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.  heart-robotMaybe 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.

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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

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

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

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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.

Progression-free survival curves for PD-0332991

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.

Cell cycle schematic

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

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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

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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 😉

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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

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A Cell/Molecular Biologist’s Guide to iPad Apps

I’ve had my iPad for a little over 2 months now and in spite of craziness revolving around moving across the state and settling in, and gazillions of meetings to select a lab (yes really gazillions!) I’ve had a chance to play around with my new toy a bit.  A certain friend of mine has been prodding me to write this post for a little while, and since this weekend has been relatively relaxing thought I’d go for it.  Here’s my fictional day using my iPad as much as possible.  The links are mostly to the iTunes app store pages for the mentioned apps.

Firstly, I turn on Pandora. I trust you’ve heard of this app so I’m not going to elaborate on its awesomeness.  My world is never quiet unless I’m asleep, whether I’m working on or playing. Unless I forget my headphones – then I’m not a happy camper at work.  Guess I should buy a backup pair for there.

Like most scientists (and most people in general nowadays), I start my day by checking my email on one of my iOS devices (iPhone or iPad).  Great, nothing urgent….now I move onto twitter.  I’ve tried most of the common apps, and because of my tweet consumption style of wanting to try to read everything, Hootsuite is my favorite since I can consistently scroll back the furthest, though interface-wise I much prefer the Twitter app.  Depending on time I may also check on Facebook and Google+ using these native apps.

Next I check my calendar to figure out what I need to do today…I keep my schedule in Apple’s calendar app on my iPhone, which can sync with iPad over Mobile Me. However it is not super reliable (an observation shared by some of my online buddies) so I have not turned on calendar sync lately, and rely on my phone which never really leaves my side anyway.

For my task list, I’ve tried a few apps and I’ve settled on the free-mium Remember the

Remember the Milk Icon

Remember the Milk Icon

Milk one since its simple but flexible (eg you can designate “Waiting for” tasks, can change the dates).  Its also available for every platform, and lots of plug-ins for your computer and online activities (gmail and such) – check out the full list here. You can also organize tasks around locations to avoid making multiple trips to places that are close proximity to each other when running errands for example.  Unfortunately to sync more than 1 device with the website requires you to go “pro” for $3/month or $25/year.  The icon is not THAT cute 😉

OK so now I know what I have to do today….so I’m likely working away either at the bench (or nowadays in the hood doing hours of cell culture!) or at my macbook pro doing these tasks.  I’m trying to get into the pattern of Mondays being a day to read – my auto Pubmed updates are set to arrive on Mondays and so now I’ll delve into reading methods. Speaking of Pubmed, Pubmed On Tap allows you to search Pubmed and read full-text of open access papers/email link to yourself for later.  Pretty useful for when you’re out and you just have to know something…

All the glamor journals (Science, Nature, Cell) have ok apps for browsing the latest tables of contents, however to get full-text its not very straightforward to use an institutional subscription currently.  But at least I can make a note of interesting sounding papers using SimpleNote, which syncs with Notational Velocity on my Mac so I can download the full-texts when I’m on the network or connected via VPN at home.  I actually have half a folder full of journal apps that include some field-specific apps (including AACR publications, my professional society and NEJM – where I aspire to publish a paper during my postdoc!)

For a quick break from work reading I might grab a coffee and check out the news on the New York Times or use Flipboard or Zite for a cool, personalized view of news in a magazine format.  But I try not to get too sucked in.

Back to reading….next I might check out my RSS feeds for my journals. On my iPhone I use Net News Wire as my RSS reader, but unfortunately the iPad version is $9.99.  I personally don’t rely on RSS that much to be worth spending that much on.  Reeder is widely thought to be the best RSS reader on the iPad (though News Rack is a worthy contender in a sizable minority), and for $5 I was willing to download it.  Not only can you read your feeds, but there are sharing options galore (including social media sites twitter and facebook, as well as Instapaper/ReadItLater/Readability and plain old email too).  Speaking of Instapaper – that is a must-buy app for me!  It allows you to save articles for later reading from your desktop/laptop or from your phone and it strips out all the distracting ads etc. and downloads for offline reading later, which for us wifi-only iPad users is great for passing the time on long flights without wifi or while cramped in coach.  As I’m reading I find an article with a useful table which I think I would like to access later, so I save it to Evernote, a great information manager app, and give it some useful tags so I can search for it later either on my computer or phone/iPad.

After all this reading I’m needing some social interaction, so I open up Words with Friends free and play some words. I’m not very good at it compared to some of my friends and my dad, but its still fun.  Then I might see if anyone is on gchat to chat using BeeJive (the iphone version, since the iPad version is $10!).  Oh bummer everyone else is working so I guilt myself back into working….

Suddenly I get a push notification that a webinar I signed up to view is starting in 10 minutes.  So I launch the GoToMeeting app, and go to my email to get the code…and soon enough I’m signed into the webinar, and maybe I eat my lunch while watching, since I gotta be always multi-tasking while eating.

After lunch I go into the lab and begin my benchwork for the day.  I open Safari and browse to my Biodata lab notebook (hopefully soon to be a real iPad app per the biodata team) and see that I have a few things to accomplish today. Firstly I have to set up some restriction digests for my latest cloning project.  But what enzymes and buffer do I need????  Promega comes to the rescue.  Out of all the science-specific apps I have downloaded, this is the most useful in my field (and no I’m not being paid by Promega to say this).  There are a variety of tools including converters, videos about lab procedures, written protocols and protocol info regarding many of their products including catalog numbers if you’re just preparing for your next experiments…..so lets say I find the perfect kit for my study, I just copy the catalog number, open my email application and shoot our lab manager a message with what I would like.  Easy peasy!  Next I realize I need to setup some PCR reactions so I get everything out to thaw, and double check my conditions using the “melting temperature for oligos” tool in Promega.  Next task accomplished.

The other useful laboratory science app I’ve found is Invitrogen’s Daily Calcs, which as it sounds is focused on calculations.  There is some overlap with the promega app here, but also there is a useful cell culture reference for newbies including useful numbers like surface areas, volume of media to use etc…(we all remember the first weeks of cell culture when we were super-anal about every detail).  There is also a useful molecular weight lookup if you know the formula of the chemical.  If only there was a way to also lookup by name.  There you go Sigma – take my idea, link it to your huge catalog and #win!

While my PCRs are running, I open the cool HHMI bulletin app to read some science outside of my field, since a too-narrowly focused scientist can miss interesting new connections.  I read an interesting epigenetics article, which discusses modifications I’m not familiar with so I open EMD Millipore’s cool Histone Map app to learn more,

Histone map

Example of information from Histone Map app

and end up sucked into this fascinating world of nuclear biology for the next half-hour.  Ooops – I’m never escaping lab today at this rate!  Still, at the end of this exploration, I have a few questions ….what do I do?  I use Wikipanion to see what Wikipedia has to say….then I quickly make a post on Quora (using Social Questions) and visit EpiExperts, a cool new scientific community for epigenetics peeps (I’ll do a post on this later) in Safari to post them as discussion items.

OK back to my day.  Digests are done, PCRs are coming along. I check on my cells…everything’s good.  So I go back to my desk and start studying my flash cards I made in Evernote Peek (covered previously here) for my test on Friday.  And soon enough my collaborator from Asia is Skyping me to discuss some cool new data, since it’s the beginning of his day now. At the end of our call, he asks me to sign a form for a grant he is about to submit, so I open iAnnotate PDF and using my stylus add my signature, save and send it back to him in 2 minutes. Quite a productive day I’m having 🙂

I guess its home time soon.  I wonder what I will make for dinner?  So I browse epicurious and AllRecipes for some quick ideas, and prop my iPad up in the kitchen so I can follow along..  Once I’ve cooked my dinner, I sit down and select a movie to watch on Netflix while I eat and wind-down.  Then it’s a quick email , twitter and Words with Friends session before bed, and hopefully I remember to set my alarm (in Apple’s clock app) on my phone before falling asleep. But before sleeping I remember to check my bank account to see if I got paid so here I come Bank of America app.

That’s all peeps.  I have mentioned a lot of apps, but as you’ve probably gathered by now, I use my iPad mainly for consumption tasks, so I don’t have a personal recommendation on work software such as to create Office documents.  GoodReader seems to be a good basic choice, or if I were needing something I’d download Documents to Go. My laptop goes almost everywhere with me so right now this isn’t a huge need.

What are your favorite iOS apps fellow scientists?

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