How social media led to my current research in IBC via twitter and blogging?

In my last post I discussed some of what drives my research and my overall goals. This post I wanted to take 1 step back and share my unusual story with how I got here starting with picking this postdoc. Usually how postdoc-seeking works is that 3-9 months before graduating (if you’re on the ball) or shortly after defending if you’re staying in your PhD lab for a while, you make a short list of PIs who you want to work for. You might have people in mind that you’ve met at a conference or followed their work for a while, or maybe your mentor has some recommendations, or maybe you’re just desperate to move to a city for personal/family reasons and you narrow it down that way. Regardless of how you attack it, you make a list, and then you generally go to PubMed and look at their work, and figure out what it is you want to do in the context of their work. Then you write emails to them with a carefully crafted CV and overview of what you would like to learn/accomplish and why you would be a good fit for their lab …and hope and wait for a response back inviting you to go interview….and if it’s a big famous PI, you might have your mentor call a few weeks later if you haven’t heard back….

Of course, like everything else in my educational background, I had to be the unusual one in my grad program….none of the above applied to me, since I had decided that my top postdoc choice would be in a new (at the time) translational training program at MD Anderson called TRIUMPH. The program not only would allow me to work in any of the program labs doing great clinically-relevant research, but the extra training experiences are unmatched anywhere else in the country. In learning about the program, I realized that I would not have to do the above research into the PIs ahead of time before applying to the program, since I would be accepted (or not) to the program as a whole and then spend the 1st month or so meeting with all the mentors to find a good match. Seemed like an easy decision to apply, especially given the pretty straightforward process.

March 2011-July 2011 = Crazy few months!

A lot happened in the few months between applying to TRIUMPH in March, getting accepted….and moving to Houston in July – lots of travel including 2 back-to-back conferences in 2 countries with entirely different posters, writing my 200+ page thesis in ~2.5 weeks, defending, graduation, big paper revisions …. etc….then literally a day after my defense (yes I have email PROOF), I get word of an upcoming fellowship opportunity through the Department of Defense that the TRIUMPH program director wants me to apply for.

The thing is….it just happens to be due ~3 weeks after graduation, and eeeek what do I even know about breast cancer??? * At first I think, “I need a break, I’ll pass this up this cycle” and “what about all the interviews I would be doing – isn’t this a big waste of time to limit myself to breast cancer” which I had thought (and still think) is a pretty crowded field compared to a few of the other tumor types I thought I might work in.

The counter arguments going through my head included “I do not want to look like a slacker before I even join the program if I refuse nicely to do it” and oh look at how much $ is involved if I did get it**. Eventually I talked myself into hanging out at my favorite Austin coffeeshops  and doing it since I’m a bit crazy and like grant writing anyway, and it would be good experience regardless of getting it….and if by chance I selected another lab but got an offer, I could turn it down (HAHA – such wishful thinking!) So I came down to Houston the next week, met with the director, looked over her grants and papers, and came up with a potential social-media-inspired project with a teeeeensy bit of preliminary data….wrote the whole thing in about 3 days (+ a weekend on the most repetitive attachments ever), got funded, and the rest is history. As an aside, for the 1st few years of grad school I was not that interested in academia because I thought I sucked at coming up with ideas for research….how times have changed now that I realize how much I like to write and think about science

Social Media as Research Inspiration?

So now you’re thinking, how on earth did she get her research idea from twitter? Tweets are only 140 characters of inane updates on what people are eating or doing, right? NO NO NO!!!. You see, behind those little 140-character status updates is a person (usually!), and there is a huge range of twitter content. Indeed social-media savvy folks use twitter for productive purposes, and frequently they also have a website listed in their profile, as well as relevant key words so they can be contacted by like-minded folks.

It turns out that as an early adopter of most technology, I joined twitter in early 2008***. But after not really investing much effort into it, I didn’t really see the point, since I wasn’t getting a lot out of it. (This is still a common theme I hear when I try to convince my IRL friends about the benefits of twitter) Anyway…I ignored twitter for more than a year, maybe close to 2 years. I didn’t even log in. But then something made me try again more seriously to follow more people and engage in conversations to see if anything worthwhile would happen. In the early days, when my twitter handle was @flutesUD, I looked for interesting people to follow by doing searches for terms like “cancer”, “research”, “science” “flute”….One of these people that popped up in one of the general science-y searches was @whymommy, (Susan Niebur) who I credit with being the inspiration for my major research direction. However, had she not had a blog, I may or may not have actually followed her and certainly wouldn’t be studying IBC or likely even know what it is.

You see, Susan was an IBC patient who blogged not only about parenting and life at her blog but her journey with IBC. I’m sure I’ve mentioned that IBC is a rare, but highly aggressive form of breast cancer that unfortunately receives very little press either in the public media or even in the scientific literature – hence I had not even heard of it prior to coming upon Susan’s blog.

Over a couple of evenings I decided to read her entire blog archive to really understand it, and also followed all of the links on her really helpful IBC links page. Clearly because of the dearth of good quality information available at the time on the internet, Susan had a passion for providing educational content and outreach to fellow patients, and in my view did an outstanding job of this. Through exploring her blog and the other sites, I realized that not very much is known about the biology of this terrible disease that presents and behaves very different clinically from “regular” breast cancer. In addition since patients with this disease don’t have many therapeutic options beyond standard chemotherapy, mastectomy and hard-core radiation, I realized that something must be done to help patients such as Susan (who was fighting her first recurrence at that point)…and thought it might be a good niche to get into, given that I also followed the MDACC IBC clinic director on twitter (@teamoncology). After a few back-and-forward emails with Dr Ueno discussing my idea, I had him lined up to be my co-mentor on the grant to help with the clinical side of the project, and to establish feasibility of the work, since nobody else in my lab works on IBC.

To come full circle on this story, it saddens me greatly to say that last year this week, unfortunately Susan passed away after a tough battle with IBC recurrences (as is unfortunately still so common in this disease). I started this post back then as a tribute since I regretted never leaving any comments on her blog to let her know the impact of her posts, but embarrassingly the first draft was too unwieldy and needed a lot of pruning and focusing. In between all my long hours in the lab & program requirements, it got tossed aside (& lost on my stolen laptop). It’s fitting however a few days after a great twitter chat (#bcsm – on Monday nights) that I post my story to thank all the patient advocates and health bloggers for writing and sharing your stories on social media. Many of you might never know the real reach of your writings even long after you post them, but please keep on doing them as long as you are able to.

~~~

* This is known as imposters syndrome within academics. It’s pretty common.

** not that I would see any extra $$$ directly, but it does pay for more of my research than pretty much any other postdoctoral fellowship would, and allows me a few extra freedoms

*** Yup, nearly my 5 year twitter-versary on 3/16/13!

Emotional investment in cancer research – how much is necessary for good research?

One of the thought-provoking articles that has come up repeatedly in my twitter feed this week, is an article in the NY Times about (and written by) a young woman who found out that she carries a BRCA1 mutation. After discussing the reasons behind wanting to know whether she carried the gene mutation, she mentions enrolling in a cancer biology class taught by a

“professor [who] filled his slides with dark oncological puns, lecturing with the almost robotic detachment I sometimes see in those who work closely with cancer”…

Reading this paragraph as a cancer researcher, I asked myself to what extent do I portray the robotic detachment she mentions, and does this lead to better research?  Its now a few days after I read the article but I don’t think I really have an answer yet.

To elaborate, my work now is really translational – if you ask me what the measure(s) of my success over the next few years is, here’s my answer: I would have designed a biomarker-driven treatment strategy for IBC patients that still appears promising after rigorous preclinical work including animal model testing and a clear understanding of mechanism. My data so far on my main project is coming along very nicely!

In addition, because I am in the TRIUMPH postdoctoral training program, I have the unique opportunity to be exposed to clinical issues at a deeper level than virtually any other PhD-track program in the country.  This year, in parallel with my lab research, I am engaging in rotations with various specialties within MDACC (pediatrics, medical oncology, radiation therapy, phase 1 trials, surgical oncology). In reflecting on my experiences so far, and talking with my peers, it is crystal clear to us why we are here.  Papers in nice high-IF journals, awards, invited talks etc are nice (and desirable qualifications for those of us who want to stay in academia), but at the end of the program, many of our goals include being able to see our work translate directly into patient care.

On top of these IRL opportunities, I have enjoyed interacting with a group of cancer survivors and patient advocates on social media and reading blogs, which has given me a deeper understanding of the impact of cancer on people’s lives than the average lab scientist, and made me even more driven to do clinically-relevant work. Time will tell whether time invested in such activities above and beyond my long days in lab, will actually make me a better researcher – but I have my suspicions it will.

In contrast, when thinking back to my PhD which was in a much more basic science-driven department, my success was measured by how elegantly I could prove a mechanism for some biological process (in my case how oxidative stress and DNA damage signals to particular pathways to regulate cell survival/death), and by most people’s definition, I was successful in this endeavor. Looking back at some of my peers I have to admit that I saw some of the “robotic detachment” mentioned in the article, not only from those who worked in cell lines/yeast on fundamental biology questions (like understanding all the binding partners of protein X or what genes ABC transcription factor regulates). Perhaps it was just such fundamental (and SLOW!) research combined with the struggles of grad school that made even the brightest students to sometimes appear uninspired.  However, even some of my colleagues who worked on mouse models of XYZ cancer seemed to care only enough to do their project to their committee’s satisfaction.  To be fair, some superficial level of detachment is probably necessary for working with animals that have to be sacrificed during/after the study, especially after the researcher induced disease (in the most humane way possible).  However deep down, I think that most cancer researchers aren’t very detached from their work. After all, cancer touches us all at some point whether individually or people close to us.  Maybe its just a question of degree instead of a black-and-white detached or not attitude. Hey, maybe we can be robots WITH hearts – if that’s what it takes to make a real difference!

*****

What do you think fellow biomedical researchers? Do you feel detached from your work i.e. is it mainly just a fun/interesting way to make a living or are you deeply invested in the broader implications of your work?  Or is the reality of the disease you are working on so depressing that you need some objectivity to survive.

SABCS mini-series post 2: What’s new and upcoming in triple negative breast cancer?

In this second overview of research presented at SABCS, I thought I would focus on the excitement building with regard to options in triple negative breast cancer (that is tumors that don’t express the estrogen receptor, progesterone receptor or HER2).

In the past, triple negative disease has been defined in terms of what proteins are NOT expressed, but at this meeting, we heard from Dr Jennifer Pietenpol how TNBC is actually a heterogenous disease with 7 subtypes based on a large scale gene expression analysis of more than 3000 tumors from 21 worldwide data sets (not a trivial bioinformatics effort!).  The major take home talk from her fabulous talk is that most of these subtypes have particular targets that may be feasible for targeting. As an example, about 11% of TNBCs actually express the Androgen Receptor (called the Luminal Androgen Receptor subtype), which is known to be a key growth regulator in prostate cancer, but until now has not received much attention in other tumors.  The availability of AR antagonists such as bicalutamide means that now it is possible to target AR in breast cancers as well, although more detailed characterization of its function in breast cancer is still needed.  As such, there will shortly be a trial available at Vanderbilt, using bicalutamide in combination with a PI3K inhibitor (because this subtype is highly enriched for PIK3Ca mutations – in TCGA dataset 50% of the LAR subtype had PIK3Ca mutations vs 3% in TNBCs as a whole).  In case you are interested in reading more, the majority of Dr Pietenpol’s data was recently published in the Journal of Clinical Investigation (Lehmann et al, see references below).

Another interesting talk in the TNBC session on Tuesday was by Trey Westbrook, a young professor at Baylor College of Medicine. His research is focused on using genetic screens to uncover new targets. This functional approach is complementary to many of the large scale genomic screens such as the TCGA and ICGC that are being performed since targets that inhibit tumorigenesis that overlap with gene-level changes (amplification/mutation) are more likely to be true drivers vs passenger changes. In addition, targets that are validated functionally allow us to narrow down a large number of potential molecules for further study, since drug development and even basic research to understand mechanism is quite expensive.

So with that background, I will describe some of Dr Westbrook’s findings from his basic screen using a shRNA library transfected into normal mammary cells that have been immortalized with telomerase and SV40.  The goal was to figure out which shRNAs induce transformation of these immortalized cells, which is tested using a standard anchorage-independent growth assay.  A total of 42 new tumor suppressors were uncovered in this screen, but he only presented data regarding one of them,  that is PTPN12.  PTPN12 is a phosphatase that is mutated in about 5% of TNBCs but when analyzed further is found to be down-regulated by other (unknown) mechanisms in about 60% of TNBC tumors. Next the lab asked what does PTPN12 do? Phosphatases act in opposition to kinases that add phosphate groups to other proteins ie they remove these phosphates, which usually (but not always) turns off a protein.

Figure 1: Network of proteins regulated by PTPN12

To figure out which proteins PTPN12 acts on, they did an elegant proteomic experiment using SILAC and compared the phospho-tyrosine proteome in cells with high PTPN12 levels and shRNA-depleted cells. What they found was that PTPN12 regulates a whole network of tyrosine kinase receptors including EGFR, HER2 and PDGFb, and that collectively these pathways drive tumorigenesis (see figure 1). This is exciting because there are currently available drugs against many of these pathways, so there is renewed enthusiasm in testing novel combinations of TKIs in this biomarker-defined subset (that is PTPN12 low). As a proof of principle preclinical study in xenograft tumors in mice, a combination of crizotinib and sunitinib to target cMet and PDGFRb (respectively) was tested. Individually each agent showed only very minimal tumor growth delay, however in combination tumor growth was halted, and the mice lived statistically longer (see key tumor growth rate in figure 2).

Figure 2: Tumor growth rate in mice treated with crizotinib and/or sunitinib

Once again, some of this work has been published recently in Cell, although this specific pharmacological combination was not presented in the publication (Sun T et al, see references)

References:

Lehmann B et al, “Identification of human triple-negative breast cancer subtypes and preclinical models for selection of targeted therapies” JCI 2011

Sun T et al, “Activation of multiple proto-oncogenic tyrosine kinases in breast cancer via loss of the PTPN12 phosphatase” Cell 2011

SABCS Mini-series post 1: Pfizer CDK4/6 inhibitor is a #win

I just returned from my first San Antonio Breast Cancer Symposium which was an information-packed week of talks, posters, and meeting interesting people.  I had a blast, learned a ton, and made a valuable connection at a company for a future study.  The next few posts on my blog are going to cover the biggest news items as well as what I personally found the most interesting at the meeting.  But outside of these topics, if you have any questions, feel free to comment and maybe I’ll add a post or just get back to you on it. The online resources available to the attendees of the meeting are vast so even if I didn’t attend that session, I should be able to get an answer for you from them or my twitter colleagues who attended.

I will kick off this short series of posts, with what I thought was the most promising new therapeutic advance, and this is the latest analysis of the trial of Pfizer’s CDK4/6 inhibitor, PD-0332991.   When I was reading up on drugs for the book chapter I just wrote on cell cycle targeted therapies, apart from my own drug of interest, I was most excited about this compound.  And indeed, the clinical results of a randomized phase 1/2 study presented by Richard Finn were stunning! The progression-free survival curve presented is shown in figure 1. “LET” stands for letrozole, a non-steroidal aromatase inhibitor, an FDA approved drug that is currently used in post-menopausal patients with hormone-sensitive tumors.

Figure 1: Progression-free survival curves for letrozole vs PD+letrozole in postmenopausal ER+ patients.

To elaborate on this study, which was a worldwide multi-center trial of postmenopausal ER+, HER2- patients based on the preclinical work that highlighted that targeting CDK4/6 only works in the context of cells with intact G1 checkpoint (ie wild-type Rb). In case you are not familiar with the cell cycle, figure 2 has a schematic of the cell cycle and proteins involved in each phase.

Figure 2: Cell cycle schematic

Note that CDK4 and CDK6, targets of this drug,  function in complex with cyclin D1 to phosphorylate and inactivate Rb, which is a major cellular brake on cell proliferation. It would make sense then that targeting CDK4/6 in the context of tumors cells that have lost Rb would be ineffective. Since luminal (ER positive) breast cancers also frequently overexpress cyclin D1, Pfizer decided to focus on these patients, however they do have an additional 3 separate trials in lymphoma and myeloma, based on preclinical data in these models too.

This drug was incredibly well tolerated, with the majority of the AEs being grades 1 or 2. The only added toxicity over letrozole alone that was observed in more than a few patients was neutropenia, which was described by Dr Finn as “uncomplicated”, and expected for this class of compounds which do affect normal cells as well.

The results of the biomarker analysis was intruiging however for the basic scientists among us. Even though it was thought that cyclin D1 amplification or loss of p16 (which is a negative regulator of CDK4/6 activity) would be predictive biomarkers of sensitivity, and were used to enrich the phase 2 part of this trial for potential responders (after phase 1 found the maximum tolerated dose). However, upon biomarker analysis at the end of the study, they found that these proteins were no better than ER alone at predicting response.  Clearly, further work is necessary to find a biomarker of response (and/or resistance), even though the clinical benefit rate of 70% seen in this study was quite impressive. In conclusion though, based on these data (both preclinical and this study), a registration study is planned to start in 2013.

References (journal articles):

Preclinical breast cancer papers:

“PD 0332991, a selective cyclin D kinase 4/6 inhibitor, preferentially inhibits proliferation of luminal estrogen receptor-positive human breast cancer cell lines in vitro.” – Breast Cancer Res Treatment 2009, pubmed link

“Therapeutic response to CDK4/6 inhibition in breast cancer defined by ex vivo analyses of human tumors.” – Cell cycle 2012, pubmed link

Preclinical other tumors:

“A novel orally active small molecule potently induces G1 arrest in primary myeloma cells and prevents tumor growth by specific inhibition of cyclin-dependent kinase 4/6.” – Cancer Res 2006, pubmed link

“Pharmacologic inhibition of CDK4/6: mechanistic evidence for selective activity or acquired resistance in acute myeloid leukemia.” – Blood 2007, pubmed link

“Pharmacologic inhibition of cyclin-dependent kinases 4 and 6 arrests the growth of glioblastoma multiforme intracranial xenografts.” – Cancer Res 2010, pubmed link

“Selective CDK4/6 inhibition with tumor responses by PD0332991 in patients with mantle cell lymphoma” – Blood 2012, pubmed link

PARP inhibitors and PI3K inhibitors – a new option in triple negative breast cancer?

This week’s Cancer Discovery had 2 exciting articles on combining PI3K inhibitors with PARP inhibitors in breast cancer. I was particularly intrigued as these papers have a solid mechanistic explanation of the mechanism of synergy so I thought I would do a post on the 2 papers. But first a little background…

PARP enzymes play important roles in a specific type of DNA repair pathway called BER (or base excision repair). PARP inhibitors have been developed to inhibit DNA repair in tumor cells that have other defects in DNA repair, such as BRCA1 or BRCA2

Figure 1: Synthetic lethality in the setting of BRCA1/2 mutation (From: Polyak K, Nature Med 2011)

mutant breast and ovarian cancers (which have defective homologous recombination).  This concept is what is known as a synthetic lethal relationship (see figure 1 for schematic) – either defect alone doesn’t have much effect, but when combined together do have an effect (ie cell killing).  Several PARP inhibitors have been developed, including olaparib and MK-4827, which have been tested in patients with BRCA1/2 mutations.  The results from these trials have been somewhat promising, with response rates between 30-40% without considerable toxicity. However these responses have not been very durable.

BRCA1 and BRCA2 germline mutations only account for 5-10% of all breast cancers however, so researchers have been trying to figure out whether PARP inhibitors might have some utility in patients who have not inherited these alleles.  This is where these new papers come in.

So why the excitement about combination with PI3K inhibition? There are 2 reasons:

* Combinations of PARP inhibitors and cytotoxic chemotherapy is effective in preclinical studies, however in patients unfortunately the toxicities are also additive, especially immunosuppression, which leads to dose reductions/delays. These results suggest that the therapeutic window for these treatment strategies may actually be pretty narrow.

* We already know that the PI3K pathway is highly relevant in most breast cancers in different contexts –as primary genetic defects or as resistance mechanisms to endocrine/HER2-targeted therapy. Specifically in triple negative breast cancer for example, alterations include PTEN mutations, INPP4B phosphatase loss and PIK3CA activating mutations (rarer). Unfortunately despite expressing these potential biomarkers of sensitivity to PI3K inhibition, cancer cells are really smart, and if we just use PI3K inhibitors alone, feedback loops are quickly turned on to help cells survive, so combinations with PI3K inhibitors are definitely going to be the way forward.  In addition, it is known that BRCA1-mutant breast tumors have elevated PI3K pathway activity.

To briefly summarize the 2 papers, starting with my favorite of the 2:

“Ibrahim et al, “PI3K inhibition impairs BRCA1/2 expression and sensitizes BRCA-proficient triple-negative breast cancer to PARP inhibition” was interesting because the premise of the whole paper is that regular triple negative breast cancers could be made more like BRCA-mutant breast cancers via PI3K inhibition. This is called “BRCAness” and is actually a pretty neat concept, since there is data showing that among triple negative tumors, those with BRCA1/2 mutations actually respond to chemotherapy better.  So why would PI3K inhibition cause “BRCAness”?  It has been known already that PI3K can regulate steady state levels of homologous recombination, so the authors took one of my favorite cell lines MDA-MB-468 which has wild-type BRCA, and knocked down either BRCA 1 or PIK3CA (the catalytic subunit of PI3K), and observed an increase in cells with gamma H2AX, a marker of DNA damage. This phenomenon was also seen with the pan PI3K inhibitor NVP-BKM120. They went on to explore the mechanism further, and showed that PI3K inhibition decreased BRCA1/2 protein level both in cell lines and in 2 out of 3 xenograft models taken from patients which correlated with response to PARP inhibitor treatment. And finally they carefully dissected out the mechanism by PI3K inhibitors decreased BRCA expression, and found the pathway to be via ERK activation of ETS1 transcription factor. The overall model they proposed is in figure 2.

Figure 2: Model for synergistic activity (From: Rehman FL et al, Cancer Discovery 2012 “In the Spotlight”)

The second study: “Juvekar et al, “Combining a PI3K inhibitor with a PARP inhibitor provides an effective therapy for BRCA1-related breast cancer” basically showed that in a transgenic mouse model of BRCA1-hereditary breast cancer, that both olaparib (the PARP inhibitor) and the PI3K inhibitor NVP-BKM120 could inhibit tumor growth by some degree alone, but when given together caused a 14-fold delay in tumor growth. The growth curves are pretty impressive given that these tumors grow exceedingly rapidly! Tumor growth inhibition by Pi3K inhibition involves many pathways, and they show specifically inhibition of AKT as a pharmacodynamic marker, as well as decreases FDG-uptake as a functional readout. Angiogenesis (growth of new blood vessels) is also significantly decreased by BKM120 treatment.

The mechanism of synergy that they go on to explore involves PI3K inhibition blocking DNA repair via impaired Rad51 recruitment to DNA damage combined with the already existing defect in homologous recombination repair. As a result the tumor cells would become more dependent on PARP-mediated repair, so if you then add a PARP inhibitor, you kill them better. However if the tumors relapsed, these markers of DNA damage were increased over baseline and MAPK signaling could compensate for PI3K survival signals.

In closing, here are a few take-home points I took from both studies together

* Based on the mechanism of action, I would postulate that combining ERK inhibitors in triple negative breast cancer with PI3K inhibitors and PARP would be counterproductive.

* Method-wise, I liked that both studies used patient-derived xenograft models which are now being viewed as superior models to traditional cell-line derived xenografts.  The fact that the Juvekar study saw greater synergy in vivo versus in cell lines, points to why doing such studies in animals is important and may lead to greater insight into mechanisms of action that are not cancer cell-intrinsic.

* Trials with PARP inhibitors and PI3K inhibitors should now routinely be adding gamma H2AX as a pharmacodynamic marker to show that the drugs are working.

References (both free! )

Ibrahim et al paper: http://cancerdiscovery.aacrjournals.org/content/2/11/1036.full

Juvekar et al paper: http://cancerdiscovery.aacrjournals.org/content/2/11/1048.full

How cheap do they think postdocs are?

I am in the lab really late tonight, and finished everything except waiting on my MTTs to be done, so I was just doing some website searching for a few products I need for my upcoming experiments, and I came across an interesting marketing spiel.

During my PhD when I needed a lot of rapamycin for my animal studies, I found this company called LC Labs, as a result of having to shop around, and overall I think they’re pretty cool – they don’t waste money on extravagant  marketing/trade shows/brightly colored catalogs/sales reps etc to keep prices low.  When I figured out how much rapamycin I would need for even the first 2 months of the study (and I had hoped it would last even longer if the mTOR pathway was important!), it would be $40K.  Yikes!   Even though my lab in grad school was very well-funded and we never worried about money, this figure was a bit shocking, so my PI asked us to look around….LC Labs to the rescue….just as an idea 1mg at Sigma is around $279, whereas LC Labs equally pure product is $225 for 500mg!….They have a handy-dandy chart on every product page with their competitors prices based on mass and purity claim which I like again, as it demonstrates transparency.

So even now I continue to check them out for drugs/reagents that I can’t just get for free from the pharmacy here.  On the staurosporine page tonight I read this funny statement that caught my eye:

“Buy 100-300 mg from LC Labs; support a postdoc for 1-2 years with the money you save!”

LOL, but really???  Lets see, if I needed a boatload of it (since it [staurosporine] inhibits many kinases at very low nanomolar doses) and wanted to order 300mg it would cost $1590 from LC Labs.  Most of their competitors don’t sell such a large size, but biorbyt does, and they charge $2245 for the same 300mg (according to the price table)….a $655 difference. Where can I find a postdoc for $655/year or even $655/month? (I’m taking notes for my future lab

Collaboration in Science Twitter Chat Tomorrow

As the complexity of performing science increases, collaboration is becoming increasingly necessary to accomplish great things.  Collaboration may occur across disciplines, continents and type of environments, but regardless of scope, there are a number of challenges and opportunities in moving forward in this new era of collaborative science especially for young scientists lacking broad networks and experience working with diverse groups of people.

Here at MD Anderson* we’re paving the way for novel types of interactions to become mainstream – who would’ve thought multiple competing pharmaceutical companies each with drugs that would work best in combination, would work together on a clinical trial. Its happening here because we have the power!!! (ie the patients, experience and the leadership)

Other examples of new types of collaborations can include company sponsorship of academic lab activities such as preclinical studies or method validation.

Tomorrow (Wed Feb 1) on the life science twitter chat, which you can participate in by following the hashtag #ls_chat, that my friend @Comprendia and I started last year, we will be discussing collaboration in science.  Some of the topics that we will be discussing include finding opportunities for academic-corporate research collaboration, determining how to make them worthwhile to both parties, and most importantly best practices for being a successful team player in such endeavors.

~~~~~~

Please join us tomorrow from 10-11am PT (noon CT/1pm ET) for this (hopefully!) useful discussion between academic scientists, industry scientists and others who are interested in discussing this.  See you on the twitterz!

* note: I’m not speaking on behalf of my employer, just commenting on what’s happening here relating to the content of this post