This is the second post of a two-part mini series on RNases with Dr Laura Strong of Quintessence Biosciences. If you haven’t yet read it, check out yesterday’s post, which focused on Ribonucleases (RNase) – what are they and why are they relevant to cancer?
Yesterday, we learned that RNases kill cancer cells by a novel mechanism – destruction of RNA – and may be synergistic with some chemotherapy agents.
At the recent American Association for Cancer Research (AACR) meeting, I had the pleasure of meeting several interesting young scientists and physicians either in the poster halls or in various scientific sessions. It seemed a great idea to encourage some of them to contribute some guess blog posts here on PSB.
Dr Laura Strong, Photo courtesy of Pieter Droppert, Biotech Strategy Blog
Amongst the people I met was Dr Laura Strong, President and COO of Quintessence Biosciences.
Yesterday, I mentioned that some of the best bits of this year’s American Association for Cancer Research (AACR) meeting were the numerous gems in the poster sessions.
Reuben Sierra, Ming Tsao's Lab (with permission)
One of the coolest such posters I came across was from Ming Tsao’s group.
Specifically, Rafael Sierra (see photo right) was hosting an excellent piece of research entitled: “Overcoming resistance to EGFR-tyrosine kinase inhibitor therapy in non-small cell lung cancer.”
This is an area of much needed research and breakthroughs.
Why?
The 2012 American Association for Cancer Research (AACR) meeting in Chicago was interesting for several reasons. While there were no truly ground breaking data such as in previous years as with, for example:
there were a lot of encouraging signs for the future.
What made the meeting exciting for me was the sheer number of new compounds emerging from late preclinical to early phase I – clearly companies are looking to restock their pipelines with the threat of major patent cliffs imminent. Not everyone is chasing new compounds to license in! The sheer breadth and depth of the pathways targeted by the new compounds took me a little by surprise.
Today marks the kick off for one of my favourite conferences on the oncology-hematology calendar, with the annual meeting of the American Association for Cancer Research (AACR) being held in Chicago. It’s all about the science and basic research here, although there are clinical sessions, usually on strategy and early emerging phase I/II data.
Wifi is usually pretty good at the AACR annual meeting, although it can be more variable at the smaller meetings. Like many attendees, wifi permitting, I’ll be tweeting from the conference and blogging some of the interesting highlights over the next few days.
One of the biggest challenges facing cancer research was aptly summarised by Levi Garraway and Pasi Jänne in this month’s Cancer Discovery journal:
“All successful cancer therapies are limited by the development of drug resistance. The increase in the understanding of the molecular and biochemical bases of drug efficacy has also facilitated studies elucidating the mechanism(s) of drug resistance.”
It will therefore come as no surprise to PSB readers that resistance occurs with two drugs approved by the FDA only last year; vemurafenib (BRAFV600E melanoma) and crizotinib (ALK+ lung cancer). We’ve discussed the development of resistance in melanoma here via several potential mechanisms in the past and potential strategies for overcoming them (eg MEK inhibitors), but what about lung cancer?
Cancer metabolism is fast becoming an area to watch out for in R&D. Last month I tweeted that I was attending a one day meeting at NY Academy of Sciences on Cancer Metabolism with keynote speakers Drs Lou Cantley and Craig Thompson. Jonathan Mandelbaum (@biotechbaumer) responded saying it looked like a dress rehearsal of another related meeting he was attending the following week. That was too good an opportunity to miss, so I invited Jonathan to consider guest posting a summary of the Keystone event he attended here on Pharma Strategy. I’m delighted to say he kindly took me up on the offer and what follows is Jonathan’s synopsis, including some references he chose to illustrate the key points, most of which are open access.
Back in 2009 at the American Association for Cancer Research (AACR) Molecular Targets meeting, a researcher (Anirban Maitra) from Boston had a most interesting poster about the use of nanotechnology to deliver nab-paclitaxel (Abraxane) to pancreatic adenocarcinomas in a more targeted fashion. You can read about it in more detail from the meeting coverage at that time.
Essentially, one of the things that stops chemotherapy being more effective in advanced pancreatic cancer is that the stromal layer forms a physical, almost impenetrable layer, that slows drugs from getting through to the tumour.
During my years in Pharmaland, I often sat in waiting rooms waiting to see the Principal Investigator (PI) for one of the studies we were doing. I would generally see them at the end of the clinic, preferring to arrive early and chat with some of the patients to learn of their experiences, the trials and tribulations of cancer therapy. This keeps your feet on the ground – drug development is not an academic exercise, there are real people involved after all.
This week I have been in Orlando for the American Association for Cancer Research (AACR) Special Conference on prostate cancer chaired by Drs Arul Chinnaiyan (U. of Michigan) and Charles Sawyers (MSKCC). It was a superb meeting, probably one of the best I’ve attended since the PI3K meeting that AACR hosted in February last year. I wrote nearly half a Moleskine of notes that vaguely resemble chicken scratch – there were so many good talks that stimulated new ideas and explained a few scientific things I also didn’t know too well. Learning is a continuous lifetime experience, after all.