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Pancreatic Neoplasms: HELP
Articles by Jennifer Man
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, Jennifer Man wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Targeting the complexity of Src signalling in the tumour microenvironment of pancreatic cancer: from mechanism to therapy. 2019

Parkin, Ashleigh / Man, Jennifer / Timpson, Paul / Pajic, Marina. ·The Kinghorn Cancer Centre, The Garvan Institute of Medical Research, Sydney, Australia. · Faculty of Medicine, St Vincent's Clinical School, University of NSW, Sydney, Australia. ·FEBS J · Pubmed #31330086.

ABSTRACT: Pancreatic cancer, a disease with extremely poor prognosis, has been notoriously resistant to virtually all forms of treatment. The dynamic crosstalk that occurs between tumour cells and the surrounding stroma, frequently mediated by intricate Src/FAK signalling, is increasingly recognised as a key player in pancreatic tumourigenesis, disease progression and therapeutic resistance. These important cues are fundamental for defining the invasive potential of pancreatic tumours, and several components of the Src and downstream effector signalling have been proposed as potent anticancer therapeutic targets. Consequently, numerous agents that block this complex network are being extensively investigated as potential antiinvasive and antimetastatic therapeutic agents for this disease. In this review, we will discuss the latest evidence of Src signalling in PDAC progression, fibrotic response and resistance to therapy. We will examine future opportunities for the development and implementation of more effective combination regimens, targeting key components of the oncogenic Src signalling axis, and in the context of a precision medicine-guided approach.

2 Review The Evolving Understanding of the Molecular and Therapeutic Landscape of Pancreatic Ductal Adenocarcinoma. 2018

Parkin, Ashleigh / Man, Jennifer / Chou, Angela / Nagrial, Adnan M / Samra, Jaswinder / Gill, Anthony J / Timpson, Paul / Pajic, Marina. ·The Kinghorn Cancer Centre, The Garvan Institute of Medical Research, 384 Victoria St, Darlinghurst, Sydney, NSW 2010, Australia. a.parkin@garvan.org.au. · The Kinghorn Cancer Centre, The Garvan Institute of Medical Research, 384 Victoria St, Darlinghurst, Sydney, NSW 2010, Australia. j.man@garvan.org.au. · The Kinghorn Cancer Centre, The Garvan Institute of Medical Research, 384 Victoria St, Darlinghurst, Sydney, NSW 2010, Australia. a.chou@garvan.org.au. · University of Sydney, Sydney, NSW 2006, Australia. a.chou@garvan.org.au. · The Kinghorn Cancer Centre, The Garvan Institute of Medical Research, 384 Victoria St, Darlinghurst, Sydney, NSW 2010, Australia. Adnan.Nagrial@health.nsw.gov.au. · Crown Princess Mary Cancer Centre, Westmead Hospital, Sydney, NSW 2145, Australia. Adnan.Nagrial@health.nsw.gov.au. · Department of Surgery, Royal North Shore Hospital, St Leonards, Sydney, NSW 2065, Australia. jas.samra@bigpond.com. · The Kinghorn Cancer Centre, The Garvan Institute of Medical Research, 384 Victoria St, Darlinghurst, Sydney, NSW 2010, Australia. Anthony.Gill@health.nsw.gov.au. · University of Sydney, Sydney, NSW 2006, Australia. Anthony.Gill@health.nsw.gov.au. · Department of Anatomical Pathology, Royal North Shore Hospital, St Leonards, Sydney, NSW 2065, Australia. Anthony.Gill@health.nsw.gov.au. · Cancer Diagnosis and Pathology Research Group, Kolling Institute of Medical Research, St Leonards, NSW 2065, Australia. Anthony.Gill@health.nsw.gov.au. · The Kinghorn Cancer Centre, The Garvan Institute of Medical Research, 384 Victoria St, Darlinghurst, Sydney, NSW 2010, Australia. p.timpson@garvan.org.au. · St Vincent's Clinical School, Faculty of Medicine, University of NSW, Sydney, NSW 2010, Australia. p.timpson@garvan.org.au. · The Kinghorn Cancer Centre, The Garvan Institute of Medical Research, 384 Victoria St, Darlinghurst, Sydney, NSW 2010, Australia. m.pajic@garvan.org.au. · St Vincent's Clinical School, Faculty of Medicine, University of NSW, Sydney, NSW 2010, Australia. m.pajic@garvan.org.au. ·Diseases · Pubmed #30428574.

ABSTRACT: Pancreatic cancer is the third leading cause of cancer-related deaths, characterised by poor survival, marked molecular heterogeneity and high intrinsic and acquired chemoresistance. Only 10⁻20% of pancreatic cancer patients present with surgically resectable disease and even then, 80% die within 5 years. Our increasing understanding of the genomic heterogeneity of cancer suggests that the failure of definitive clinical trials to demonstrate efficacy in the majority of cases is likely due to the low proportion of responsive molecular subtypes. As a consequence, novel treatment strategies to approach this disease are urgently needed. Significant developments in the field of precision oncology have led to increasing molecular stratification of cancers into subtypes, where individual cancers are selected for optimal therapy depending on their molecular or genomic fingerprint. This review provides an overview of the current status of clinically used and emerging treatment strategies, and discusses the advances in and the potential for the implementation of precision medicine in this highly lethal malignancy, for which there are currently no curative systemic therapies.

3 Article PAK inhibition by PF-3758309 enhanced the sensitivity of multiple chemotherapeutic reagents in patient-derived pancreatic cancer cell lines. 2019

Wang, Kai / Huynh, Nhi / Wang, Xiao / Pajic, Marina / Parkin, Ashleigh / Man, Jennifer / Baldwin, Graham S / Nikfarjam, Mehrdad / He, Hong. ·Department of Surgery, University of Melbourne, Austin Health Studley Road, Heidelberg, Victoria 3084, Australia. · The Kinghorn Cancer Centre, The Garvan Institute of Medical Research 384 Victoria St, Darlinghurst, Sydney, NSW 2010, Australia. · St Vincent's Clinical School, Faculty of Medicine, University of NSW Australia. ·Am J Transl Res · Pubmed #31312349.

ABSTRACT: BACKGROUND/OBJECTIVE: Pancreatic ductal adenocarcinoma (PDA) remains the most lethal malignancy due to lack of an effective treatment. P21-activated kinases (PAKs) play a key role not only in cell proliferation and migration, but also in mediating chemo-resistance in PDA. The aim of this study was to investigate the combined effect of a PAK inhibitor PF-3758309 with multiple chemotherapeutic reagents on a panel of patient-derived PDA cell lines, and potential mechanisms involved. METHODS: Cells were treated with PF-3758309 plus or minus gemcitabine, 5-fluorouracil (5-FU) or abraxane, and cell growth was determined using a cell proliferation assay kit. Protein expression profiles were measured by Western blot. PDA cells were subcutaneously injected into the flanks of SCID mice which were then treated with saline, gemcitabine, PF-3758309, gemcitabine plus PF-3758309 or abraxane. Tumour growth was measured by volume and weight. RESULTS: PAK1 was correlated with CK19 expression, and PAK4 with α-SMA and palladin expression. Combination of PF-3758309 with 5-FU, gemcitabine or abraxane further suppressed cell growth of patient-derived PDA cell lines CONCLUSIONS: PAK inhibitor PF-3758309 can enhance anti-tumour effects of multiple chemotherapeutic reagents on a panel of patient-derived PDA cell lines. Combination of PF-3758309 with gemcitabine achieves comparable efficacy to combination of gemcitabine with abraxane, and thus provides a potential targeted therapy in the management of PDA.