This month has brought a flurry of regulatory activity in the prostate cancer landscape with several companies seeing noticeable action in the new product development area:
While thoughts have already turned to the forthcoming ASCO 2012 meeting and today I am off to AUA 2012 in Atlanta, the annual meeting of the American Association Association for Cancer Research (AACR) last month continues to generate insights.
At AACR I was delighted to meet up with Philippe Aftimos, MD, a Clinical Research Fellow at the Jules Bordet Institute in Brussels, Belgium. Philippe is medical coordinator of the Clinical Research Unit and someone who I met through social media (@aftimosp), so it was a pleasure to meet in person.
It’s that time of the year again where we cogitate and contemplate on what might be hot at the annual meeting of the American Society of Clinical Oncology (ASCO) before the abstracts are available (they’re released online tomorrow at 6pm ET).
This year, while interesting early data from up and coming small biotechs is likely to be eagerly presented in poster sessions, the focus is more likely going to be on big Pharma with various phase III and also late phase II trials that are due to report data. Unfortunately, not all of these will produce overwhelmingly positive results though!
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.
Amongst the people I met was Dr Laura Strong, President and COO of Quintessence Biosciences.
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:
- vemurafenib in BRAFV600E melanoma
- vismodegib in basal cell carcinoma (BCC)
- crizotinib in ALK+ lung cancer
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.
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.
A couple of recent controversies in the field of angiogenesis have fascinated scientists and clinicians alike, namely:
- Does VEGF inhibition lead to more aggressive tumours?
- What drives metastases and invasion?
- What is the role of tumour hypoxia in this process?
Data was originally presented in glioblastoma by Rubenstein et al., (2000), showing that anti-VEGF antibody treatment prolonged survival, but resulted in increased vascularity caused quite a stir. Several other groups subsequently demonstrated in preclinical models that VEGF signaling shrinks tumours, but also results in increased invasion and metastases (see Casanovas et al., (2005), Ebos et al., (2009), Paez-Ribes et al., (2009), for examples).
Every now and then my eye is caught by reports of new fusion genes being found in different cancers. Often these descriptions involve researchers across multiple laboratories due to the rarity of the target. Following a discussion on Twitter yesterday, a friend sent me the link to this interesting paper published in Science Translational Medicine. Naturally, one of the first things that came to mind was ‘is the identified target druggable?’
Tanas et al., (2011) used deep gene sequencing and conventional cytogenetics to identify two genes involved in chromosomal translocation in epithelioid hemangioendothelioma (EHE), a rare vascular sarcoma that arises out of endothelial cells, namely: