Following on from yesterday’s post on the potential for small basket trials in ER+ breast cancer with the ESR1 mutation, I wanted to highlight another area where these type of highly focused and rational studies appear to be not only useful but also potentially produce stunning responses.
Today brings the launch of our series on the AACR annual meeting Previews. A variety of different topics will be covered over the next two weeks, not just by tumour type and pathway, but also to highlight some novel research that is emerging on various driver mutations that not only can cause resistance to occur, but may also be viable targets for therapeutic intervention.
Every year at AACR meetings there seems to be a new update on how researchers are doing with their work on overcoming resistance in metastatic melanoma. We’ve seen some stunning photos where targeting the BRAF V600E mutation with a specific kinase inhibitor such as vemurafenib (Zelboraf) or dabrafenib (Tafinlar) results in dramatic reduction, and sometimes even complete disappearance of the lesions, only for resistance to set in and the melanoma sadly comes back with a vengeance. Adding a MEK inhibitor such as trametinib (Mekinist) was originally thought to be a rather promising strategy, until it became clear that this only gave a few extra months with exactly the same result.
The next few weeks will see quite a lot of activity here on Biotech Strategy Blog with the segue from Miami Breast Cancer Conference to the World Lung Conference in Geneva and then onto the annual AACR meeting in San Diego.
One area that is finally seeing a lot more research results of late is neo-adjuvant therapy in breast cancer, i.e. therapeutic intervention prior to surgery.
Following on from yesterday’s update on how proteomics and genomics can help us make better decisions in breast cancer at the Miami Breast Cancer Conference (#MBCC14) organised by PER, today also looks at the complexity of genomics, but from a different lens – can genomics impact the way we actually treat patients?
On Friday, I headed uptown to attend the Miami Breast Cancer Conference (#MBCC14) held at the Fontainebleau Hotel and organised by the Physicians Education Resource (PER). It was fun to grab a local Deco Bike and furiously cycle over 45 blocks in under half an hour – most probably the only attendee who arrived on two wheels that day!
During the recent American Society of Hematology meeting, much of the focus in immuno-oncology was squarely on the pediatric and adult data using the chimerica antigen receptor T cell product being developed by Novartis, CTL019, in acute lymphoblastic leukemia (ALL) from Children’s Hospital of Philadelphia (CHOP, not to be confused with the chemotherapy regimen!) and U Penn, respectively. We wrote about that data earlier this year.
This morning, I woke up early to a sad announcement from Genentech that:
In today’s post, we discuss multiple myeloma and the proteasome inhibitors (bortezomib, carfilzomib and ixazomib), in particular. One of the ongoing debates concerns the toxicities and how the drugs in this class might differ. Whereas melphalan and the immunomodulatory drugs or IMiDs (lenalidomide, pomalidomide and thalidomide) have both been associated with secondary primary malignancies including AML and MDS, especially in combination, cardiotoxicity has been the main focus of debate for the proteasome inhibitors.