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Posts tagged ‘Nanotechnology’

Way back in November 2009 at the American Association of Cancer Research (AACR) Molecular Targets meeting in Boston, there was a fascinating poster on the early promise for nanotechnology as a new form of efficient drug delivery for cancer therapeutics (see the blog post here).

Fast forward 18 months and my attention was drawn to a new article published in Cancer Research about how nanotechnology has been used preclinically to deliver therapy for breast cancer into the cancer cells rather than to the cells.  This is a subtle, but important, difference.

For those of your wondering what nanotechnology is, my colleague Pieter Droppert reviewed some basics earlier this month in a blog post:

“Nanotechnology is the application of science and engineering to materials that are between 1 and 100 nanometers (nm) in size.”

He went on to put this in layman terms:

“1nm is one-billionth of a meter.   To put this in context, 1nm is one seven-thousandth of the width of a red blood cell or one eighty-thousandth of the width of a human hair.  These are unimaginably small materials that are engineered to operate at the molecular and atomic level.”

The approach in the latest preclinical research (see references below) is to take trastuzumab (Herceptin) and combine it with biodegradable polymers to form nanoconjugates that are small enough to enter cancer cells because they are more water soluble rather than attack the outside of the cells, thereby potentially reducing toxicities associated with the therapy.

The same group also tried this technique with brain cancer (see references below), allowing the nanocells to cross the usually impenetratable blood-brain barrier, which:

“resulted in a marked inhibition of tumor angiogenesis and growth.”

In the breast cancer research, the group compared the results of their polymer-trastuzumab conjugate with trastuzumab alone in mice:

“Our experiments confirmed that a proper design of the lead nanobiopolymer was possible for efficient blocking of HER2/neu-positive breast tumor growth through dual inhibition of HER2/neu and Akt phosphorylation, and as a result, promoting enhanced tumor cell apoptosis.

The nanobiopolymer’s unique combination of features resulted in highly specific drug accumulation in the tumor tissue and inside tumor cells.”

It will be most interesting to see if this idea is developed clinically in human trials and whether the results will be reproducible or not.

Significance of the findings:

The nanoconjugate concept has promise, not just in allowing a novel drug delivery system to cross impenetrable barriers, but also in reducing the toxicities associated with systemic targeted therapy.  Randomised clinical trials in patients with cancer are required to determine if there is viability in humans.

References:

ResearchBlogging.orgInoue, S., Ding, H., Portilla-Arias, J., Hu, J., Konda, B., Fujita, M., Espinoza, A., Suhane, S., Riley, M., Gates, M., Patil, R., Penichet, M., Ljubimov, A., Black, K., Holler, E., & Ljubimova, J. (2011). Polymalic Acid-Based Nanobiopolymer Provides Efficient Systemic Breast Cancer Treatment by Inhibiting both HER2/neu Receptor Synthesis and Activity Cancer Research, 71 (4), 1454-1464 DOI: 10.1158/0008-5472.CAN-10-3093

Ljubimova, J., Fujita, M., Ljubimov, A., Torchilin, V., Black, K., & Holler, E. (2008). Poly(malic acid) nanoconjugates containing various antibodies and oligonucleotides for multitargeting drug delivery Nanomedicine, 3 (2), 247-265 DOI: 10.2217/17435889.3.2.247

Ding, H., Inoue, S., Ljubimov, A., Patil, R., Portilla-Arias, J., Hu, J., Konda, B., Wawrowsky, K., Fujita, M., Karabalin, N., Sasaki, T., Black, K., Holler, E., & Ljubimova, J. (2010). Inhibition of brain tumor growth by intravenous poly( -L-malic acid) nanobioconjugate with pH-dependent drug release Proceedings of the National Academy of Sciences, 107 (42), 18143-18148 DOI: 10.1073/pnas.1003919107

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Treatment for ovarian cancer hasn't changed much in the last ten years, reflecting the lack of biomarkers and biochemical targets for the disease. Chemotherapy with a platinum (carboplatin or cisplatin) and a taxane (paclitaxel or docetaxel) has therefore formed the bedrock of therapy, along with other options such as gemcitabine or pemetrexed, as illustrated in the latest NCCN Guidelines.

The good news is that the use of paclitaxel-based combination chemotherapy has been shown to increase progression free survival (PFS) and overall survival (OS) in women with primary peritoneal or ovarian cancers.

While a proportion of ovarian cancers have been shown to be highly chemosensitive, a large number unfortunately fail to respond to primary taxane therapy, leading to the emergence of resistant disease.

The big unanswered questions are therefore why does this happen and what can be done about it to improve outcomes and overall prognosis?

It was with great interest that I read about the findings of a new study just published in Cancer Cell from researchers at MD Anderson (see e-link in the references below).  According to the MD Anderson news alert:

"For the first time, Salt Inducible Kinase 2 (SIK2) has been found to play a critical role in cell division and to regulate the response of some ovarian cancers to chemotherapy."

It's not often when you see the mention of both a potential target and prognostic/predictive biomarker mentioned in the same sentence as ovarian cancer, so this is huge news!  The press release went on to claim:

"Researchers found that depleting SIK2 from ovarian cancers sensitized the cancer cells to paclitaxel, a commonly prescribed chemotherapeutic agent that inhibits cell division, making the drug more effective in stopping the cancer's growth. Levels of the SIK2 protein are increased in approximately 30 percent of ovarian cancers and are associated with poorer survival in women with the disease."

The researchers analysed nearly 780 pools of siRNAs to identify proteins that alter sensitivity to paclitaxel. They found that SIK2 regulates sensitivity to paclitaxel and prevents cell division. This means that SIK2 may offer a useful therapeutic target for pipeline drugs to be developed in ovarian cancer.

What was even more fascinating was that another related article on ovarian cancer from Bast's group appeared in the same journal. In essence, they used siRNA-loaded nanoparticles to stifle a protein, Zeste homolog 2 (EZH2), which is associated with poor survival. This resulted in inhibition of angiogenesis (formation of new blood vessels) to the tumour and caused a steep reduction in the tumour burden in a mouse model of ovarian cancer.

In this study, the authors looked at human 180 ovarian cancer tumours and found that the protein was overexpressed in the tumour samples (66%) and in the endothelial cells (67%). It is relevant to note that endothelial cells line the inside of blood vessels and play a crucial role in angiogenesis.

In practice, they found that women with increased EZH2 levels in their tumours had a median survival of 2.5 years compared to 7.33 years for those without. Looking at overexpression in the endothelial cells, the difference was 2.33 years versus 8.33 years for those with normal levels.

Like me, you're probably wondering how these nanoparticles work.  According to MD Anderson:

"The nanoparticles accumulate in the cancer cell and vasculature passively as they circulate in the blood stream. Chitosan nanoparticles are so small that they can flow through tiny holes in the tumor vasculature. They also accumulate in other organs, so the researchers are working to add a targeting molecule that will limit nanoparticle uptake to tumors and their vasculature."

Targeting EZH2 may have application beyond ovarian cancer, since it been associated with the progression and spread of bladder, breast, prostate and gastric cancers and cancer of the pharynx.

All in all, a really interesting pair of papers from Bast's group, which may have clinical promise and real application to the future treatment of ovarian cancer.

 

ResearchBlogging.org Ahmed, A., Lu, Z., Jennings, N., Etemadmoghadam, D., Capalbo, L., Jacamo, R., Barbosa-Morais, N., Le, X., Vivas-Mejia, P., & Lopez-Berestein, G. (2010). SIK2 Is a Centrosome Kinase Required for Bipolar Mitotic Spindle Formation that Provides a Potential Target for Therapy in Ovarian Cancer Cancer Cell, 18 (2), 109-121 DOI: 10.1016/j.ccr.2010.06.018

Lu, C., Han, H., Mangala, L., Ali-Fehmi, R., Newton, C., Ozbun, L., Armaiz-Pena, G., Hu, W., Stone, R., & Munkarah, A. (2010). Regulation of Tumor Angiogenesis by EZH2 Cancer Cell, 18 (2), 185-197 DOI: 10.1016/j.ccr.2010.06.016

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Nanotechnology is a topic that fascinates me, ever since hearing some interesting data in pancreatic cancer at the American Association of Cancer Research (AACR) meeting last November on Molecular Targets in Boston.

Someone kindly sent me a paper from PNAS recently (link below), from 2008, which got my attention essentially because:

"Integrin aBv3 is found on a subset of tumor blood vessels where it is associated with angiogenesis and malignant tumor growth. We designed a targeted aBv3 nanoparticle (NP) encapsulating the cytotoxic drug doxorubicin (Dox) for targeted drug delivery to the expressing tumor vasculature."

Now, giving doxorubicin by the normal route of administration results in noticeable weight loss and other side effects when given systemically.  Using nanotechnology, a 15-fold increase in anti-metastatic activity without concomitant weight loss, which is very interesting indeed.

The authors noted that integrin could represent an ideal vascular targeting receptor since it is highly expressed on the angiogenic endothelium and expression of this receptor on tumor vessels correlates with disease progression.  This was first shown by Gasparini et al., in 1998 (see reference source below).

Meanwhile, in this 2008 study, the researchers used models from renal cell and pancreatic carcinoma to determine the effectiveness of the nanoparticle delivery system. Given that the results appear better with metastatic rather than primary tumour growth, I wondered if anyone was looking at this concept with currently approved drugs for metastatic disease?

A quick search for nanoparticle and cancer in the clinical trials database brought up mostly trials associated with nanoparticle paclitaxel (Abraxane) from Abraxis ($ABII). Of course, one of the challenges here is that in animal research, drugs and nanoparticles can be injected directly into the tumour thus avoiding systemic effects, whereas in human research, nanoparticle drugs are more typically combined with regular drugs and infused as normal.

It was, hover, no surprise to learn earlier this year that Abraxane is looking promising in 2nd line advanced pancreatic cancer as a single agent after failure of gemcitabine-based chemotherapy.  At AACR last year, researchers from Mass General showed that Abraxane targets the tumour stroma, depleting it, thereby reducing the impediment to chemotherapy.  The Nab-paclitaxel utilises endogenous albumin pathways via binding of the albumin to secreted proetin acid rich in cysteine or SPARC.  Interestingly, pancreatic cancer is known to overexpress SPARC and therefore offers a logical target for the drug.  Abraxis reported in May that the median overall survival was 7.3 months, which is impressive in a very hard to treat refractory population.

I wonder what the Nab paclitaxel data would look like in front-line treatment in combination with gemcitabine?  Or what about using it in advanced renal cancer with any of the half dozen drugs already approved but with limited effectiveness? Would adding a nanoparticle delivery system such as Abraxane to the mix reduce metastasis, deplete the stroma and improve access to the tumour for the anti-angiogenic agents?

Overall, it's an interesting technology concept for improving drug delivery and we're still at relatively early stages of research.  Hopefully, we'll hear more about nanotechnology and the broader application of new combination nanoparticles to cancer treatment in the near future.  It takes significant investment, creativity in trial design and an intensive yet broad research program to drive results though. Celgene ($CELG) have since bought Abraxis and may be more willing to aggressively invest in the growth of this interesting drug.

I must say that the AACR Molecular Targets and Cancer Therapeutics meeting every November is one of my all time favourites, but it alternates with Europe every other year and will be in Berlin this November, so depending upon my schedule I may not be able to make it this time 🙁

 

ResearchBlogging.org Murphy, E., Majeti, B., Barnes, L., Makale, M., Weis, S., Lutu-Fuga, K., Wrasidlo, W., & Cheresh, D. (2008). From the Cover: Nanoparticle-mediated drug delivery to tumor vasculature suppresses metastasis Proceedings of the National Academy of Sciences, 105 (27), 9343-9348 DOI: 10.1073/pnas.0803728105

Gasparini G, Brooks PC, Biganzoli E, Vermeulen PB, Bonoldi E, Dirix LY, Ranieri G, Miceli R, & Cheresh DA (1998). Vascular integrin alpha(v)beta3: a new prognostic indicator in breast cancer. Clinical cancer research : an official journal of the American Association for Cancer Research, 4 (11), 2625-34 PMID: 9829725

'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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