in patients without advanced liver disease
  publication-title: Hepatology
– volume: 80
  start-page: 22
  year: 1997
  end-page: 33
  article-title: In situ simultaneous detection of hepatitis C virus RNA and hepatitis C virus‐related antigens in hepatocellular carcinoma
  publication-title: Cancer
– volume: 71
  start-page: 44
  year: 2020
  end-page: 55
  article-title: Long‐term risk of hepatocellular carcinoma in HCV patients treated with direct acting antiviral agents
  publication-title: Hepatology
– volume: 67
  start-page: 358
  year: 2018
  end-page: 380
  article-title: AASLD guidelines for the treatment of hepatocellular carcinoma
  publication-title: Hepatology
– volume: 83
  start-page: 168
  year: 2014
  end-page: 173
  article-title: The distribution of KIR‐HLA functional blocks is different from north to south of Italy
  publication-title: Tissue Antigens
– volume: 9
  start-page: 207
  year: 2019
  end-page: 214
  article-title: Therapy with oral directly acting agents in hepatitis C infection is associated with reduction in fibrosis and increase in hepatic steatosis on transient elastography
  publication-title: J. Clin. Exp. Hepatol.
– volume: 157
  start-page: 1253
  year: 2019
  end-page: 1263
  article-title: Direct‐acting antiviral therapy for hepatitis C virus infection is associated with increased survival in patients with a history of hepatocellular carcinoma
  publication-title: Gastroenterology
– volume: 13
  start-page: 3267
  year: 2021
  article-title: Investigation of the effect of KIR‐HLA pairs on hepatocellular carcinoma in hepatitis C virus cirrhotic patients
  publication-title: Cancers
– ident: e_1_2_9_11_1
  doi: 10.1016/j.jhep.2016.04.008
– ident: e_1_2_9_25_1
  doi: 10.1016/j.jhep.2016.01.029
– ident: e_1_2_9_2_1
  doi: 10.1002/hep.30823
– ident: e_1_2_9_5_1
  doi: 10.1002/hep.29855
– ident: e_1_2_9_20_1
  doi: 10.4049/jimmunol.1501358
– ident: e_1_2_9_31_1
  doi: 10.1111/tan.13754
– ident: e_1_2_9_15_1
  doi: 10.1016/j.coi.2004.07.010
– ident: e_1_2_9_23_1
  doi: 10.1182/blood-2008-02-137521
– ident: e_1_2_9_19_1
  doi: 10.1084/jem.182.2.605
– ident: e_1_2_9_27_1
  doi: 10.1111/j.1600-065X.1997.tb00935.x
– ident: e_1_2_9_8_1
  doi: 10.1001/jamaoncol.2017.3055
– ident: e_1_2_9_18_1
  doi: 10.1111/j.1399-0039.1995.tb02408.x
– ident: e_1_2_9_28_1
  doi: 10.1038/ng2077
– ident: e_1_2_9_7_1
  doi: 10.1002/hep.29086
– ident: e_1_2_9_16_1
  doi: 10.1093/infdis/jit801
– ident: e_1_2_9_4_1
  doi: 10.1002/hep.29811
– ident: e_1_2_9_21_1
  doi: 10.1016/j.humimm.2008.05.001
– ident: e_1_2_9_30_1
  doi: 10.1016/j.humimm.2017.10.008
– ident: e_1_2_9_14_1
  doi: 10.1002/(SICI)1097-0142(19970701)80:1<22::AID-CNCR4>3.0.CO;2-H
– ident: e_1_2_9_6_1
  doi: 10.1053/j.gastro.2019.07.033
– ident: e_1_2_9_9_1
  doi: 10.1002/hep.29811
– ident: e_1_2_9_29_1
  doi: 10.4049/jimmunol.168.5.2307
– ident: e_1_2_9_26_1
  doi: 10.1016/j.cell.2020.11.041
– ident: e_1_2_9_17_1
  doi: 10.1111/j.1399-0039.2007.00923.x
– ident: e_1_2_9_10_1
  doi: 10.1016/j.jhep.2016.06.009
– ident: e_1_2_9_32_1
  doi: 10.1111/tan.12299
– ident: e_1_2_9_33_1
  doi: 10.3390/cancers13133267
– ident: e_1_2_9_24_1
  doi: 10.1053/j.gastro.2019.07.040
– ident: e_1_2_9_12_1
  doi: 10.1371/journal.pone.0167934
– ident: e_1_2_9_13_1
  doi: 10.1002/1097-0142(19940501)73:9<2253::AID-CNCR2820730904>3.0.CO;2-9
– ident: e_1_2_9_3_1
  doi: 10.1016/j.jceh.2018.06.009
– ident: e_1_2_9_22_1
  doi: 10.1093/nar/gkq1128
SSID ssj0009659
Score 2.4499657
Snippet Background and aims Second‐generation direct‐acting antivirals (2G DAA) to cure HCV have led to dramatic clinical improvements. HCV‐associated hepatocellular...
Second-generation direct-acting antivirals (2G DAA) to cure HCV have led to dramatic clinical improvements. HCV-associated hepatocellular carcinoma (HCC),...
Background and aimsSecond‐generation direct‐acting antivirals (2G DAA) to cure HCV have led to dramatic clinical improvements. HCV‐associated hepatocellular...
In patients with hepatitis C cirrhosis who are treated with 2G DAA, predicted weak NK cell-mediated immunity may predispose to HCC development more than...
SourceID pubmedcentral
proquest
pubmed
crossref
wiley
SourceType Open Access Repository
Aggregation Database
Index Database
Publisher
StartPage e2350678
SubjectTerms Adult
Aged
Antiviral Agents
Antiviral Agents - therapeutic use
Antiviral drugs
Carcinoma
Carcinoma, Hepatocellular - immunology
Cirrhosis
Complementation
Female
Follow-Up Studies
Hepacivirus - immunology
Hepatitis C
Hepatitis C - complications
Hepatitis C - drug therapy
Hepatitis C - immunology
Hepatitis C, Chronic - complications
Hepatitis C, Chronic - drug therapy
Hepatitis C, Chronic - immunology
Hepatocellular
Hepatocellular carcinoma
HLA Antigens - immunology
Humans
Immunity
Immunity, Cellular
Innate
Killer cell immunoglobulin-like receptors
Killer Cells
Killer Cells, Natural - immunology
Liver cancer
Liver cirrhosis
Liver Neoplasms - immunology
Male
Middle Aged
Natural
Natural killer cells
Receptors, KIR - immunology
Tissue typing
Title Hepatocellular carcinoma after direct‐acting antivirals for hepatitis C is associated with KIR‐HLA types predicting weak NK cell‐mediated immunity
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Feji.202350678
https://www.ncbi.nlm.nih.gov/pubmed/38700055
https://www.proquest.com/docview/3089842181
https://www.proquest.com/docview/3050938349
https://pubmed.ncbi.nlm.nih.gov/PMC11745084
Volume 54
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV3NTtwwEB61SK16oS39S0uRK1W9VFmysb2JjwiBFiioQkXilsaODVtKFrFZVfTUR-DI8_EkzNjZ0C1SpaqHbKKNJ46TmfFnZ_wNwPtEGV7mXMR2UJmY2O9iJVITqzTJnHQm45oGirt7g-GB2D6Uh22eU1oLE_ghugk3sgzvr8nASz1ZvSUNtd9GPcr9Lcnfog-meC0CRfu39FFElhc8sYhTlSctxybKr85Jz_dJd4Dm3XjJ33Gs74g2H8PXWRNC_MlJb9ronvn5B7vjf7TxCSy2IJWtBa16CvdsvQQPQtrKiyV4uNt-kH8GV0PszpoxTf9TPCszlJqoHp-WzCcfZ6HHvP51Sesn6iOG73FEYcXfJwzRMjsmaWJVYusMf8pWV2zFaH6Y7Wzto-jw0xqjmeIJOzuniv2FftjyhO3tMKoZy_gFMCQ38utdmovncLC58WV9GLfJHmJDhDJxpgyCH-dcP9fGytQaaTMxENaoNLO50JJbyysuha6MduiorckQCzncmZIr_gIW6nFtXwEzLuVaJk5WKheuj8cEy3JXSdyETSP4MHvdxVng9CgCe3Na4BMvuicewfJMGYrWtCcFT_BagpBRBO-602iU1OCytuMplUEchmN_oSJ4GXSnq4mjhyTmswjyOa3qChDh9_yZenTsib_7OHxEQC0i-Oi15u93X2xsb0mEp6__qfQbeIT_iRDjuAwLzfnUvkXc1egVuJ-KzyvexG4ACcQtcA
linkProvider Wiley-Blackwell
linkToHtml http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1Lb9QwEB5BEY8Lj1IgUMBIiAvKNhvbm-RYlVbZ7uNQtVJvUeLYdClkq25WqD31J_TY38cvYcbOpl0qISEOeUh-xcnM-LMz_gbgY5Aonsdc-LpXKp_Y7_xEhMpPwiAy0qiIFzRRHI176YHYPZSHN3bxO36IdsGNNMPaa1JwWpDeuGYN1d8mHQr-Lcng3oV7FNWb2PO_7F0TSBFdnrPFwg-TOGhYNrGCjaXiy6PSLah522PyJpK1Q9HOE8gXnXAeKMedeV101Pkf_I7_08un8LjBqWzTCdYzuKOrVbjvIleercKDUfNP_jlcpTii1VP6A0AurUxRdKJq-iNnNv44c4Pmr4tL2kJRfWX4KSfkWfx9xhAwsyMqTcRKbIvhKW_ERZeMlojZoL-HRdPhJqPF4hk7OaWGbUU_dX7MxgNGLWMeuweGyk3slpf6bA0Odrb3t1K_iffgK-KU8aNEIf4xxnTjQmkZaiV1JHpCqySMdCwKybXmJZeiKFVh0FZrFSEcMnhROU_4C1ipppV-BUyZkBcyMLJMYmG6eE_ILDalxEPo0INPi--dnThaj8wROIcZvvGsfeMerC-kIWu0e5bxAOsSBI48-NAmo15Sh_NKT-eUB6EYTv9F4sFLJzxtSxyNJJGfeRAviVWbgTi_l1OqyZHl_u7iDBIxtfDgsxWbvz99tr3bl4hQX_9T7vfwMN0fDbNhfzx4A48wXTiXx3VYqU_n-i3CsLp4ZzXtN5f0MLU
linkToPdf http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1LT9wwEB4VqiIuVUt5pKWtK1W9VIGsH5v4iCirXRZWCIHELUocG7aP7IpdVHHrT-ixv6-_pDN2CF0hVeohD8mvJJPxfLbH3wC8T7QRRSZkbLuViYn9LtaSm1jzJHXKmVSUNFA8HnX75_LwQl00cU5pL0zgh2gn3EgzfH9NCj6t3O49aaj9PN6h2N-K-tsleEwLfuTTxeXJPetuVwX825Ex11nSkGxiBbsLxReN0gOk-dBh8m8g6y1R7xk8bSAk2wsyfw6PbL0GT0JQyds1WDlulstfwK8-Gpv5hCbnyduUGQocVE--FcyHBmfBnv3-8ZN2N9SXDL_ymJx-v84YYll2RaWJ84jtMzwVjSRtxWj2lg0Hp1i0f7THaB53xqbX1LCv6LstvrDRkFHLmMdvT6FyY78bZX67Due9g7P9ftyEYogN0b3EqTYITZxznaw0VnFrlE1lV1qjeWozWSphraiEkmVlSofdqDUpIhWHF1MILTZguZ7UdguYcVyUKnGq0pl0Hbwn0JS5SuEhLY_gw50s8mlg3MgDtzLPUWh5K7QItu8klTeKN8tFgnVJwi0RvGuTUWXohYvaTm4oD6IkHJlLHcFmEGzbksD-i3jJIsgWRN5mIDruxZR6fOVpuTs4uEO4KyP46P-Ofz99fnA4UAgeX_5X7rewcvKplx8NRsNXsIrJMjgjbsPy_PrGvkaANC_feCX4A5i1DmY
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Hepatocellular+carcinoma+after+direct%E2%80%90acting+antivirals+for+hepatitis+C+is+associated+with+KIR%E2%80%90HLA+types+predicting+weak+NK+cell%E2%80%90mediated+immunity&rft.jtitle=European+journal+of+immunology&rft.au=Ryan%2C+James+C.&rft.au=Haight%2C+Christina&rft.au=Niemi%2C+Erene+C.&rft.au=Grab%2C+Joshua+D.&rft.date=2024-08-01&rft.issn=0014-2980&rft.eissn=1521-4141&rft.volume=54&rft.issue=8&rft.epage=n%2Fa&rft_id=info:doi/10.1002%2Feji.202350678&rft.externalDBID=10.1002%252Feji.202350678&rft.externalDocID=EJI5727
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0014-2980&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0014-2980&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0014-2980&client=summon