PDF - 924K, Supplementary Figure 1: Morphology and growth curves of MHCC97L, MHCC97L/CisR and MHCC97L/DoxR cells. Supplementary Figure 2: In vivo growth rate of MHCC97L, MHCC97L/CisR and MHCC97L/DoxR cells in nude mice. Supplementary Figure 3: Experimental flow for identification of chemoresistant targets. Supplementary Figure 4: Expression profiles of candidate genes in chemoresistant cells. Supplementary Figure 5: The persistence of TMEM98 expression after drug treatment. Supplementary Figure 6: The expression level of TMEM98 after transfection of TMEM98 siRNA. Supplementary Figure 7: MTT cytotoxic assay of PLC-pcDNA3.1 and PLC-TMEM98 cells in cisplatin or doxorubicin treatment. Supplementary Figure 8: MTT cytotoxic assay of MHCC97L-pcDNA3.1 and MHCC97L-TMEM98 cells under the treatment of sorafenib.

Supplementary Figure 1: Computational Modeling Study.

PDF file - 104KB, Clinical features of IDH1-mutant intrahepatic cholangiocarcinoma patients in the Screening cohort.

PDF file - 67KB, Characteristics of all intrahepatic cholangiocarcinoma patients evaluated across the two cohorts.

Supplementary Figure Legends 1-3 from Lupeol Suppresses Cisplatin-Induced Nuclear Factor-κB Activation in Head and Neck Squamous Cell Carcinoma and Inhibits Local Invasion and Nodal Metastasis in an Orthotopic Nude Mouse Model

Supplementary Figure 1. CONSORT diagram

Association of NR1I3 haplotype with TTP (Supplementary Online only). CAT/CAT carriers, median TTP 1.92 months vs 6.21 months for CAT/â^' or â^'/â^' carriers.

Supplementary Tables 1-8 and Supplementary Figures 1-3 legends Supplementary Table 1: List of Investigators for the HEAT Study Supplementary Table 2: Summary of RFA Treatment Supplementary Table 3: Stepwise Multivariate Cox Modelling Results Supplementary Table 4: Overall Survival According to Stage Supplementary Table 5: Evaluation of Treatment Failure Supplementary Table 6: Overview of Treatment-Emergent Adverse Events Supplementary Table 7: Treatment-Emergent Adverse Events by Preferred Term Supplementary Table 8: Key Treatment-Emergent Adverse Events Among Subjects With a Solitary Tumor by 45-Minute RFA Cutpoint

Supplementary Figure 2b: Kaplan-Meier Survival Estimates:(B) Subset: Solitary lesion and RFA dwell time {greater than or equal to}45 min, n=285.

Supplementary Figures 1-6 from The Kringle 1 Domain of Hepatocyte Growth Factor Has Antiangiogenic and Antitumor Cell Effects on Hepatocellular Carcinoma

Background and Objective Hong Kong, like many parts of Asia, faces a high burden of hepatocellular carcinoma (HCC) caused by high endemic rates of hepatitis B virus infection. Hong Kong clinicians have developed a high level of expertise in HCC treatment across surgical, transarterial, ablative, radiotherapeutic and systemic modalities. This publication summarizes the latest evidence-based recommendations on how these modalities should be used. Methods In two meetings held in 2020, a multidisciplinary panel of surgeons, oncologists and interventional radiologists performed a narrative review of evidence on the management of HCC, with an emphasis on treatment of HCC not amenable to surgical resection. Close attention was paid to new evidence published since the previous version of these statements in 2018. Key Content and Findings The expert panel has formulated 60 consensus statements to guide the staging and treatment of unresectable HCC. Since the previous version of these statements, considerable additions have been made to the recommendations on use of targeted therapies and immunotherapies because of the large volume of new evidence. Conclusions Our consensus statements offer guidance on how to select HCC patients for surgical or non-surgical treatment and for choosing among non-surgical modalities for patients who are not candidates for resection. In particular, there is a need for more evidence to aid physicians in the selection of second-line systemic therapies, as currently most data are limited to patients with disease progression on first-line sorafenib.

PDF file - 57KB, Levels of serum 2HG relative to tumor burden in IDH1-mutant and IDH2-mutant intrahepatic cholangiocarcinoma patients in the Validation cohort.

Supplementary Figure 3: Forest Plot of Hazard Ratio of Treatment Effect on Progression-Free Survival, According to Baseline Prognostic Factors. (A) Intent-to-treat population, n=701; (B) Subset: Solitary lesion (BCLC A) and RFA dwell time {greater than or equal to}45 min, n=285.

PDF - 150K, Supplementary Table 1: List of primers. Supplementary Table 2: List of commonly up-regulated genes in drug resistant sublines. Supplementary Table 3: List of commonly down-regulated genes in drug resistant sublines. Supplementary Table 4: List of differential genes with 10-fold changes in MHCC97L/CisR and MHCC97L/DoxR sublines. Supplementary Table 5: Expression pattern of 5 up-regulated differential genes in 37 pairs of HCC patients. Supplementary Table 6: Cox proportional hazard regression analysis.

Supplementary Figure 2 from Lupeol Suppresses Cisplatin-Induced Nuclear Factor-κB Activation in Head and Neck Squamous Cell Carcinoma and Inhibits Local Invasion and Nodal Metastasis in an Orthotopic Nude Mouse Model

Table S1: Summary of pharmacokinetic parameters (days 1 and 15); Table S2: Significant changes in circulating biomarkers from baseline; Table S3: Multivariate models for selected covariates, Overall Survival.

Supplementary Figure 2a: Kaplan-Meier Survival Estimates: Interim Overall Survival. (A) Intent-to-treat population, n=701.

Supplementary Figures S1-S4; Supplementary Tables S1-S5.

Supplementary Figure 3 from Lupeol Suppresses Cisplatin-Induced Nuclear Factor-κB Activation in Head and Neck Squamous Cell Carcinoma and Inhibits Local Invasion and Nodal Metastasis in an Orthotopic Nude Mouse Model

Objective: The aim of this study was to evaluate the short- and long-term outcome of associating liver partition and portal vein ligation for staged hepatectomy (ALPPS) for hepatitis-related hepatocellular carcinoma (HCC). Summary Background Data: ALPPS has been advocated for future liver remnant (FLR) augmentation in liver metastasis or noncirrhotic liver tumors in recent years. Data on the effect of ALPPS in chronic hepatitis or cirrhosis-related HCC remained scarce. Methods: Data for clinicopathological details, portal hemodynamics, and oncological outcome were reviewed for ALPPS and compared with portal vein embolization (PVE). Tumor immunohistochemistry for PD-1, VEGF, and AFP was evaluated in ALPPS and compared with PVE and upfront hepatectomy (UH). Results: From 2002 to 2018, 148 patients with HCC (hepatitis B: n = 136, 92.0%) underwent FLR modulation (ALPPS, n = 46; PVE: n = 102). One patient with ALPPS and 33 patients with PVE failed to proceed to resection (resection rate: 97.8% vs 67.7%, P < 0.001). Among those who had resections, 65 patients (56.5%) had cirrhosis. ALPPS induced absolute FLR volume increment by 48.8%, or FLR estimated total liver volume ratio by 12.8% over 6 days. No difference in morbidity (20.7% vs 30.4%, P = 0.159) and mortality (6.5% vs 5.8%, P = 1.000) with PVE was observed. Chronic hepatitis and intraoperative indocyanine green clearance rate <= 39.5% favored adequate FLR hypertrophy in ALPPS. Five-year overall survival for ALPPS and PVE was 46.8% and 64.1% (P = 0.234). Tumor immunohistochemical staining showed no difference in expression of PD-1, V-EGF, and AFP between ALPPS, PVE, and UH. Conclusions: ALPPS conferred a higher resection rate in hepatitis-related HCC with comparable short- and long-term oncological outcome with PVE.