Member Q+A - Dr Abhishek D. Garg

In the second of our series showcasing active community members - we meet Abhishek who is currently working as a Senior Postdoc in Belgium

Go to the profile of Dr Alison Halliday
Feb 09, 2018
  1. What is your full name, job title and where do you work?

Abhishek D. Garg; I currently work as a Senior Postdoctoral Scientist at the Cell Death Research & Therapy (CDRT) Lab, Dept. Cellular Molecular Medicine (CMM), KU Leuven University of Leuven, Belgium.

2. What are your main research interests?

Cell death immunology, Tumour immunology & immunotherapy, Immunological predictive or prognostic biomarkers in cancer patients.

3. Describe your work in a tweet

Exploiting knowledge of cell death immunology to understand tumour-immune cross-talk and pave way for advancement of biomarkers-driven cancer immunotherapy.

4. What big projects are you working on right now?

We are trying to understand the molecular features of cancer cell death that ultimately govern the outcome of anticancer immunity and influence success of immunotherapy.

5. Who do you collaborate with?

We widely collaborate with a number of researchers at KU Leuven, various labs at some Belgian universities and some international labs. Mostly the subject of our collaboration is either molecular biology of cell death or tumour immunology.

6. Tell us a bit about your career so far

I started my career with the study of cancer cell death mechanisms during my MSc at University of Leeds, UK (under Dr. Simon Wood). Over the course of my PhD at KU Leuven (under Prof. Patrizia Agostinis), I worked on molecular mechanisms of immunogenic cell death (ICD) in cancer. During continuation of my postdoc at KU Leuven, I have worked on translational and biomarker aspects of ICD in cancer.

7. What are you most proud of?

I am proud of being able to complete the whole therapeutic 'pipeline' for ICD induction in cancer. Over 9 years, in a period covering my PhD and postdoc stints, I started off with the aim of molecularly optimizing ICD in cancer - a very basic, foundational research line; and was able to advance this towards its logical 'end' i.e., a translatable ICD-based next-generation anticancer vaccine that can be hopefully translated towards the clinic in the near future.

8. What’s your interest in the Cancer Immune Setpoint?

My future research aims to understand the positive and negative immunological feedback loops originating from cancer cell death, and its consequences for tumour immunology & immunotherapy. I believe there are several overlaps in my future research vision and the scope of Cancer Immune Setpoint.

9. What do you hope it will achieve?

The Cancer-Immune Setpoint should hopefully achieve a consensus view of different positive or negative drivers of cancer immunology & immunotherapy. I hope this leads to a consensus article that gives a consolidated view to the readers. I have been part of such articles for the fields of cell death, autophagy, danger signals and ICD, and consider that such a strategy works well for the field at large (especially for young researchers who often get confused by differing personal opinions expressed in individual reviews by few labs or researchers).

10. What are your hopes for the future of cancer immunotherapy?

It is clear, with the rapid FDA approvals for several cancer immunotherapies, that this modality is here to stay. But much like targeted therapies, it is necessary to understand the reasons behind why majority of patients fail to respond to immunotherapies. I hope in the future, more attention could be paid to biomarkers-driven application of immunotherapy rather than applying it in an indiscriminate manner (the latter might create a bigger burden on healthcare system).

11. What advice do you have for others working in the field?

It is necessary to prioritize research on different mechanisms governing cancer immunology & immunotherapy. At the same time it is necessary to be highly critical of pre-clinical data. Trade-of-the-mill combinations tested in mice models that fail to create tumour-free surviving mice, and only create incremental prolongation in survival without tumour regression, may not be worth pursuing in long term.

12. What do you do to wind down?

I love spending time with my 1.5 years old daughter! Beyond that I like reading stuff like socio-political commentaries, NatGeo-style articles and comics. I have also recently developed an 'obsession' for the AR-game, Pokemon Go.

13. Tell us something unusual about yourself

In my school days, I wanted to be a dinosaur palaeontologist. I wonder how that would have worked out!

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Go to the profile of Dr Alison Halliday

Dr Alison Halliday

Community Manager, Nature Research

Molecular Biologist turned freelance science communicator, with 10 year's experience at Cancer Research UK.


Go to the profile of David Hicks
David Hicks 2 months ago


The best, (and probably easiest), proposed immunotherapy treatment for many cancers would be an inhibitor of TGF-beta. This should definitely work for beta lineage cancers, most likely for alpha lineage cancers, and probably not for real gamma lineage cancers. You shouldn't assume all brain cancers are caused in the gamma lineage. Researchers should always remain cognitive of which lineage the cancer is instigated in. This will help in the understanding of the multiple outcomes derived with existing treatments.

The immune system is only one of the many pathways that is altered in cancer and other diseases, so on its own, inhibited TGF-beta will not be a cure, but use it as a concomitant treatment that inhibits the correct isoform of PARP that matches the targeted cancer, and it should be as close to a cure that you can get. There are already a number of FDA approved PARP inhibitors on the market.

These two concomitant treatments both alter the cell cycle, so they must be administered intermittently.

Chronically activated TGF-beta locks in the G1 phase producing chronic activation of the adaptive immune system and type 1 interferon, (INF), and CD4+ T cell activation. The inhibition of TGF-beta will allow the activation of Cyclin E and A, allowing the cell cycle to progress. This will prevent the so called immunosuppression that occurs in many chronic diseases.

David Hicks.