Dr Debashis Sarker

Oncologist, Honorary Consultant in Medical Oncology, Guy’s and St Thomas’ NHS Foundation Trust

London, GB
En, En
Best at: Hepato-pancreatic-biliary malignancies

Dr Sarker is a Senior Lecturer and Honorary Consultant in Medical Oncology at Guy’s and St Thomas’ NHS Foundation Trust, and King’s College Hospital NHS Foundation Trust. He specialises in the treatment of hepato-pancreatic-biliary malignancies: Liver Cancer, Bile Duct Cancer, Pancreatic Cancer, Neuro-endocrine Cancer, Adrenal Glands Cancer, Gall Bladder Cancer. His main research focus is in the development of novel therapies for cancer, and together with Dr James Spicer, runs the Early Phase Clinical Trials Unit based at Guy’s Hospital. He is also actively involved in the management of hepato - pancreatic-biliary malignancies at King's College Hospital Liver Unit, and has a specific interest in the development of new therapies and molecular imaging for these tumours. Dr Sarker graduated in medicine from the University of Liverpool in 1997, and subsequently trained in internal medicine and medical oncology. In 2003 he was appointed to a Cancer Research UK Clinical Research Fellowship in the Drug Development Unit of The Royal Marsden Hospital and Institute of Cancer Research, leading to the award of a PhD. He completed his medical oncology training at The Royal Marsden in 2010.

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Statistics.

Achievements of Dr Debashis Sarker

Trustedoctor credentials

-

Clinical endorsements

30

Articles

121

Scientific
co-authors

Trustedoctor credentials

16

General specialty

17

Subspeciality

Languages

About.

Information about Dr Debashis Sarker

Timeline

Place

Country

Position

Focus

2010

Institute of Cancer Research

United Kingdom

PhD

Cancer molecular pharmacology

1997

University of Liverpool

United Kingdom

MBBS

Medicine

Timeline

Place

Country

Position

Focus

Since 2010

King's College London

United Kingdom

Senior Lecturer in Medical Oncology

Medical Oncology

Since 2010

Guy’s and St Thomas’ NHS Foundation Trust

United Kingdom

Consultant Medical Oncologist

Gastrointestinal Cancer

Since 2010

King's College Hospital NHS Foundation Trust

United Kingdom

Consultant Medical Oncologist

Gastrointestinal Cancer

2007-2010

The Royal Marsden NHS Foundation Trust

United Kingdom

Specialist Registrar in Medical Oncology

Medical Oncology

Timeline

Place

Organization

Position

-

United States

American Society of Clinical Oncology

Member

-

Europe

European Society for Medical Oncology

Member

-

United States

American Cancer Society

Member

-

United States

American Association of Cancer Research

Member

-

International

International Liver Cancer Association

Member

-

Europe

European Neuroendocrine Tumour Society

Member

-

United Kingdom and Ireland

UK and Ireland Neuroendocrine Tumor Society

Member

Timeline

Description

Collaboration

-

Timeline

Place

Award

Position

-

Clinical Experience.

General speciality (4)

Patients per year

Patients total

chemotherapy

0-50

-

chemoradiotherapy

0-50

-

targeted therapy

0-50

-

general gallbladder cancer oncology

0-100

-

Sub-speciality (5)

Patients per year

Patients total

adenocarcinoma

0-50

-

small cell carcinomas

0-50

-

hepatoid adenocarcinoma

0-50

-

gallbladder sarcoma

0-50

-

signet ring cell carcinoma

0-50

-

General speciality (4)

Patients per year

Patients total

general liver tumour oncology

0-100

-

chemotherapy

0-100

-

immunotherapy

0-100

-

targeted therapy

0-100

-

Sub-speciality (6)

Patients per year

Patients total

hepatocellular carcinoma (hcc)

0-50

-

fibrolamellar carcinoma

0-50

-

hepatoblastoma

0-50

-

haemangioma

0-50

-

hepatic adenoma

0-50

-

focal nodular hyperplasia

0-50

-

General speciality (4)

Patients per year

Patients total

chemotherapy

0-100

-

immunotherapy

0-100

-

targeted therapy

0-100

-

general pancreas tumour oncology

0-100

-

Sub-speciality (4)

Patients per year

Patients total

fibrolamellar carcinoma

0-50

-

pancreatic ductal adenocarcinoma

0-50

-

acinar cell carcinoma

0-50

-

somatostatinomas

0-50

-

General speciality (4)

Patients per year

Patients total

general bile duct cancer oncology

0-100

-

chemotherapy

0-50

-

immunotherapy

0-50

-

targeted therapy

0-50

-

Sub-speciality (2)

Patients per year

Patients total

adenocarcinoma

0-50

-

small cell carcinoma

0-50

-

Skills & Endorsements.

General specialty

chemotherapy

chemoradiotherapy

targeted therapy

general gallbladder cancer oncology

General specialty

chemotherapy

immunotherapy

general liver tumour oncology

targeted therapy

General specialty

targeted therapy

immunotherapy

chemotherapy

General specialty

general bile duct cancer oncology

immunotherapy

chemotherapy

targeted therapy

Academic research.

30
Total articles

chemotherapy - 12
surgery - 1
chemoradiation - 1

6
liver cancer articles - Impact Factor

liver - 6

oncology therapy - 6

Hepatocellular Carcinoma in Perinatally Acquired HIV and HBV Coinfection: A Case Report.

This report describes a case of hepatocellular carcinoma in an adolescent with perinatally acquired HIV and hepatitis B virus coinfection, arising despite more than a decade of suppressive antiretroviral therapy for both HIV and hepatitis B virus. This case raises important questions regarding optimal hepatocellular carcinoma screening in this high-risk group and the oncogenic potential of even very well-controlled viral infection.

Efficacy and safety of sorafenib in patients with advanced hepatocellular carcinoma: age is not a problem.

Sorafenib is the standard of care for patients with advanced hepatocellular carcinoma (HCC), but data on its use in the elderly are inconclusive.

Histological heterogeneity in primary and metastatic classic combined hepatocellular-cholangiocarcinoma: a case series.

Combined hepatocellular-cholangiocarcinoma (cHCC-CC) is a rare and aggressive primary liver cancer with both hepatocellular and cholangiocellular differentiation. Due to its bi-phenotypic component, cHCC-CC is a heterogeneous tumour and histopathological analysis of metastatic deposits is poorly characterized. In this retrospective study, we describe four patients in whom the histology from resected specimens of both primary and recurrent and/or metastatic tumour was available for comparison and immunohistochemical characterization. Our study shows that recurrent or metastatic deposits replicate the heterogeneity of the primary cHCC-CC, that even originally small foci of divergent differentiation can become predominant later on and that hepatocellular and cholangiocellular components can show different tropism in distant organs. In our experience, the behaviour of recurrent/metastatic cHCC-CC is unpredictable and histological examination is necessary to guide treatment options at present.

Lenvatinib: a potential breakthrough in advanced hepatocellular carcinoma?

Treatment of advanced hepatocellular carcinoma (HCC) has reached a plateau after the approval of sorafenib in 2007. Several molecularly targeted therapies have failed to show significant improvement in survival outcomes compared with sorafenib, due to flaws in the design of clinical trials or failure to understand and correct for the competing co-morbidity of liver dysfunction. Lenvatinib is a multitargeted tyrosine kinase inhibitor with potent antiangiogenic effects, and has recently been approved for differentiated thyroid cancer. Lenvatinib has shown highly promising response data in Phase I/II clinical trials in HCC, although with some concerns regarding its toxicity profile. The pivotal Phase III REFLECT trial comparing lenvatinib to sorafenib has been completed, and the results of this trial will determine whether lenvatinib represents a breakthrough in the current crisis affecting HCC drug development.

Tubulin β-III: a novel immunohistochemical marker for intrahepatic peripheral cholangiocarcinoma.

Our recent proteomic study identified tubulin β-III (TUBB3) as a potential tissue marker for intrahepatic cholangiocarcinomas (CCs). This validation study was conducted to see whether or not TUBB3 can serve as a novel immunohistochemical marker for peripheral CCs, using a large cohort (n = 197) covering various liver tumours and premalignant conditions.

Quantification of pancreatic cancer proteome and phosphorylome: indicates molecular events likely contributing to cancer and activity of drug targets.

LC-MS/MS phospho-proteomics is an essential technology to help unravel the complex molecular events that lead to and propagate cancer. We have developed a global phospho-proteomic workflow to determine activity of signaling pathways and drug targets in pancreatic cancer tissue for clinical application.

5
pancreatic cancer articles - Impact Factor

pancreas - 5

oncology therapy - 5

Deciphering the link between PI3K and PAK: An opportunity to target key pathways in pancreatic cancer?

The development of personalised therapies has ushered in a new and exciting era of cancer treatment for a variety of solid malignancies. Yet pancreatic ductal adenocarcinoma (PDAC) has failed to benefit from this paradigm shift, remaining notoriously refractory to targeted therapies. Chemotherapy is the cornerstone of management but can offer only modest survival benefits of a few months with 5-year survival rates rarely exceeding 3%. Despite these disappointing statistics, significant strides have been made towards understanding the complex biology of pancreatic cancer, with deep genomic sequencing identifying novel genetic aberrations and key signalling pathways. The PI3K-PDK1-AKT pathway has received great attention due to its prominence in carcinogenesis. However, efforts to target several components of this network have resulted in only a handful of drugs demonstrating any survival benefit in solid tumors; despite promising pre-clinical results. p-21 activated kinase 4 (PAK4) is a gene that is recurrently amplified or overexpressed in PDAC and both PAK4 and related family member PAK1, have been linked to aberrant RAS activity, a common feature in pancreatic cancer. As regulators of PI3K, PAKs have been highlighted as a potential prognostic marker and therapeutic target. In this review, we discuss the biology of pancreatic cancer and the close interaction between PAKs and the PI3K pathway. We also suggest proposals for future research that may see the development of effective targeted therapies that could finally improve outcomes for this disease.

Ki-67 index and response to chemotherapy in patients with neuroendocrine tumours.

Chemotherapy (CT) is widely used for neuroendocrine tumours (NETs), but there are no validated biomarkers to predict response. The Ki-67 proliferation index has been proposed as a means of selecting patients for CT, but robust data are lacking. The aim of this study was to investigate the relationship between response to chemotherapy and Ki-67 in NET. We reviewed data from 222 NET patients treated with CT. Tumours were graded according to Ki-67 index: G1 ≤2%, G2 3-20% and G3 >20%. Response was assessed according to RECIST and survival calculated from start of chemotherapy to death. To explore Ki-67 as a marker of response, we calculated the likelihood ratio and performed receiver operating characteristic analysis. Overall, 193 patients had a documented Ki-67 index, of which 173 were also evaluable for radiological response: 10% were G1, 46% G2 and 43% G3; 46% were pancreatic NET (PNET). Median overall survival was 22.1 months. Overall response rate was 30% (39% in PNET vs 22% in non-PNET) and 43% of patients had stable disease. Response rate increased with grade: 6% in G1 tumours, 24% in G2 and 43% in G3. However, maximum likelihood ratio was 2.3 at Ki-67=35%, and the area under the ROC curve was 0.60. As reported previously, a high Ki-67 was an adverse prognostic factor for overall survival. In conclusion, response to CT increases with Ki-67 index, but Ki-67 alone is an unreliable means to select patients for CT. Improved methods to stratify patients for systemic therapy are required.

Prospects for adoptive immunotherapy of pancreatic cancer using chimeric antigen receptor-engineered T-cells.

Adoptive immunotherapy using chimeric antigen receptor (CAR) engineered T-cells is emerging as a powerful new approach to cancer immunotherapy. CARs are fusion molecules that couple the antibody-like binding of a native cell surface target to the delivery of a bespoke T-cell activating signal. Recent studies undertaken by several centers have demonstrated highly compelling efficacy in patients with acute and chronic B-cell malignancies. However, comparable therapeutic activity has not been achieved in solid tumors. Modern management of pancreatic ductal adenocarcinoma (PDAC) remains ineffective, reflected in the virtual equivalence of annual incidence and mortality statistics for this tumor type. Increasing evidence indicates that these tumors are recognized by the immune system, but deploy powerful evasion strategies that limit natural immune surveillance and render efforts at immunotherapy challenging. Here, we review preclinical and clinical studies that have been initiated or completed in an effort to develop CAR-based immunotherapy for PDAC. We also consider the hurdles to the effective clinical development of this exciting new therapeutic modality.

FOLFIRINOX - a new paradigm in the treatment of pancreatic cancer.

Treatment of metastatic and locally advanced pancreatic cancer has made slow progress during the last decade. Single agent gemcitabine or in combination with capecitabine or erlotinib remained the preferred systemic treatment options until 2010 when the ACCORD study demonstrated significantly improved outcomes achieved with FOFIRINOX compared with gemcitabine monotherapy. Since 2010, use of FOLFIRINOX has increased both in metastatic and locally advanced cancer. Despite its gaining popularity among oncologists, unanswered questions remain. Do the often necessary dose modifications affect its efficacy? Are the toxicities manageable and how applicable are the results of the ACCORD study in the general population of patients with newly diagnosed pancreatic cancer? In the present manuscript, we review the published literature regarding the use of FOLFIRINOX, the challenges associated with its use and how it will be optimally incorporated into the management of patients with different stages of pancreatic cancer and ultimately, in a more biomarker-driven pathway algorithm.

Quantification of pancreatic cancer proteome and phosphorylome: indicates molecular events likely contributing to cancer and activity of drug targets.

LC-MS/MS phospho-proteomics is an essential technology to help unravel the complex molecular events that lead to and propagate cancer. We have developed a global phospho-proteomic workflow to determine activity of signaling pathways and drug targets in pancreatic cancer tissue for clinical application.

2
bile duct cancer articles - Impact Factor

bile duct - 2

oncology - 2

Tubulin β-III: a novel immunohistochemical marker for intrahepatic peripheral cholangiocarcinoma.

Our recent proteomic study identified tubulin β-III (TUBB3) as a potential tissue marker for intrahepatic cholangiocarcinomas (CCs). This validation study was conducted to see whether or not TUBB3 can serve as a novel immunohistochemical marker for peripheral CCs, using a large cohort (n = 197) covering various liver tumours and premalignant conditions.

Histological heterogeneity in primary and metastatic classic combined hepatocellular-cholangiocarcinoma: a case series.

Combined hepatocellular-cholangiocarcinoma (cHCC-CC) is a rare and aggressive primary liver cancer with both hepatocellular and cholangiocellular differentiation. Due to its bi-phenotypic component, cHCC-CC is a heterogeneous tumour and histopathological analysis of metastatic deposits is poorly characterized. In this retrospective study, we describe four patients in whom the histology from resected specimens of both primary and recurrent and/or metastatic tumour was available for comparison and immunohistochemical characterization. Our study shows that recurrent or metastatic deposits replicate the heterogeneity of the primary cHCC-CC, that even originally small foci of divergent differentiation can become predominant later on and that hepatocellular and cholangiocellular components can show different tropism in distant organs. In our experience, the behaviour of recurrent/metastatic cHCC-CC is unpredictable and histological examination is necessary to guide treatment options at present.

Connections.

Map of connections

121

Scientific
co-authors