Pancreatic cancer is one of those conditions I never hope to get. Why? Well, for starters, it’s one of the most difficult to treat tumour types, largely because so many patients are detected late, that is with stage IV metastatic disease. The annual incidence and prevalence are pretty much equal, suggesting that the for many with advanced disease, the lifespan is approximately one year or less. In fact, to put things even more succinctly, despite surgical resection, radiation and chemotherapy, more than 90% of people with pancreatic cancer do not survive beyond 5 years.
Today I’m heading off to attend the ASCO GI meeting in San Fransciso, and in particular, the pancreatic cancer sessions on Friday.
The event promises to be an interesting day with a keynote from Margaret Tempero (UCSF), as well as Daniel van Hoff (TGEN) presenting the much awaited nab-paclitaxel (Abraxane) data in advanced pancreatic ductal carcinoma and a poster on masitinib from the French researchers.
Many of you will recall the excitement expressed at ESMO in this data, although the topline data in the Celgene press release on the MPACT study this week suggests the overall responses were good rather than great.
Today, I’m heading off to The New York Academy of Sciences (NYAS) for an afternoon of lectures on pancreatic cancer. It’s free for members and only $40 for non-members. Previous 1-day and half day meetings I’ve attended at NYAS have been packed with information and very enjoyable.
Why am I interested in this meeting?
Well, aside from Icarus Consultants being one of the media partners for this worthy event, we like to support scientific causes that facilitate cancer research and the communication of the data.
One of the most interesting highlights of this ESMO for me has actually not been some new data or science that was presented here, but the sense of anticipation about the forthcoming nab-paclitaxel (Abraxane) data in pancreatic cancer.
The pancreatic cancer KOLs are a relatively dour group, much as melanoma specialists were until the advent of BRAF inhibitors. It’s largely a function of toiling away in a known graveyard zone with few effective therapies to offer patients and their families and then, suddenly, a new breakthrough is borne that re-energises the sub-specialty and propels it forward again.
Aside from the already published Part 1 and Part 2 blog posts about AACR here on PSB, you can also find some more coverage, including summaries of other topics, on the companion Biotech Strategy Blog, such as the following:
- SARDs, an emerging potential new class of agents for advanced prostate cancer
- Cool robots that automate cell profiling in cancer research
- Update on next generation Bcl–2 inhibitors in CLL
- Novel-novel combinations are emerging in cancer research
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.
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).
Pancreatic cancer as many readers know, is one of those cancers that is generally diagnosed later than most in stage IV and as a result, has a poor prognosis, often only a year or so from diagnosis.
It has been known for a decade that constitutive Kras and NF-kB activation is one of the signature changes in the disease in the majority (80-95% ) of patients. Kras is a particularly important gene because it is often involved with on-off signaling of other genes. In addition, mutational inactivation of a key tumour suppressor gene (Ink4a/Arf) also occurs in over half (50-75%) of pancreatic adenocarcinomas. What is not known, however, is what are the key signaling pathways downstream of Kras and how they relate to pancreatic cancer.
Today on 10th November, it’s the Second Annual Worldwide NET (Neuroendocrine Tumor) Cancer Awareness Day. Granted that’s a bit of a mouthful, but it also seems poignant given so many of my news feeds this morning were still full of Steve Jobs, who sadly passed away from the disease last month.
I’ve been meaning to post an update on this rare form of cancer all year, given that we now have targeted therapies now approved by the FDA for treatment, but things were hectic at the office and then with Jobs passing, the timing just seemed tacky and inappropriate.
Perhaps one of the most beautiful articles I’ve ever read on the internet:
You might want to have some tissues handy before reading.