Hunter Cancer Research Alliance

As a multidisciplinary and multi-institutional alliance, the Hunter Cancer Research Alliance (HCRA) functions to provide capacity building, funding and strategic support to cancer research across the translational research continuum – from basic research through clinical trials to behavioural, implementation and health services research.

With the support of our partnering institutions, executive leaders and a membership that consists of 250+ cancer-focused researchers, we are working to promote the excellence of cancer research in the Hunter and ultimately improve cancer patient outcomes in our region and beyond.

HCRA Director, Professor Stephen Ackland, explains the work of HCRA in the video below:



An Immune Atlas of Clear Cell Renal Cell Carcinoma

St├ęphane Chevrier, Jacob Harrison Levine, Vito Riccardo Tomaso Zanotelli, Karina Silina, Daniel Schulz, Marina Bacac, Carola Hermine Ries, Laurie Ailles, Michael Alexander Spencer Jewett, Holger Moch, Maries van den Broek, Christian Beisel, Michael Beda Stadler, Craig Gedye, Bernhard Reis, Dana Pe’er, Bernd Bodenmiller


Immune cells in the tumor microenvironment modulate cancer progression and are attractive therapeutic targets. Macrophages and T cells are key components of the microenvironment, yet their phenotypes and relationships in this ecosystem and to clinical outcomes are ill defined. We used mass cytometry with extensive antibody panels to perform in-depth immune profiling of samples from 73 clear cell renal cell carcinoma (ccRCC) patients and five healthy controls. In 3.5 million measured cells, we identified 17 tumor-associated macrophage phenotypes, 22 T cell phenotypes, and a distinct immune composition correlated with progression-free survival, thereby presenting an in-depth human atlas of the immune tumor microenvironment in this disease. This study revealed potential biomarkers and targets for immunotherapy development and validated tools that can be used for immune profiling of other tumor types.

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Gelatin-albumin hybrid nanoparticles as matrix metalloproteinases-degradable delivery systems for breast cancer therapy

Vahid Heravi Shargh, Hubert Hondermarck & Mingtao Liang


Aim: To develop matrix metalloproteinase-responsive gelatin-albumin hybrid nanoparticles encapsulating a selective tropomyosin receptor kinase A (TrkA) inhibitor GNF-5837 (Gel-Alb-GNF HNPs) and to demonstrate their anticancer effects in breast cancer. Methods: Gel-Alb-GNF HNPs were prepared using a pH-controlled complexation process from cationic gelatin, dextran sulfate and albumin-bound GNF-5837. The anticancer activities of Gel-Alb-GNF HNPs were tested in a panel of subtype-specific breast cancer cell lines. Results: Gel-Alb-GNF HNPs (∼130 nm) displayed excellent stability and matrix metalloproteinase-triggered drug release. Compared with GNF-5837 alone, Gel-Alb-GNF HNPs not only significantly enhanced the antiproliferative and anti-invasive effects but also restored the apoptosis of cancer cells. Conclusion: Gel-Alb-GNF HNPs may be adaptable for stand-alone therapies or used in combination with traditional chemotherapies for breast cancer treatment.

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MicroRNA-645 is an oncogenic regulator in colon cancer

S T Guo, X Y Guo, J Wang, C Y Wang, R H Yang, F H Wang, X Y Li, H Hondermarck, R F Thorne, Y F Wang, L Jin, X D Zhang and C C Jiang


Despite advances in early diagnosis and the development of molecularly targeted therapy, curative treatment of colon cancer once it has metastasized is yet to be accomplished. This is closely associated with deregulated CRC cell proliferation and resistance to apoptosis. Here we reveal that upregulation of microRNA-645 (miR-645) through DNA copy number gain is responsible for enhanced proliferation and resistance to apoptosis in colon cancer. MiR-645 was upregulated in most colon cancer tissues related to adjacent normal mucosa. This appeared to be associated with amplification of a section of chromosome 20q13.13, where miR-645 is located. Inhibition of miR-645 reduced proliferation and enhanced sensitivity to apoptosis triggered by the chemotherapeutic drugs 5-fluorouracil and cisplatin in CRC cells, and retarded colon cancer xenograft growth. Conversely, overexpression of miR-645 in normal colon epithelial cells enhanced proliferation and triggered anchorage-independent cell growth. Although SRY-related HMG-box 30 (SOX30) was identified as a miR-645 target, its expression was only partially affected by miR-645, suggesting that miR-645 is a fine-tuning mechanism of SOX30 expression. Moreover, overexpression of SOX30 only moderately inhibited promotion of CRC cell proliferation by miR-645, indicating that miR-645 may have more targets that contribute to its pro-proliferation effect in colon cancer. Together, this study reveals that miR-645 can regulate oncogenesis in colon cancer with SOX30 being one of its targets.

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March 2017

The University of Newcastle, Australia Hunter New England Local Health District Calvary Mater Newcastle Hunter Medical Research Institute Cancer Institute NSW