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  • 1
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    Online Resource
    Prognostic Value of Ventricular‐Arterial Coupling After Transcatheter Aortic Valve Replacement on Midterm Clinical Outcomes
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Journal of the American Heart Association Vol. 10, No. 18 ( 2021-09-21)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 10, No. 18 ( 2021-09-21)
    Abstract: Ventricular‐arterial coupling predicts outcomes in patients with heart failure. The arterial elastance to end‐systolic elastance ratio (Ea/Ees) is a noninvasively assessed index that reflects ventricular‐arterial coupling. We aimed to determine the prognostic value of ventricular‐arterial coupling assessed through Ea/Ees after transcatheter aortic valve replacement to predict clinical events. Methods and Results We retrieved data on 1378 patients (70% women) who underwent transcatheter aortic valve replacement between October 2013 and May 2017 from the OCEAN‐TAVI (Optimized transCathEter vAlvular iNtervention) Japanese multicenter registry. We determined the association between Ea/Ees and the composite end point of hospitalization for heart failure and cardiovascular death by classifying the patients into quartiles based on Ea/Ees values (group 1: 〈 0.326; group 2: 0.326–0.453; group 3: 0.453–0.666; and group 4: 〉 0.666) during the midterm follow‐up after transcatheter aortic valve replacement. During a median follow‐up period of 736 days (interquartile range, 414–956), there were 247 (17.9%) all‐cause deaths, 89 (6.5%) cardiovascular deaths, 130 (9.4%) hospitalizations for heart failure, and 199 (14.4%) composite events of hospitalization for heart failure and cardiovascular death. The incidence of the composite end point was significantly higher in group 2 (hazard ratio [HR], 1.76; 95% CI, 1.08–2.87 [ P =0.024]), group 3 (HR, 2.43; 95% CI, 1.53–3.86 [ P 〈 0.001]), and group 4 (HR, 2.89; 95% CI, 1.83–4.57 [ P 〈 0.001]) than that in group 1. On adjusted multivariable Cox analysis, Ea/Ees was significantly associated with composite events (HR, 1.47 per 1‐unit increase; 95% CI, 1.08–2.01 [ P =0.015]). Conclusions These findings suggest that a higher Ea/Ees at discharge after transcatheter aortic valve replacement is associated with adverse clinical outcomes during midterm follow‐up. Registration URL: https://www.upload.umin.ac.jp/ . Unique identifier: UMIN000020423.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.120.019267
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
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  • 2
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    Gab1 in livers with persistent hepatocyte apoptosis has an antiapoptotic effect and reduces chronic liver injury, fibrosis, and tumorigenesis
    American Physiological Society ; 2021
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 320, No. 6 ( 2021-06-01), p. G958-G968
    Details
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 320, No. 6 ( 2021-06-01), p. G958-G968
    Abstract: Grb2-associated binder 1 (Gab1) is an adaptor protein that is important for intracellular signal transduction by receptor tyrosine kinases that are receptors for various growth factors and plays an important role in rapid liver regeneration after partial hepatectomy and during acute hepatitis. On the other hand, mild liver regeneration is induced in livers of individuals with chronic hepatitis, where hepatocyte apoptosis is persistent; however, the impact of Gab1 on such livers remains unclear. We examined the role of Gab1 in chronic hepatitis. Gab1 knockdown enhanced the decrease in cell viability and apoptosis induced by ABT-737, a Bcl-2/-xL/-w inhibitor, in BNL.CL2 cells, while cell viability and caspase activity were unchanged in the absence of ABT-737. ABT-737 treatment induced Gab1 cleavage to form p35-Gab1. p35-Gab1 was also detected in the livers of mice with hepatocyte-specific Mcl-1 knockout (KO), which causes persistent hepatocyte apoptosis. Gab1 deficiency exacerbated hepatocyte apoptosis in Mcl-1 KO mice with posttranscriptional downregulation of Bcl-XL. In BNL.CL2 cells treated with ABT-737, Gab1 knockdown posttranscriptionally suppressed Bcl-xL expression, and p35-Gab1 overexpression enhanced Bcl-xL expression. Gab1 deficiency in Mcl-1 KO mice activated STAT3 signaling in hepatocytes, increased hepatocyte proliferation, and increased the incidence of liver cancer with the exacerbation of liver fibrosis. In conclusion, Gab1 is cleaved in the presence of apoptotic stimuli and forms p35-Gab1 in hepatocytes. In chronic liver injury, the role of Gab1 in suppressing apoptosis and reducing liver damage, fibrosis, and tumorigenesis is more important than its role in liver regeneration. NEW & NOTEWORTHY Grb2-associated binder 1 (Gab1) is known to contribute to liver regeneration after acute liver injury. However, in chronic liver diseases, Gab1 plays a greater role in suppressing hepatocyte apoptosis than in liver regeneration, resulting in suppression of hepatocyte proliferation, liver fibrosis, and liver carcinogenesis.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    URL: Article
    DOI: 10.1152/ajpgi.00370.2020
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2021
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  • 3
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    Immunosuppressive CD29 + Treg accumulation in the liver in mice on checkpoint inhibitor therapy
    BMJ ; 2023
    In:  Gut
    Details
    In: Gut, BMJ
    Abstract: Liver metastases are often resistant to immune checkpoint inhibitor therapy (ICI) and portend a worse prognosis compared with metastases to other locations. Regulatory T cells (Tregs) are one of several immunosuppressive cells implicated in ICI resistance of liver tumours, but the role played by Tregs residing within the liver surrounding a tumour is unknown. Design Flow cytometry and single-cell RNA sequencing were used to characterise hepatic Tregs before and after ICI therapy. Results We found that the murine liver houses a Treg population that, unlike those found in other organs, is both highly proliferative and apoptotic at baseline. On administration of αPD-1, αPD-L1 or αCTLA4, the liver Treg population doubled regardless of the presence of an intrahepatic tumour. Remarkably, this change was not due to the preferential expansion of the subpopulation of Tregs that express PD-1. Instead, a subpopulation of CD29 + ( Itgb1 , integrin β1) Tregs, that were highly proliferative at baseline, doubled its size in response to αPD-1. Partial and full depletion of Tregs identified CD29 + Tregs as the prominent niche-filling subpopulation in the liver, and CD29 + Tregs demonstrated enhanced suppression in vitro when derived from the liver but not the spleen. We identified IL2 as a critical modulator of both CD29 + and CD29 − hepatic Tregs, but expansion of the liver Treg population with αPD-1 driven by CD29 + Tregs was in part IL2-independent. Conclusion We propose that CD29 + Tregs constitute a unique subpopulation of hepatic Tregs that are primed to respond to ICI agents and mediate resistance.
    Type of Medium: Online Resource
    ISSN: 0017-5749 , 1468-3288
    URL: Article
    DOI: 10.1136/gutjnl-2023-330024
    RVK:
    XA 10000
    Language: English
    Publisher: BMJ
    Publication Date: 2023
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  • 4
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    Letter: serum growth differentiation factor 15 predicts hepatocellular carcinoma occurrence after hepatitis C virus elimination—authors' reply
    Wiley ; 2022
    In:  Alimentary Pharmacology & Therapeutics Vol. 55, No. 8 ( 2022-04), p. 1061-1062
    Details
    In: Alimentary Pharmacology & Therapeutics, Wiley, Vol. 55, No. 8 ( 2022-04), p. 1061-1062
    Abstract: This article is linked to Myojin.et al’s paper. To view this article, visit https://doi.org/10.1111/apt.16691 and https://doi.org/10.1111/apt.16834
    Type of Medium: Online Resource
    ISSN: 0269-2813 , 1365-2036
    URL: Issue
    URL: Article
    DOI: 10.1111/apt.v55.8
    DOI: 10.1111/apt.16862
    Language: English
    Publisher: Wiley
    Publication Date: 2022
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    SSG: 15,3
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  • 5
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    Interleukin-6 Is a Circulating Prognostic Biomarker for Hepatocellular Carcinoma Patients Treated with Combined Immunotherapy
    MDPI AG ; 2022
    In:  Cancers Vol. 14, No. 4 ( 2022-02-10), p. 883-
    Details
    In: Cancers, MDPI AG, Vol. 14, No. 4 ( 2022-02-10), p. 883-
    Abstract: Atezolizumab/bevacizumab (Atezo/Bev) combination therapy has become a front-line therapy for advanced hepatocellular carcinoma (HCC), but approximately 20% of patients are nonresponders. We investigated circulating biomarkers to predict therapeutic outcomes. We performed simultaneous measurement of 34 proteins using a multiplex bead-based immunoassay in baseline plasma from 34 patients who underwent Atezo/Bev therapy as first- or second-line treatment. Logistic regression analysis showed that plasma IL-6 and interferon alpha (IFNα) levels were significant predictors of non-responders (odds ratio of 13.33 and FDR p = 0.021 for IL-6 and IFNα). The progression-free survival (PFS) and overall survival (OS) of patients with high IL-6 levels were significantly shorter than those of patients with low IL-6 levels. Next, we measured baseline plasma IL-6 levels in 64 HCC patients who underwent Atezo/Bev therapy by ELISA. The IL-6-high group showed higher female ratio, AST levels, tumor markers, Child–Pugh score, and vascular invasion ratio. The PFS and OS of the IL-6-high group were significantly shorter than those of the IL-6-low group. Multivariate Cox proportional hazards analysis showed that IL-6 level and age were independent risk factors for disease progression (hazard ratio of 2.785 and p = 0.015 for IL-6, and hazard ratio 0.306 and p = 0.03 for age). In conclusion, circulating IL-6 levels are a novel prognostic biomarker for advanced HCC patients who undergo combined immunotherapy.
    Type of Medium: Online Resource
    ISSN: 2072-6694
    URL: Article
    DOI: 10.3390/cancers14040883
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2527080-1
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  • 6
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    Generation and Detection of Media Clones
    Institute of Electronics, Information and Communications Engineers (IEICE) ; 2021
    In:  IEICE Transactions on Information and Systems Vol. E104.D, No. 1 ( 2021-1-1), p. 12-23
    Details
    In: IEICE Transactions on Information and Systems, Institute of Electronics, Information and Communications Engineers (IEICE), Vol. E104.D, No. 1 ( 2021-1-1), p. 12-23
    Type of Medium: Online Resource
    ISSN: 0916-8532 , 1745-1361
    URL: Article
    DOI: 10.1587/transinf.2020MUI0002
    Language: English
    Publisher: Institute of Electronics, Information and Communications Engineers (IEICE)
    Publication Date: 2021
    detail.hit.zdb_id: 2214518-7
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  • 7
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    Phase I/II study of PexaVec in combination with immune checkpoint inhibition in refractory metastatic colorectal cancer
    BMJ ; 2023
    In:  Journal for ImmunoTherapy of Cancer Vol. 11, No. 2 ( 2023-02), p. e005640-
    Details
    In: Journal for ImmunoTherapy of Cancer, BMJ, Vol. 11, No. 2 ( 2023-02), p. e005640-
    Abstract: Oncolytic immunotherapy represents a unique therapeutic platform for the treatment of cancer. Here, we evaluated the safety and efficacy of the combination of pexastimogene devacirepvec (PexaVec) plus durvalumab (anti-programmed death ligand 1) with and without tremelimumab (anti-cytotoxic T-lymphocyte associated protein 4) in patients with standard chemotherapy refractory mismatch repair proficient (pMMR) metastatic colorectal cancer (mCRC) in a phase I/II trial. Methods Adult patients with histologically confirmed advanced pMMR mCRC, who had progressed on at least two prior lines of systemic chemotherapy were studied in four cohorts. Patients received four doses of PexaVec IV at a dose of 3×10 8 plaque forming units (pfu) (dose level 1) or 1×10 9  pfu (dose level 2) every 2 weeks. Twelve days after the first PexaVec administration, patients received either 1500 mg of durvalumab every 28 days alone or an additional single dose of 300 mg tremelimumab on day 1. Responses were assessed every 8 weeks by CT or MRI. AEs were recorded. The primary endpoints were safety and feasibility. Secondary endpoints included progression-free survival (PFS) and overall survival. Paired tumor samples and peripheral blood were collected to perform immune monitoring. Results Thirty-four patients with mCRC enrolled on to the study: 16 patients in the PexaVec/durvalumab cohorts and 18 patients in the PexaVec/durvalumab/tremelimumab cohorts. Overall, the combination of PexaVec plus immune checkpoint inhibitors did not result in any unexpected toxicities. Most common toxicities observed were fever and chills after PexaVec infusion. Two cases of grade 3 colitis, one case of a grade 2 myositis and one case of grade 3 hypotension resulted in discontinuation of immune checkpoint inhibitor and PexaVec treatment, respectively. The median PFS in the PexaVec/durvalumab/tremelimumab cohorts was 2.3 months (95% CI: 2.2 to 3.2 months) vs 2.1 months (95% CI: 1.7 to 2.8 months; p=0.57) in the PexaVec/durvalumab cohorts. Flow cytometry analysis of peripheral blood mononuclear cells revealed an increase in Ki67 + CD8 + T cells on treatment. Conclusion PexaVec in combination with durvalumab and tremelimumab is safe and tolerable. No unexpected toxicities were observed. The combination of PexaVec/durvalumab/tremelimumab demonstrated potential clinical activity in patients with pMMR mCRC, but further studies are needed to identify the predictive biomarkers. Trial registration number NCT03206073 .
    Type of Medium: Online Resource
    ISSN: 2051-1426
    URL: Article
    DOI: 10.1136/jitc-2022-005640
    Language: English
    Publisher: BMJ
    Publication Date: 2023
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  • 8
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    Table_1.xlsx
    Frontiers Media SA ; 2022
    In:  Frontiers in Immunology Vol. 13 ( 2022-6-27)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 13 ( 2022-6-27)
    Abstract: Innate lymphoid cells (ILC) are a heterogeneous and plastic population of cells of the innate immune system. Their role in cancer and specifically in hepatocellular carcinoma is unraveling. The presence of ILCs in peripheral blood of HCC patients has not been explored yet. Their role and function in response to checkpoint inhibitor therapy have also not been explored. Here, we characterized ILCs in PBMC of HCC patients at baseline and after treatment with immune checkpoint inhibitors (ICI) by flow cytometry and single-cell sequencing. Characterization of ILC subsets in PBMCs of HCC patients showed a significant increase in ILC1 and a decrease in ILC3 frequencies. Single-cell RNA-sequencing identified a subgroup of NK-like ILCs which expressed cytotoxicity markers as well as NKp80/ KLRF1 . This KLRF1 high NK-like population showed low abundance in patients with HCC and was enhanced after combined anti-CTLA-4 and anti-PD-1immunotherapy. Trajectory analysis placed this population in between ILC1 and ILC3 cells. The transcriptomic signature of KLRF1 high NK-like ILCs was associated with better progression-free survival in large HCC cohorts. This study shows a previously unknown effect of ICI on the composition and plasticity of ILCS in peripheral blood. Thus, ILCs from PBMC can be used to study changes in the innate immune system under immunotherapy.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fimmu.2022.849958
    DOI: 10.3389/fimmu.2022.849958.s001
    DOI: 10.3389/fimmu.2022.849958.s002
    DOI: 10.3389/fimmu.2022.849958.s003
    DOI: 10.3389/fimmu.2022.849958.s004
    DOI: 10.3389/fimmu.2022.849958.s005
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
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  • 9
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    Abstract 2582: Regulatory T cells restrain efficacy of immunotherapy in murine liver tumors
    American Association for Cancer Research (AACR) ; 2022
    In:  Cancer Research Vol. 82, No. 12_Supplement ( 2022-06-15), p. 2582-2582
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 82, No. 12_Supplement ( 2022-06-15), p. 2582-2582
    Abstract: Background: Checkpoint blockade immunotherapy (CBI) can induce a durable response for some patients with hepatic tumors, but many derive no or incomplete oncologic benefit for unclear reasons. Regulatory T cells (Tregs) in the liver play a central role in maintaining the tolerogenic local immune environment, both in homeostasis and disease. Here we sought to explore the impact of CBI on hepatic Tregs to determine if they play a role in CBI resistance of liver tumors in mice. Methods: High-dimensional flow cytometry was used to examine the ex vivo characteristics of lymphocytes from both tumor-free and orthotopic tumor-bearing livers of mice treated with CBI or other immunomodulatory agents. Results: All hepatic T cell subsets examined displayed higher proliferative and apoptotic indices compared with those of splenic T lymphocytes. We found that hepatic Tregs intensely proliferate and undergo apoptosis compared with splenic Tregs under homeostatic conditions. Hepatic Treg proliferation was enhanced after administration of CBI treatment. This effect was abrogated by co-treatment with sirolimus. CD8, macrophages, and the gut microbiome were found to be dispensable for the in vivo in response to αPD1. Co-treatment of mice with αPD1 and αCD25 sensitized MC38-bearing liver tumors. Conclusion: Murine liver Tregs naturally proliferate and undergo apoptosis due to the mTOR rheostat at homeostasis making them highly responsive to CBI. This behavior potentially explains liver-specific CBI-resistance in tumors. Citation Format: Benjamin L. Green, Chi Ma, Qianfei Zhang, Benjamin Ruf, Umberto Rosato, Jonathan Qi, Simon Wabitsch, Kylynda Bauer, Yuta Myojin, Justin McCallen, John C. McVey, Varun Subramanyam, Vanessa Catania, Amran Nur, Firouzeh Korangy, Changqing Xie, Tim F. Greten. Regulatory T cells restrain efficacy of immunotherapy in murine liver tumors [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2582.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2022-2582
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
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  • 10
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    Abstract 351: Serum ST6GAL1 is a novel biomarker for predicting efficacy of tyrosine kinase inhibitors in hepatocellular carcinoma by detecting FGF19 expressing tumor
    American Association for Cancer Research (AACR) ; 2021
    In:  Cancer Research Vol. 81, No. 13_Supplement ( 2021-07-01), p. 351-351
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 81, No. 13_Supplement ( 2021-07-01), p. 351-351
    Abstract: Background: Several tyrosine kinase inhibitors (TKIs) have been developed for hepatocellular carcinoma (HCC). However, their efficacy is limited partly due to the diversity of its genetic drivers. In this study, we sought for HCC oncogenes involved in susceptibility of TKIs and aimed to develop their serum biomarkers. Methods: We created a novel HCC mouse model in which tumor diversity of genetic drivers was recapitulated by transposon-based intrahepatic delivery of a pooled barcode-tagged 10-oncogene cDNA library. Tumor-bearing mice were then treated with lenvatinib (LEN), or sorafenib (SOR), or vehicle until moribund. The relative abundance of each oncogene cDNA in each tumor was quantified by a high-throughput barcode sequence. In vitro LEN susceptibility was assessed in 9 human HCC cell lines and LEN-resistant Hep3B cells (LEN-R) established by its long-term exposure. Tumor-derived secreted proteins were screened via cellular proteomic and secretomic analyses of Huh7 and Hep3B cells. Serum and tumor levels of identified proteins were examined in 62 HCC patients who underwent hepatectomy. Efficacy of biomarker candidates was assessed using pre-treated serum of 96 HCC patients who underwent TKI therapy. Results: Mice developed multiple genetically heterogeneous liver tumors as early as 2 weeks after delivery of the pooled library. Upon TKI administration, their sequencing analysis showed that LEN selectively eliminated FGF19-expressing tumors, whereas SOR did MET- and NRAS-expressing tumors. Among 9 HCC cell lines, HuH7 and Hep3B cells showed the highest FGF19 levels and LEN susceptibility. FGF19 inhibition eliminated their susceptibility. LEN-R cells showed reduction of FGF19 levels and got resensitized to LEN by FGF19 replenishment. Thus, FGF19-driven HCC is susceptible to LEN. Proteomics identified 6 secreted proteins downregulated by FGF19 inhibition in Hep3B cells. Among them, ST6GAL1 was the most positively correlated with FGF19 in HCC cell lines and in mouse and human HCC tissues. FGF19 knockdown in Hep3B cells decreased phosphorylation of STAT3, whereas FGF19 overexpression increased its phosphorylation with ST6GAL1 upreguation. Silencing of STAT3 signal by inhibitor or siRNA significantly decreased ST6GAL1 expression. In surgically-resected HCC patients, serum ST6GAL1 levels were positively correlated with tumor site FGF19 expression and were markers for disease progression. In TKI-treated HCC patients with high baseline serum ST6GAL1 levels, LEN therapy showed significantly longer survival than SOR. Conclusion: ST6GAL1 is a tumor-derived secreted protein downstream of FGF19 and may be a useful serum biomarker for identification of patients with FGF19-driven HCC who may benefit from LEN therapy. Citation Format: Yuta Myojin, Takahiro Kodama, Hayato Hikita, Ryotaro Sakamori, Tetsuo Takehara. Serum ST6GAL1 is a novel biomarker for predicting efficacy of tyrosine kinase inhibitors in hepatocellular carcinoma by detecting FGF19 expressing tumor [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 351.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2021-351
    RVK:
    XA 36000
    RVK:
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
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