Hi All,
I’m back to briefly answer some of the questions posed on this thread last weekend. I’ll do them in order given…
justAfterTEM: I’m not a MD so I can’t give medical advice but I do give scientific opinions on clinical trial drugs. There are so many variables (e.g. genetic) in cancer patients that it is impossible to make a blanket statement of what specific current trials I think are scientifically most interesting for all patients. As a general statement, along with many on this forum, I am particularly hopeful that one of the upcoming/in progress immunotherapy trials will identify the trick needed to work for CRC. It is a tough nut to crack (CRC is usually poorly immunogenic) but I am hopeful since there are “so many shots on goal” being taken within the next few years, that at least one will work. Immunotherapy as a “concept” has been the Holy Grail of oncology for many many years but it is much easier said than done – research is finally catching up to the much easier to make “concept”. Every major company/research university/cancer center & countless small biotechs are simultaneously working very hard on immunotherapies right now ever since the CTLA-4 inhibitor Yervoy first showed proof-of-principle in melanoma a few years ago. In the non-immunotherapy space, I think RRx-001 is a very scientifically intriguing molecule with an unique preliminary clinical profile. Likewise, I am intrigued by ADAPT although I wish they would publish more data or at least case studies in oncology journals…
Sleen: STING is the acronym name of the protein “Stimulator of interferon genes”
http://en.wikipedia.org/wiki/Stimulator ... eron_genes Keeping things simple, it is one of the main regulators of half of your immune system called the “innate immune system”. This is an extremely powerful (but historically tough to control) side of the immune system that is an area of intense oncology immunotherapy research right now. The famous PD-1 inhibitors impact the other half of the immune system (the adaptive immune system). They are just now finding new tricks to activate the innate immune system, e.g. with STING activators as well as other targets. There is hope that by activating BOTH sides of your immune system, a broader list of cancer types (e.g. hopefully CRC
) will respond to immunotherapy…
Lilacbreastedroller: See above. In the paper, they also added an immune-activating tumor vaccine called STINGVAX. Historically cancer vaccines have not worked very well because e.g. a vaccine won’t do its job if the associated tumor is shooting out immunosuppresive signals turning off the immune system. In this study they combined 3 things: 1.) a vaccine to teach the immune system/activate it 2.) a STING agonist to activate the innate half of the immune system and 3.) a PD-1 inhibitor to stop the tumor from suppressing the adaptive half of the immune system. Their goal was to impact three different major aspects of immune response simultaneously as a cocktail. And... (in mice at least!) it worked…
Vilca11: I wouldn’t hazard a guess... In broad terms: 1.) many many things work in mice but fail in the clinic. 2.) Even if this strategy ends up working in the clinic, I can’t imagine ever getting a 100% response rate (human cancers are very heterogeneous, the mouse model used was not) 3.) On the positive side, compared to most mouse studies – this one had abnormally excellent results/high activity (in one of the best mouse models) – which is why it was published in a top journal and will generate a lot of attention for follow-up...
-DK
6/4/2012 Dx Stage 3C CRC @ 40 yo. MSS, KRAS-WT, BRAF-WT, p53-mut
7/12 FOLFOX/FOLFIRI
2/13 NED!
8/13 Enlarged lymphs - Stable
10/14 Stage IV. Lung & Lymph mets. 5-FU+bev
3/15 Cetuximab
11/15 FOLFIRI + bev
11/16 Signs of FOLFIRI resistance (Lymph mets)
1/17 Palliative radiation for resistant mets
2/17 FOLFIRI + bev + Maraviroc (off-label)
3/17 FOLFIRI + Erbitux + Maraviroc (off-label)
MSS-CRC Clinical Trial Finder: http://trialfinder.fightcrc.org/2016 Colondar 2.0 ModelDK37 Science Posts List