• 5.1. Clinical Trial
    • 5.1.1. Liver Cancer
    • 5.1.2. Cholangiocarcinoma
  • 5.2. Basic Research

5.0 Hepatobiliary

 

5.1 Clinical Trial

 

5.1.1.1 Liver Cancer

 

Non-metastatic, Unresectable

 

Specific Selection Criteria: PD-L1, CTLA-4

 

First-line treatment: Phase 2

TACE + SBRT + Immunotherapy (Anti-PD-L1/ Anti-CTLA-4 antibody)

 

Study Title

Main Inclusion/Exclusion

Investigational Product

Principal Investigator

Department

Email

Contact number

 

Sequential TransArterial chemoembolization and stereotactic radiotherapy Followed by durvalumab (MEDI4736) and tremelimumab for downstaging hepatocellular carcinoma for hepatectomy (START-FIT double IO).

Key Inclusion Criteria:

  1. Diagnosis of unresectable HCC.

     

  2. No prior systemic therapy nor immunotherapy.

     

  3. No prior trans-arterial chemo-embolization (TACE).

     

  4. No prior radiotherapy to the liver or selective internal radiation (SIRT).

 

Key Exclusion Criteria:

  1. Participation in another clinical study with an investigational product within 4 weeks prior to the first dose of study treatment.

     

  2. Any concurrent chemotherapy, IP, biologic, or hormonal therapy for cancer treatment.

     

  3. Prior radiotherapy to the region of liver or selective internal radiotherapy.
  4. History of primary immunodeficiency or allogenic organ transplantation.

     

  5. Prior randomisation or treatment in a previous durvalumab and/or tremelimumab clinical study regardless of treatment arm assignment.

     

  6. Active or prior documented gastrointestinal variceal bleeding.

Transarterial Chemoembolisation (TACE) + Stereotactic Body Radiation Therapy (SBRT) + Durvalumab (Anti-PD-L1 Monoclonal Antibody)

+ Tremelimumab (Anti-CTLA-4 Monoclonal Antibody)

Prof. Albert Chi-Yan Chan

Department of Surgery

isabelw@hku.hk

Isabel Chan

2255 5362

 

5.1.1.2 Liver Cancer

Locally Advanced or Metastatic, Unresectable

First-line treatment: Phase 2

Targeted therapy (Anti-VEGF Antibody / VEGFR Inhibitor)

GEMINI-Hepatobiliary (Protocol ID: D7987C00001):

A Phase II, Open-Label, Multi-Drug, Multi-Centre, Master Protocol to Evaluate the Efficacy and Safety of Novel Immunomodulators as Monotherapy and in Combination with Anticancer Agents in Participants with Advanced Hepatobiliary Cancer.

Key Inclusion Criteria:

  1. Confirmed locally advanced or metastatic and/or unresectable HCC based on histopathology.

     

  2. Must not have received prior systemic therapy for HCC.

     

  3. At least 1 measurable lesion, not previously irradiated, that can be accurately measured at baseline as ≥ 10 mm in the longest diameter (except lymph nodes, which must have a short axis ≥ 15 mm) with CT or MRI. A lesion which progressed after previous ablation or TACE could be measurable if it meets these criteria.

 

Key Exclusion Criteria:

  1. History of allogeneic organ transplantation or in the waiting-list of allogeneic organ transplantation.

Medi5752 (Monovalent bispecific antibody (PD-1 + CTLA-4)

 

Vs.

 

Medi5752 (Monovalent bispecific antibody (PD-1 + CTLA-4) + bevacizumab (Anti-VEGF Monoclonal Antibody)

 

Vs.

 

Medi5752 (Monovalent bispecific antibody (PD-1 + CTLA-4) + lenvatinib (VEGFR Inhibitor)

Dr. Chiang Chi Leung

Department of Clinical Oncology

ychwilly@hku.hk

Will Yeung

22555125

5.1.1.3 Liver Cancer

Advanced, Unresectable

Specific Selection Criteria: Naïve to tyrosine kinase inhibitors

Second-line treatment: Phase 2

Targeted therapy (VEGFR inhibitor)

OUTREACH2 (Protocol ID: MNA-3521-014-RNDZ):

An Open Label, Randomised Phase 2 Study to Evaluate the Safety and Efficacy of MTL-CEBPA Administered in Combination with sorafenib or sorafenib Alone in TKI naïve Participants with Previously Treated Advanced Hepatocellular Carcinoma (HCC) and Hepatitis B or Hepatitis C Virus.

Key Inclusion Criteria:

  1. Histologically confirmed advanced HCC with cirrhosis in a participant with a history of hepatitis B and/or C.

     

  2. Unsuitable for liver tumour resection and/or refractory to loco regional therapy.

     

  3. Had progression or recurrence of HCC following previous treatment with atezolizumab in combination with bevacizumab; Participants with progression or recurrence of HCC on non-atezolizumab anti-PD-1/PD-L1 inhibitors and non-bevacizumab anti-VEGF agent in combination or as any as single agents; No prior treatment with atezolizumab and bevacizumab.

     

  4. Naïve to tyrosine kinase inhibitors, including sorafenib, regorafenib, cabozantinib, and lenvatinib.

MTL-CEBPA + sorafenib (TKI Inhibitor)

 

Vs.

 

Sorafenib

Dr. Thomas Yau

Department of Medicine (Medical Oncology)

medicaloncology@hku.hk

  • 2255 5582

5.1.1.4 Liver Cancer

Advanced or Metastatic

First-line treatment: Phase 1/2

Immunotherapy (anti-LAG-3/ anti-PD-1 monoclonal antibody), Targeted therapy (Anti-VEGF Monoclonal Antibody)

Study Title

Main Inclusion/Exclusion

Investigational Product

Principal Investigator

Department

Email

Contact number

RELATIVITY-106 (Protocol ID: CA224-106):

A Phase 1/2, Safety Confirmation, Placebo-controlled, Randomized Study of Nivolumab in Combination With Relatlimab and Bevacizumab in Treatment-naive Advanced/Metastatic Hepatocellular Carcinoma

Key Inclusion Criteria:

  1. Histologically confirmed advanced/metastatic hepatocellular carcinoma (HCC).

     

  2. Naïve to systemic therapy for advanced/metastatic HCC

Relatlimab (anti-LAG-3 monoclonal antibody)

+

Nivolumab (anti-PD-1 monoclonal antibody)

+

Bevacizumab (Anti-VEGF Monoclonal Antibody)

 

Vs.

 

Placebo

+

Nivolumab

+

Bevacizumab

Dr. Thomas Yau

Department of Medicine (Medical Oncology)

medicaloncology@hku.hk

2255 5582

5.1.1.5 Liver Cancer

Advanced, Metastatic, Non-resectable, Recurrent

Specific Selection Criteria: Tumor association with MYC oncogene

Second-line or Subsequent treatment: Phase 1/2

mRNA therapeutic, Targeted Therapy (tyrosine kinase inhibitor), Immunotherapy (Anti-PD-1/ PD-L1 antibody)

Study Title

Main Inclusion/Exclusion

Investigational Product

Principal Investigator

Department

Email

Contact number

A Phase 1/2 open-label study to evaluate the safety, tolerability, pharmacokinetics, pharmacodynamics, and preliminary antitumor activity of OTX-2002 as a single agent and in combination with standard of care in patients with hepatocellular carcinoma and other solid tumor types known for association with the MYC oncogene.

Key Inclusion Criteria:

  1. Participants with metastatic, advanced (non-resectable), or recurrent solid tumor who progressed on, relapsed after, are refractory to, or intolerant of standard of care (only applicable to Part 1 escalation).

     

  2. Participants with BCLC Stage B (intermediate stage) or C (advanced stage), Child-Pugh A hepatocellular carcinoma who is not amenable to locoregional therapy, refractory to locoregional therapy or not amenable to curative treatment approach.

     

  3. Progressed on, have relapsed after, be refractory to, or be intolerant of at least 1 prior systemic therapy, and without available subsequent standard of care.

OTX-2002 (mRNA therapeutic)

 

Vs

 

OTX-2002

+

TKI 1

 

Vs.

 

OTX-2002

+

TKI 2

 

Vs.

 

OTX-2002

+

Anti-PD-1/L1 antibody

Dr. Thomas Yau

Department of Medicine (Medical Oncology)

medicaloncology@hku.hk

2255 5582

5.1.1.6 Liver Cancer

Advanced or Metastatic, Unresectable

Second-line or Subsequent treatment: Phase 1

RNA transcription modulator

Study Title

Main Inclusion/Exclusion

Investigational Product

Principal Investigator

Department

Email

Contact number

A Phase I, Single-arm, Open-label, Dose-escalation, Safety and Pharmacokinetic Study of AU409 Capsule in Hepatocellular Carcinoma Patients Who Failed Standard Treatment (AU409-LEES-2021-03)

Key Inclusion Criteria:

  1. Subjects with histologically and/or cytologically confirmed advanced (unresectable or metastatic) hepatocellular carcinoma (HCC) that have failed any of standard treatment (including Immunotherapies and/or Tyrosine Kinase Inhibitor therapies, or Oxaliplatin-based systemic chemotherapies), recurrence, or are intolerant.

     

  2. Subjects must have previously completed chemotherapy, radiotherapy, interventional therapy for more than 4 weeks.

 

Key Exclusion Criteria:

  1. Subjects of central nervous system metastasis with clinical symptoms.

     

  2. Allergies to any ingredients or excipients in AU409.

AU 409 (RNA transcription modulator)

Dr. Chiang Chi Leung

Department of Clinical Oncology

ychwilly@hku.hk

Will Yeung

2255 5125

5.0 Hepatobiliary

5.2.1 Basic Research

Study Title

Principal Investigator

Department

Email

Contact number

A study of the regulation of TAX1 binding protein 2 by p21-activated protein kinase 4 in liver cancer metastasis

Dr Yick Pang Ching

School of Biomedical Sciences

ypching@hku.hk

Dr Yick Pang Ching

3917 9434

5.2.2 Basic Research

A study of the role of salt-inducible kinase 2 in regulating chemo-resistance of liver cancer cells

Dr Yick Pang Ching

School of Biomedical Sciences

ypching@hku.hk

Dr Yick Pang Ching

3917 9434

Characterization of the role of liver cancer stem cell marker, CD133 in promoting chromosome instability in hepatocarcinogenesis

Dr Yick Pang Ching

School of Biomedical Sciences

ypching@hku.hk

Dr Yick Pang Ching

3917 9434

5.2.3 Basic Research

Functional characterization of the roles of NIMA-related kinase, Nek2 in liver cancer development and metastasis

Dr Yick Pang Ching

School of Biomedical Sciences

ypching@hku.hk

Dr Yick Pang Ching

3917 9434

5.2.4 Basic Research

Functional characterization of the roles of Polo-like kinase 4, Plk4 in hepatocarcinogenesis

Dr Yick Pang Ching

School of Biomedical Sciences

ypching@hku.hk

Dr Yick Pang Ching

3917 9434

5.2.5 Basic Research

The therapeutic potential of Polo-like protein kinase 4 in liver cancer

Dr Yick Pang Ching

School of Biomedical Sciences

ypching@hku.hk

Dr Yick Pang Ching

3917 9434

5.2.6 Basic Research

Characterization of novel HBx regulated gene in hepatocellular carcinoma

Dr Yick Pang Ching

School of Biomedical Sciences

ypching@hku.hk

Dr Yick Pang Ching

3917 9434

5.2.7 Basic Research

A study of the role of p21-activated kinase 4 (PAK4) in chromosome instability

Dr Yick Pang Ching

School of Biomedical Sciences

 

ypching@hku.hk

Dr Yick Pang Ching

3917 9434

5.2.8 Basic Research

Molecular mechanisms of Pumilio-Regulated Chromosomal Instability in Hepatocellular Carcinoma

Dr Yick Pang Ching

School of Biomedical Sciences

 

ypching@hku.hk

Dr Yick Pang Ching

3917 9434

5.2.9 Basic Research

Development of a P-21 activated protein kinase 4 specific inhibitory peptide as a novel hepatocellular carcinoma therapeutic agent

Dr Yick Pang Ching

School of Biomedical Sciences

ypching@hku.hk

Dr Yick Pang Ching

3917 9434

5.2.10 Basic Research

A study of the role of transgelin-2 in hepatocarcinogenesis

Dr Yick Pang Ching

School of Biomedical Sciences

ypching@hku.hk

Dr Yick Pang Ching

3917 9434

5.2.11 Basic Research

The role of centrosomal protein CEP295 in chromosome instability and liver cancer progression

Dr Yick Pang Ching

School of Biomedical Sciences

ypching@hku.hk

Dr Yick Pang Ching

3917 9434

5.2.12 Basic Research

Delineating and translating the mechanistic determinants to improve the clinical management of liver cancer

Dr Clive Yik Sham Chung

School of Biomedical Sciences

 

cyschung@hku.hk

Dr Clive Yik Sham Chung

3917 9172

5.2.13 Basic Research

Understanding Cancer Stemness in Liver Cancer - From Regulation to Translational Applications

Prof. Oi Lin Irene Ng

Department of Pathology

iolng@hku.hk

2255 2664

5.2.14 Basic Research

A Multidisciplinary Study on CD133 Liver Cancer Stem Cells: Molecular Mechanisms, Clinical Relevance and Therapeutic Implications

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.15 Basic Research

A study of the role and therapeutic potential of targeting protein tyrosine kinase 7 (PTK7) in liver cancer

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.16 Basic Research

AGPAT4: a novel metabolic driver of stemness in hepatocellular carcinoma?

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.17 Basic Research

An Immune Perspective on Exploiting Stemness as a Cancer Cell Vulnerability for the Treatment of Liver Cancer.

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

 

 

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.18 Basic Research

Annexin A3: potential predictive factor for the efficacy of sorafenib and new therapeutic potential in hepatocellular carcinoma.

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.19 Basic Research

Development and applications of a driver-dependent tumor organoid biobank for translational liver cancer research.

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

 

 

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.20 Basic Research

Development and Pre-clinical Evaluation of a Humanized ANXA3 Neutralizing Monoclonal Antibody for Hepatocellular Carcinoma Treatment.

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.21 Basic Research

An immune perspective on exploiting stemness as a cancer cell vulnerability for the treatment of liver cancer (CRF).

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.22 Basic Research

PRMT6 in the control of glucose metabolic reprogramming in CD133+ liver cancer stem cells.

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.23 Basic Research

Establishment of a novel ANXA3 neutralizing antibody and its use, alone or in combination with sorafenib, as a potential therapeutic regimen against liver cancer.

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.24 Basic Research

PRMT6 regulates ERK1/2 signal transduction in liver cancer through CRAF.

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.25 Basic Research

Establishment, characterization and applications of normal liver and hepatocellular carcinoma organoid cultures.

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.26 Basic Research

PRMT6 binds to and methylates BAG5, BAG6, AMBRA1 and SQSTM1 to regulate autophagy in liver cancer.

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.27 Basic Research

A pre-clinical study to evaluate the therapeutic efficacy of FSTL1 neutralizing antibody in combination with sorafenib for the treatment of HCC.

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.28 Basic Research

Molecular and mechanistic characterization of FUT1 mediated cancer stemness in a glucose restricted liver tumor microenvironment

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.29 Basic Research

A pre-clinical study to evaluate the therapeutic efficacy of PTK7 neutralizing antibody in combination with other approved chemotherapy or molecular targeted drugs for the treatment of HCC

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.30 Basic Research

Molecular and mechanistic characterization of SERPINA12 mediated cancer stemness in hepatocellular carcinoma

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.31 Basic Research

Molecular and mechanistic characterization of FUT2 mediated cancer stemness in hepatocellular carcinoma with PTEN loss

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.32 Basic Research

Molecular and mechanistic characterization of SPINK1 mediated cancer stemness in hepatocellular carcinoma

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.33 Basic Research

Functional characterization of fucosyltransferase 1 (FUT1) in promoting cancer stemness properties in hepatocellular carcinoma

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

 

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.34 Basic Research

Regulatory role of microRNA-1246 and Wnt/β-catenin pathway interaction in CD133+ liver cancer stem cells-driven hepatocellular carcinoma

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.35 Basic Research

Role of PRMT6 in regulating cancer and stemness properties in hepatocellular carcinoma

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.36 Basic Research

Role of protein arginine methyltransferase 6 (PRMT6) in metabolic reprogramming in hepatocellular carcinoma

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.37 Basic Research

Role of the lipid metabolic regulator DGKH in driving stemness in hepatocellular carcinoma

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.38 Basic Research

Significance of serine protease inhibitor Kazal-type 1 (SPINK1) in liver cancer: function, regulation and therapeutic implication

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.39 Basic Research

Annexin A3 (ANXA3) as a novel therapeutic target for liver cancer

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.40 Basic Research

Prom1+ tumor-propagating cells and their dynamic cellular transition during liver cancer progression

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.41 Basic Research

Targeting uPAR in tumor-associated macrophages of hepatocellular carcinoma

Dr. Rio Ryohichi Sugimura

School of Biomedical Sciences

rios@hku.hk

Dr Rio Ryohichi Sugimura

3917 9269

5.2.42 Basic Research

The immune microenvironment of recurrent hepatocellular carcinoma

Dr. Rio Ryohichi Sugimura

School of Biomedical Sciences

rios@hku.hk

Dr Rio Ryohichi Sugimura

3917 9269

5.2.43 Basic Research

Exploiting stemness as a cancer cell vulnerability using hepatocellular carcinoma (HCC) as a model system

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.44 Basic Research

Using tumour mutational landscape to resolve the cellular origin of hepatocellular carcinoma at single cell level

Dr. Jason Wing Hon Wong

School of Biomedical Sciences

jwhwong@hku.hk

Dr. Jason Wing Hon Wong

3917 9187

5.2.45 Basic Research

Role of MAPK11 in liver cancer stem cells.

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238

5.2.46 Basic Research

A multidisciplinary study on hepatic cancer stem cells.

Prof. Stephanie Kwai Yee Ma

School of Biomedical Sciences

stefma@hku.hk

Prof. Stephanie Kwai Yee Ma

3917 9238