In my final post from the 2013 annual meeting of the American Association for Cancer Research (AACR), I wanted to
I will be writing in the next few days about some of the Pharma and Biotech winners and losers at the 2013 annual meeting of the American Association for Cancer Research (AACR) that just finished in Washington D.C.
However, what was noticeable to me was the disappointing lack of Twitter conversation from the 18,000 cancer scientists at the meeting.
Part of this may reflect the culture of AACR, where it is forbidden to take photographs, record or transmit information. “Thou shalt not tweet” may be thought of as a logical extension of this. It’s certainly not easy to distil complex science into 140 characters.
However, some people did tweet from the meeting and a quick look at the Symplur analytics for the #AACR meeting hashtag, shows the following:
- Highest number of tweets came from Dr Naoto Ueno (@teamoncology), a breast cancer medical oncologist from MD Anderson Cancer Center in Houston, who was not even at the meeting, but clearly would have liked to have been.
- The second highest number of tweets came from Dr Philippe Aftimos (@aftimosp), a hematologist/oncologist from Institut Jules Bordet in Brussels. Philippe wins my award for the most outstanding social media contribution from AACR 2013. He shared insights throughout the meeting in English; I could not do that in a foreign language. Outstanding!
- Also on the AACR twitter leader board was patient advocate/cancer survivor AnneMarie Ciccarella (@chemobrainfog) who presented a poster at the meeting on the power of social media for breast cancer advocacy (#BCSM). Blog readers may recall AnneMarie and other patient advocates did a phenomenal job of live tweeting #SABCS last year.
There were many others too numerous to mention who live-tweeted from AACR this year, and my post is not intended to showcase some people over others, but offer my impression that cancer scientists have not embraced social media in the way that cancer doctors and patient advocates have at clinical meetings such as ASH and ASCO.
There was no public display of Tweets or a conference Twitter Board, as there is now at leading medical meetings organized by ECCO, ESMO, AUA or ASH where delegates can watch meeting tweets in real time in the common areas. A heavily tweeted session will attract new attendees while it is ongoing.
At these meetings, I have often seen people go to sessions based on how interesting the tweets are. I follow the “law of two feet” that says if the tweets are more interesting in another session, time to get up and move there. It’s funny to watch others do the same thing and converge on a room at the same time.
While watching the Twitter board at ECCO or ESMO, I have been asked how to sign up for Twitter in order to follow the conversation (and hopefully be part of it). There was no twitter board at AACR to encourage such behaviour.
Those attending the ASCO annual meeting, will know the unofficial Tweet-up attracts a large party. The AACR unofficial tweetup had just 5, and did not as far as I am aware even merit a RT from @AACR!
To highlight the enormous gap between cancer researchers and cancer physicians when it comes to social media, one only has to look at the annual meetings of the American Society of Clinical Oncology (ASCO) and American Urological Association (AUA).
In recent years both ASCO and AUA have offered a workshop on how oncologists or surgeons can use social media in their practice. It is increasingly important as a tool for sharing and communicating information. There was no workshop at AACR on how cancer researchers could use social media to collaborate or share their research.
Why is this important you may ask? The reason that I am taking the time to write this is that if cancer researchers want the public to support the funding of research, then they need to communicate the value of what they do.
Last year, leading cancer researchers, including a past president of AACR and several Professors of Medicine, tried to obtain 25,000 signatures for a White House Petition in support of maintaining the budget for the National Institutes of Health (NIH) given the important role it plays in funding cancer research. AACR decided not to support this initiative and the petition sadly fell short by a few hundred signatures of the number needed to force an official response.
This year during their annual meeting, AACR organized a Rally for Medical Research (#RallyMedRes) to protest against the forced NIH funding cuts that were implemented as a result of the failure of the United States Congress to agree a budget deficit program.
An expensively organized rally with a stage that resembled a rock concert preached to the converted on the need to spread the word on the value of medical research. Whether it will have any effect in reversing NIH cuts remains to be seen. I fear it was too little too late and an attempt to metaphorically close the stable door after the horse has already bolted.
If cancer researchers want the public to fund their research, in my view one of the things they need to do is communicate the value of the scientific research they conduct. One way to do this is to embrace social media more, particularly at meetings such as AACR, where there is the opportunity to share information with a worldwide audience.
Next year at AACR, I hope we will see a Twitter board at the entrance to the meeting and more cancer researchers encouraged to participate in the conversation and share their thoughts and experiences. AACR could learn a lot from medical oncologists and patient advocates on how to embrace the true power of social media.
Genentech’s next generation PI3-kinase inhibitor, GDC-0032, was the topic of two presentations yesterday at the 2013 annual meeting of the
The cherry blossoms are finally blooming in Washington DC for the 2013 annual meeting of the American Association
The forthcoming annual meeting of the American Association for Cancer Research (AACR) in Washington DC is a must attend for anyone interested in cancer research and new cancer drugs in development.
Many readers will know that one of the hallmarks of cancer is the evasion of apoptosis or cell death. Drugs in development that act as an inhibitor of apoptosis proteins (IAP) are starting to show promise against this target.
Novartis IAP Inhibitor LCL161
At the 2012 San Antonio Breast Cancer Symposium (SABCS), a phase 1 trial with LCL161, a novel-IAP antagonist from Novartis, showed promising responses in triple negative breast cancer when given in combination with paclitaxel chemotherapy. The SABCS data showed that in the 52 patients treated with LCL161, a complete response was observed in 1 patient, and a partial response was seen in 15 patients.
Caution must obviously be expressed at extrapolating from early-stage data in a non-randomized trial.
Several other companies have IAP antagonists in early development, including Curis (CUDC-427).
- Curis announced in November they had licensed GDC-0917 from Genentech. I am hopeful there will be new data on CUDC-427 at the AACR annual meeting. At the recent Citi Global Healthcare Conference on Feb 25, 2013, Curis stated they could start phase 2 development of CUDC-427 by mid-2013 and were looking at it in combination with capecitabine (Xeloda) in breast cancer as well as monotherapy.
- Ascenta Therapeutics licensed their IAP inhibitor AT-406 to Debiopharm in August 2011.
Nature Reviews Drug Discovery has a review article on “Targeting IAP proteins for therapeutic intervention in cancer” for those interested in learning more about some of the compounds in preclinical and clinical development, and the scientific rationale behind this target.
IAP inhibitors are an interesting class of compounds to watch as they move forward in clinical development.
IAP Inhibitors may promote Bone Metastasis
Research published in the February 2013 issue of the AACR journal Cancer Discovery shows that in mouse experiments a side-effect of IAP inhibitors is promotion of osteoclast activity. Whether these preclinical results in animal models translate to man remains to be seen, but the research by Chang Yang and colleagues from the Washington University School of Medicine in St Louis, MO is worth noting.
In simple terms, osteoclasts are the cells that remove bone as part of a dynamic equilibrium with osteoblasts, the cells that produce and lay down new bone.
An increase in osteoclasts caused by IAP antagonists activating alternative NF-κB signalling through NF-κB-inducing kinase (NIK) results in the disruption of normal bone metabolism. In mouse experiments, this led to over-degradation of bone and osteoporosis (pathological bone loss), as well as providing a microenvironment that favors tumor expansion and metastasis.
Osteoclasts embedded in the bone matrix also release tumor growth factors, so if there are more osteoclasts then more growth factors are produced resulting in the creation of a more favourable microenvironment for bone metastasis.
In addition to showing the effects of IAP antagonists on the bone microenvironment, Chang Yang and colleagues demonstrated that drugs that prevent bone resorption such as zoledronic acid were able to decrease the incidence and severity of bone metastasis.
Many breast, cancer, prostate and lung cancer patients end up with bone metastases, which is why bone targeted agents have an important role to play in the treatment of the disease.
They conclude in their Cancer Discovery research paper that “future clinical trials of IAP antagonist-based therapy may require detailed examination of this potential for enhanced bone metastasis and osteoporosis, as well as possible combination with antiresorptive agents.”
The potential implications of this research is that bisphosphonates such as zoledronic acid and RANKL-targeted compounds, such as denosumab, may need to be used in conjunction with IAP antagonist treatment.
This is an important finding. If the animal results translate to humans, then concomitant administration of a bone target agent may be necessary. Future clinical trials of IAP antagonists could end up with more complex and expensive study designs if bone side effects needs to be monitored and addressed.
I look forward to learning more about IAP antagonists at the AACR meeting in April, and to following progress in this novel class of new drugs that seek to address one of the hallmarks of cancer.
Yang, C., Davis, J., Zeng, R., Vora, P., Su, X., Collins, L., Vangveravong, S., Mach, R., Piwnica-Worms, D., Weilbaecher, K., Faccio, R., & Veis Novack, D. (2012). Antagonism of Inhibitor of Apoptosis Proteins Increases Bone Metastasis via Unexpected Osteoclast Activation Cancer Discovery, 3 (2), 212-223 DOI: 10.1158/2159-8290.CD-12-0271