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Commentary on Pharma & Biotech Oncology / Hematology New Product Development

Posts by MaverickNY

The decade we learned the language of life

By on December 31, 2009

In the last 10 years, scientists have looked deeper into the mechanics of life than ever before. They have learned how molecules come together to make living organisms, how biological glitches cause common diseases, and have come within a whisker of creating new lifeforms in the laboratory.

Genetics was at the heart of the revolution. Scientific and technological advances allowed researchers to read every letter of an organism’s genome. The letters make genes, which are the templates for proteins that make cells. And the cells, in the tens of trillions, build the animals and plants around us.

The first major achievement came in 2001 when the 13-year, $4bn (£2.5bn) human genome project produced the first draft of the human genetic code. The huge task became a race between a global consortium of publicly funded scientists and an American genetics pioneer, Craig Venter.

via guardian.co.uk

This vividly reminds me of a summer school biology project we had to write way back in 1980 entitled “Life on Earth – what will the next decade hold in Biology?”

My biology teacher was rather annoyed at the annual PTA meeting my parents attended with what she called my “incredulous futuristic sci-fi” predictions that the human genome would be sequenced and we would start to unlock the code to health and disease.

Hmmm, well, wrong decade and only by 10 years, but hey! it’s happening right here, right now.

Sometimes all you need is a little imagination, patience and a few billion dollars to make dreams come true 🙂

Posted via web from sally church’s posterous

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A Happy New Year to y'all…

By on December 31, 2009

'Tis New Year's Eve and time to wish everyone all the best for 2010 from us at Pharma Strategy Blog. 2009 has been a very long year and it's time to draw it to a close and look forward rather than back.  A quick review of 2009 and a forward look at 2010 can be found here.  

Ice_age

All the comments, suggestions and email correspondence that we've received has been sincerely appreciated.  When this blog restarted in Feb 2008, I never thought it would be half as successful or as fun as it has been, so a big thank you to all our readers, we appreciate it and enjoy learning from you too.

For starters, today I'm going to resist the temptation to post the top 5 blogs of the year or even the five I liked the most, which are not necessarily the same thing, as that would be somewhat self serving.

Instead, I'm going to think about 5 things that I hope to see in 2010 and beyond gain some traction in the cancer field:

  1. Nanotechnology
  2. Maintenance therapy
  3. Better techniques for earlier detection of carcinomas
  4. Predictive and prognostic biomarkers
  5. Improvement in overall survival in NSCLC
  6. New inhibitors making progress such as MET/MEK/ALK

Nanotechnology got hot at AACR this year with several groups using nanocells to deliver more drug inside the tumour, to great effect.  Better options for maintenance therapy is very much needed, especially in AML, where there is a big need to improve durability of remission.  It seems odd that there are guidelines for such treatment in ALL but not AML. Time to change that, methinks.  

Obviously, the earlier you detect a cancer, can treat it with surgery with or without therapy, the better the long term survival. Numerous cancers are not detected until later stages, eg pancreatic cancer, but there is a lot of basic research going on to delineate biochemical changes that suggest a cancer is there. Biomarkers have only begun to scratch the surface in oncology; I have a feeling we will start to see more progress in this area next year, perhaps by AACR in April.

There are a number of exciting compounds in late stage (phase III) development, some of which may well have some interesting data at next year's ASCO.  Expect more posts on this throughout 2010.

Last, but by no means least, I've been following various MET/ALK and MEK inhibitors at AACR for a few years now and while they clearly may not be effective as single agent therapy, data may well mature next year in various combination trials.  Watch this space on that area!

What are you looking forward to in 2010?

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links for 2009-12-30

By on December 30, 2009

#ASH09 meeting report: Myelodysplastic Syndromes (MDS)

By on December 30, 2009

This is my second to last report on the interesting new data coming out from the American Society of Hematology (ASH) meeting in New Orleans, LA earlier this month. They've taken a little long than I expected to get through due to our current workload and client reports, so sincere apologies for the backlog.

The final update will be a comprehensive one on chronic myeloid leukemia (CML), but today I wanted to focus on myelodysplastic syndromes or MDS for short.  Let's start with a basic question: what are they?

According to the NCI:

"The myelodysplastic syndromes (MDS) are a group of disorders characterized by one or more peripheral blood cytopenias secondary to bone marrow dysfunction.  MDS are diagnosed in slightly more than 10,000 people in the United States yearly for an annual age-adjusted incidence of 3.4/100,000 people."

MDS can arise naturally or as a result of chemotherapy given to treat acute myeloid leukemia (AML). Unfortunately, secondary MDS has a much poorer prognosis than de novo.

Standard treatment options include:

  • myeloablative allogeneic stem cell transplantation
  • azacitadine or decitabine
  • lenalidomide for patients with deletions of chromosome 5q31.

A few years ago I remember sitting in a packed plenary session and getting goosebumps hearing about the lenalidomide data in patients with 5q31 deletions, or maybe it was the freezing hangar where the presentations were being held, but the science behind the concept was fascinating.  

The question is, what was hot this year at ASH in MDS?  Here's a roundup of some of the interesting data I thought was interesting and relevant to this disease:

  1. Bortezomib (Velcade): This study suggested that Millennium's drug, currently approved for the treatment of myeloma and mantle cell lymphoma, may be effective in MDS. The study included 10 MDS patients with a median age of 64 years. Bortezomib was given at a dose of 1.3 mg/m² on days 1, 4, 8 and 11 every 28 days for a maximum of eight cycles. 6 patients completed all eight cycles. Of the 6 evaluable patients, 3 patients (50%) achieved a minor red blood cell response, and three patients (50%) achieved stable disease. 7 out of 10 patients survived to the median follow-up of 24 months.

    Four patients experienced severe neutropenia (low white blood cell count), and six patients experienced severe thrombocytopenia (low platelet count). 7 patients experienced other non-blood cell-related side effects including diarrhea, fever, skin rash, and pneumonia. 

    It was concluded that single agent bortezomib has some initial efficacy in achieving hematological improvement in MDS patients but a larger sample of MDS patients is needed to confirm these results.

  2. Lenalidomide (Revlimid): Some German researchers looked at gene expression profiles to try and predict responses to therapy in MDS.  They found that single sample prediction could discriminate 3 out of 8 patients as possible responders to lenalidomide, but this was not correlated with the clinical course of those patients while on treatment with the drug.  In addition, it appeared that none of the MDS-patients receiving lenalidomide showed significant clinical response as defined by reduction of transfusion requirement by 50% or transfusion independence.  The researchers concluded that prediction of response to treatment with lenalidomide in patients with Non-Del 5q myelodysplastic syndrome by gene expression profiling remains difficult.

    A phase III trial looked at the optimal dosing for lenalidomide in 205 patients wo were randomised to receive either 5mg or 10mg of lenalidomide versus placebo.  Previous phase II trials have shown that lenalidomide resulted in transfusion-dependence (RBC-TI) in 67% of patients and complete cytogenetic response (CyR) in 45% of patients with RBC transfusion-dependent low or intermediate risk MDS with del5q.

    The researchers concluded that both doses of lenalidomide were generally well tolerated and achieved significant transfusion dependence and CyR. Lenalidomide 10 mg was associated with better RBC-TI and CyR than 5 mg, while maintaining a comparable safety profile.  The data supported the use of 10 mg as a starting dose, with dose reductions or discontinuations, if needed.

  3. Arsenic trioxide (Trisenox):  A phase II study investigated the combination of ATO and ascorbic acid is tolerable.  The drug was administrated intravenously over 1 hour at the loading dose of 0.30mg/kg/day for 5 consecutive days, followed by 0.25mg/kg/day twice weekly for 15 weeks. Ascorbic acid 1000mg was given by IV within 30 minutes after each arsenic trioxide infusion.

    44 patients were enrolled in the study and 10 obtained a response (23%), including 1 complete remission. In 8 out of 10 responders, the response was evident within the first 8 weeks of treatment. 52% patients discontinued treatment because of various factors including disease progression (11%), severe adverse events (32%), drug unrelated adverse events (5%) and withdrawal of consent (5%).  Severe neutropenia and thrombocytopenia were observed respectively in 45% and 23% patients. 

    4. Overall, the researchers concluded that the combination of ATO and ascorbic acid was tolerable and active in about 25% of MDS patients. The addition of ascorbic acid to ATO does not increase neither the toxicity nor the response rate to ATO.  The tolerability of this regimen is reduced in elderly and high risk patients.


  4. Vorinostat (Zolinza): Merck's HDAC was initially approved for CTCL, a rare form of NHL, but we have seen little dramatic data from other clinical trials since.  There is, however, significant logic in testing epigenetic therapy in MDS.

    This phase I study looked at the combination of vorinostat with decitabine in the treatment of newly diagnosed AML or MDS using 6 different dosing schedules including concurrent and sequential therapy.  72 patients were entered into the study with a median age of 68 years and 58% were male. To date, 69 patients have discontinued. Of the 70 patients evaluable for safety, 69 experienced AEs, the majority of which were relatively mild ie grade 1/2 in severity and included nausea, diarrhea, fatigue, constipation, and vomiting.  In MDS patients receiving concurrent therapy, complete remission (CR) was achieved in 2 out of 5 patients, stable disease (SD) in 1 patient, partial remission (PR) in 1 patient, and hematologic improvement in 1 patient; all 6 of the patients who received sequential treatment experienced SD.

    Overall, although preliminary, the data is promising and indicates that the combination of vorinostat and decitabine, either concurrently or sequentially, is possible without significant toxicity.

In all, while MDS is a particular difficult to treat disease, the initial results suggest that further investigation of drugs such as bortezomib, lenalidomide, arsenic trioxide and vorinostat is warranted and if further studies show more durable and repeatable responses, we may potentially see some new treatment options for MDS in the near future.

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Pfizer terminates figitumumab trial in lung cancer for futility

By on December 29, 2009

At the end of each day I do a spot check of my Twitter stream to see what's going on.  Imagine my surprise to see the following suddenly appear:

Picture 67
Oh wow, that was the trial we reported on when Pfizer suspended the patient enrollment into the study back in September and notified the clinical trial database, but did not put out a press release about it.  It subsequently turned out that there were more deaths from strokes in the figitumumab arm, suggesting that either the groups were unbalanced for co-morbidities or cardiotoxicity might possibly be an issue.  Previously, we posted a blog expressing concern about the potential for cardiotoxicity with this class of drug.

Here is the actual press release from Pfizer relating to the tweet above.

It seems that the study has now been terminated because the results suggested that adding figitumumab to standard carboplatin plus paclitaxel would not meet the primary endpoint, ie overall survival.  Pfizer were at pains to state that other figitumumab trials were ongoing, including studies in refractory NSCLC, prostate and breast cancers and Ewings sarcoma.

Meanwhile, the IGF-1R inhibitors once looked very promising, but with the termination of Pfizer's trial in NSCLC and Roche/Genentech declining to continue development of Genmab's R1507 due to a portfolio review rather than safety concerns, it will leave a lot of other companies wondering what to do with their IGF-1R inhibitor in development. 

Sometimes though, a particular class of drug can go through a whole pile of different inhibitors until one emerges from the pack triumphantly, as Genentech's VEGF inhibitor, bevacizumab (Avastin), did a few years ago.

2009 has not been a particularly good year for Pfizer Oncology with several Sutent trials being terminated in colorectal cancer, GIST and breast cancer and now the figitumumab lung cancer trial flopping.  Hopefully, they will bounce back in 2010 with their ALK inhibitor in NSCLC.

Fortune sometimes favours the brave.

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When NICE lives up to it's name…

By on December 29, 2009

Lately, we seem to have heard nothing but bad news from across the pond with the National Institute for Clinical Effectiveness (NICE) seemingly rejecting approval for reimbursement of many new cancer drugs, causing an outcry in the physician and patient communities alike.  One such example was the recent rejection of the second generation tyrosine kinase inhibitors (TKIs), dasatinib (Sprycel) and nilotinib (Tasigna) after failure of imatinib (Glivec) in chronic myeloid leukemia (CML).

However, this morning I heard from industry friends that actually, NICE has finally approved something without too much drawn out hassle.

The drug?

PharmaMar/J&J's trabectedin (Yondelis) in soft tissue sarcomas.

Interestingly, the same drug is getting a rather rough ride with the FDA and ODAC in ovarian cancer over here in the US, but anecdotally, I have heard from several oncologists who participated in the EU trials that the drug has a role to play in refractory STS given the lack of choices beyond ifosfamide based regimens.

So, what can we learn from the NICE decision, especially given that J&J also managed to obtain reimbursement for Velcade in the UK?

It is clear that companies not only need to show some pharmacoeconomic benefit, but also offer some discount or incentive for the cash strapped NHS to see a bargain.  J&J made a creative deal whereby they would cover the cost of bortezomib (Velcade) in cases where the drug did not work, so the NHS would only pay for those that did. 

What happened in this case? 

NICE originally issued draft guidance earlier this year not recommending trabectedin
for use on the NHS due to its high cost.  According to the final appraisal document published on Dec 21st, a workable solution had been hammered out:

"Trabectedin is recommended as a treatment option for people with advanced soft tissue sarcoma if:

  • treatment with anthracyclines and ifosfamide has failed or
  • they are intolerant of or have contraindications for treatment with anthracyclines and ifosfamide and
  • the acquisition cost of trabectedin for treatment needed after the fifth cycle is met by the manufacturer."

All in all, that seems a fair enough solution with a win-win for everyone involved.  In 2010, we may well see more sensible approaches like this with some flexibility to work towards compromise on both sides. Drug companies are learning that they can't just charge what they like willy nilly expecting approval based on limited resources and NICE is learning to be creative in seeking effective solutions to increase patient access to new therapies that may make a difference to their daily lives.

Who knows, the US may well gravitate towards the inclusion of cost-effectiveness measures in decision making over the next 2-3 years as well.

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#ASH09 meeting report: Non-Hodgkins Lymphoma

By on December 28, 2009

There was so much new data presented at the recent American Society of Hematology (ASH) meeting in New Orleans that I'm still digesting it all!

Today, I thought it was time to summarise what's hot in lymphomas, in particular, NHL.

Non-Hodgkins lymphomas (NHL) are a heterogeneous group of diseases affecting white blood cells with distinct clinical, morphologic, immunohistochemical, and molecular subtypes as defined in the 2008 World Health Organization (WHO) classification (PDF download).

In Europe, the German and French NHL groups are very methodical in taking each new potential regimen and comparing it in a randomised trial to the current stand of care to determine which is better, whether that be in terms of safety, tolerability or efficacy.  In New Orleans, a number of particularly interesting studies were presented for discussion in indolent NHL.

Impact on the current standard of care

One of the most interesting findings
was a realisation that the standard of care for non-Hodgkins lymphoma
(NHL) is likely changing soon with the new data on the
bendamustine-rituximab combination looking to overtake standard R-CHOP
in first line treatment of newly diagnosed patients.

At ASH, Mathias Rummel presented data on an upfront study of bendamustine plus rituximab (BR) versus R-CHOP in patients with indolent (slow growing) lymphoma.  The study population included mostly patients with follicular lymphoma, which accounted for probably 50% or so of the population, but about 20% or so of the patients had mantle cell lymphoma and the remainder had other indolent lymphomas. 

What was interesting about the results was the complete response rate significantly favoured BR, as did the progression-free survival.  When looking at the safety profile, the two-drug regimen versus the five-drug R-CHOP regimen seemed to be associated with a far superior safety profile, with patients having much less neutropenic fever and all of the other associated hematologic toxicities seen in patients with R-CHOP. 

When I interviewed Dr Owen O'Connor from the NYU Cancer Institute for Clinical Research about the data, he described the study as "potentially paradigm changing" in indolent lymphomas.  This may well turn out to be an accurate conclusion clinically, although it should be noted that the BR regimen will inevitably cost more than R-CHOP.

A long standing issue that has been unaddressed in diffuse large B-cell lymphomas has been the debate on whether a shorter R-CHOP regimen over 14 days would lead to better results than the standard 21 day regimen.  The Germans, lead by Dr Pfreundschuh and colleagues, have long suggested that accelerated CHOP-based chemotherapy was superior to classic or conventional R-CHOP21 therapy based on data from the RICOVER trial. 

This year, a heated debate apparently broke out in the NHL oral session after the French presented data from the GELA trial, demonstrating that R-CHOP21 was superior to R-CHOP14, both in terms of safety and toxicity profile, as well as efficacy, presumably because the shorter regimen was associated with more adverse events.  It should be noted that the French study inclusion criteria was for patients over 65, so these results may well be applicable to that specific population, where tolerability is very important.

W2W4 (Watch to watch for) in the future?

A walk round the poster sessions left me struck with how many interesting compounds are now being tested in NHL, after a bleak period of disappointing data.  Such compounds included AT-101, a gossypol and Mcl-1 inhibitor, and ABT-263, a Bcl-2 inhibitor. 

It is early days yet for determining true efficacy, but both compounds appear to have manageable tolerability in the phase I trials completed to date.  The rationale for ABT-263 is probably strongest in follicular lymphoma given the t(14:18) translocation, which gives rise to constituitive overproduction of Bcl-2. 

In the future, we may well see studies with either agent in combination with rituximab to determine if efficacy and tolerability can be further improved.

I missed the oral NHL sessions as they clashed with the CML sessions (more on that tomorrow), but a quick check of several experts who attended them brought the following additional suggestions of new agents in development in NHL from Novartis and Roche:

  1. Use of mTOR inhibitors such as everolimus (Afinitor) in refractory Waldenström macroglobulinemia (WM), a rare, indolent non-Hodgkin lymphoma, was considered very interesting. The data showed that everolimus had high single-agent activity with an overall response rate of 70% and manageable toxicity in patients with relapsed WM, and offers a potential new therapeutic strategy for this patient group.
  2. RO5072759 (GA101) is the first humanized and glycoengineered type II monoclonal anti-CD20 antibody to enter clinical trials and is being developed by Roche.  In vitro data show RO5072759 exhibits increased antibody-dependent cytotoxicity and strongly enhanced cell death (apoptosis) compared to rituximab.  The ORR in refractory NHL data presented in a phase I study at this meeting was 43%, with many of the patients being heavily pre-treated.  RO5072759 is now being explored as a single agent in phase II in relapsed/refractory indolent/aggressive NHL and B-CLL and in combination with chemotherapy in a phase Ib study.

Conclusions

Overall, the bendamustine-rituximab data was probably one of the stories of the conference and will likely see take-up in favour of R-CHOP in first-line NHL given the efficacy and tolerability benefits.  Trials are also ongoing in CLL, and thus if positive, we may well see some CLL patients being given with BR over fludarabine-based regimens such as FC and FCR in 2010.

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The transcriptional network for mesenchymal transformation of brain tumours: Nature

By on December 27, 2009

The inference of transcriptional networks that regulate transitions into physiological or pathological cellular states remains a central challenge in systems biology. A mesenchymal phenotype is the hallmark of tumour aggressiveness in human malignant glioma, but the regulatory programs responsible for implementing the associated molecular signature are largely unknown. Here we show that reverse-engineering and an unbiased interrogation of a glioma-specific regulatory network reveal the transcriptional module that activates expression of mesenchymal genes in malignant glioma. Two transcription factors (C/EBPβ and STAT3) emerge as synergistic initiators and master regulators of mesenchymal transformation. Ectopic co-expression of C/EBPβ and STAT3 reprograms neural stem cells along the aberrant mesenchymal lineage, whereas elimination of the two factors in glioma cells leads to collapse of the mesenchymal signature and reduces tumour aggressiveness. In human glioma, expression of C/EBPβ and STAT3 correlates with mesenchymal differentiation and predicts poor clinical outcome. These results show that the activation of a small regulatory module is necessary and sufficient to initiate and maintain an aberrant phenotypic state in cancer cells.

via nature.com

Glioblastoma is a nasty, aggressive form of cancer but no one has really known why or how to stop it growing, as a long line of therapies have proven largely ineffective.

This fascinating and important study identifies two genes, C/EBP and Stat3, which are active in about 60% of glioblastoma patients.  They appear to work in tandem to turn on many other genes that make brain cells cancerous.

Patients in the study whose tumours showed evidence of both genes being active died within 140 weeks of diagnosis. In comparison, half of patients without activity from these genes were alive after that time, suggesting the two genes may have a role to play as 'master controls' in the disease, driving cells in the brain to become glioblastoma cells.

Of course, future focus will shift to developing effective targeted therapy against the genes to determine whether inactivating them will have any effect on the cancer.

Time will tell. Watch this space!

Posted via web from sally church's posterous

ResearchBlogging.orgCarro, M., Lim, W., Alvarez, M., Bollo, R., Zhao, X., Snyder, E., Sulman, E., Anne, S., Doetsch, F., Colman, H., Lasorella, A., Aldape, K., Califano, A., & Iavarone, A. (2009). The transcriptional network for mesenchymal transformation of brain tumours Nature DOI: 10.1038/nature08712


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New trends in Pharma: the growth of generics

By on December 23, 2009

Earlier this year, we were deep into a consulting report on general trends in the Pharma industry and were struck by data in different yearly reports from PhRMA, the industry body in the US.  Basically, when we pieced the data together, it was clear that the market share of generics was not only growing but also likely to get worse in the next 2-3 years with major expiries expected.

Take a look at this chart we put together from PhRMA reports:

Picture 63
In the last 8 years, the share of generics has increased by an amazing 21% and the future growth may well increase to 9-10% per annum in the near term.

We were therefore not in the slightest bit surprised to read this report in The Economist last month predicting that a huge drop in branded sales revenues is to be expected in 2011, which is very much in line with our own analysis and predictions:

Picture 61 In case you're wondering what's happening in 2011, think blockbusters such as Lipitor, Plavix, Seroquel and Zyprexa to name a few and some of those will experience patent challenges before then.  Interestingly, between 2009 and 2011 Pfizer (Lipitor), Lilly (Gemzar and Zyprexa) and sanofi-aventis (Eloxatin, Taxotere and Plavix) will all see major losses in revenues due to patent erosion as they scramble to make up for the losses with various approaches.

In addition on the oncology front, Taxotere, Doxil and Gemzar are all due to expire next year, so the biggest impact in overall revenues will likely be seen in 2011 when multiple generic entries will further drive the price down significantly.

It's no wonder, then, that Pharma and Biotech companies are starting to rethink their future strategies given the dearth of new products coming through the pipeline at a rate that isn't fast enough to replace the blockbusters going generic. 

What options are out there that can be considered?

a) License late stage or 'hot' products from smaller pharma or biotech companies at a premium.  Many oncology companies are racing to do this such as J&J with abiraterone, Astellas with Medivation and Celgene with romidepsin, for example.

b) Creative life cycle management such as new formulations, branded generics or own-label medications (eg Novartis has successfully tried combinations of these with Voltaren, Sandogobulin and lactulose)

c) Expand into generics in emerging countries such as China, Brazil, Russia and Asia where their is a rapidly growing middle class demand for new medicines to treat lifestyle and aging diseases (eg sanofi-aventis, Pfizer, Novartis, Merck and GSK)

d) Consolidate therapy areas and have a narrower focus with increased licensing ties or acquisitions in specialty areas of interest (eg BMS, Genentech)

e) Greater focus on rarer diseases with a strong focus on rationale drug design and efficacy, leading to higher per patient prices (eg Genzyme, Novartis, Allos Therapeutics)

The recent round of mergers is unlikely to be the last for a while as others are already happening or being worked on.  The rate of licensing deals has begun to pick up significantly lately, driving up the asking price in the process, as Biogen IDEC found recently when Facet Biotech tartly declined their $17.50/share offer for the company.

Overall, I think the general trend for utilising more creative strategies with generics, emerging markets and better life cycle management strategies are here to stay.  There will always be new products coming onto the US market, but with an increasing focus by the Obama Government on pharmacoeconomics and cost effectiveness of new medicines, the Pharma industry must either innovate, diversify or struggle as patent expiries focus everyone's attention on the bottom line.  

It will be interesting to see who comes out stronger and better positioned for the future and who dies.  The difference between winning and losing is sometimes very small, as Vion found this year with Onrigin. Others may well follow suit and seek bankruptcy protection in 2010 if their Russian Roulette strategy doesn't come up trumps.

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The roller coaster of life

By on December 22, 2009

One of the things about running a consulting company is that life is more like a roller coaster than comfy slippers by the fire.  The workload is extremely uneven and veers between insanely busy and very quiet, with little in between.  As Kipling said, one should treat the two imposters the same and make the most of each.  Here at Icarus, we've been insanely busy since my mother unexpectedly passed away on July 6th and we're still busy now while all around us clients are taking their much needed time off over the Holidays.

YONGIN-SI, SOUTH KOREA - NOVEMBER 26: South K...Image by Getty Images via Daylife

Thankfully, a quieter inbox means less urgent demands and allows more time for reflection and analysis, as we have several reports due the first week of January, so not much opportunity for slacking here.  Aside from finishing off 2009 projects, we're also spending some time thinking about new ideas for collaboration projects in 2010 and some exciting new services we'll be rolling out to help our Pharma new product development and marketing clients too.  It's easy to forget that it's not about the technology per se, but the benefits tools bring and how they can be used to make a difference.

This weekend we had a huge snow dump on the East Coast and while many were stressed with flights and travel arrangements or digging their cars out of several feet of snow, one of my fellow consultant Twitter buddies, Steve Woodruff, posted this joyful video of his one year old pup gamboling wildly in the snow with great energy.  I loved it; the unbridled enthusiasm reminded me exactly how I feel about understanding the science and biology of disease:

Don't you just love the joy she brings?  Thank you Mystic for brightening my day!

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