Given the complexities of cancer, there is not – and likely never will be – a single way to destroy it. Instead, the oncologist’s armamentarium must be stocked with many weapons, which include diverse advances in chemotherapy, radiation, surgery and stem cell technologies. For the full story CLICK HERE!
An antibody therapy already in clinical trials to treat chronic lymphocytic leukemia (CLL) may also prove effective against ovarian cancer – and likely other cancers as well, reported researchers at the University of California, San Diego School of Medicine and the Blood Cancer Research Fund, in a study published in the Nov. 17 online early edition of the Proceedings of the National Academy of Sciences (PNAS). http://tinyurl.com/op7g28k
ASCO 2014: Dr. Kipps on ABT-199 and more on CLL (chronic lymphocytic leukemia): “Cancer is not an alien from outer space, cancer is us”
Here is a link to Dr. Koffman’s interview with Dr. Kipps: http://youtu.be/lEpN_58IcKc
An announcement earlier this month by the California Institute for Regenerative Medicine (CIRM), the state’s stem cell agency, is big news for innovative cancer treatment and the BCRF is right in the mix!
The Sanford Stem Cell Clinical Center at UC San Diego Health System, which is led by Lawrence Goldstein, PhD, and Catriona Jamieson, MD, PhD, was named one of three new “alpha clinics” by CIRM. Dr. Jamieson is the principal investigator on the alpha grant and co-leader of the Moores Cancer Center Hematologic Malignancies program. This designation comes with an $8 million award which will help provide vital infrastructure for establishing a comprehensive regenerative medicine clinical hub for first-in-human stem cell-related clinical trials including cancer treatment.
Recently, the Sanford Center launched three such trials including a Phase I trial to assess the safety and efficacy of a new monoclonal antibody for patients with chronic lymphocytic leukemia (CLL). The drug, called cirmtuzumab,was developed at Moores Cancer Center in the laboratory of Thomas Kipps, MD, PhD, co-leader of the Moores Cancer Center Hematologic Malignancies program.
The concept of ‘teaching’ the immune system to recognize and destroy cancer cells is over a century old, but the development of immunotherapeutic strategies for cancer was slow for many decades. However, much has been learned about the immune system in the meantime, and with the recent approval of two new immunotherapeutic anticancer drugs and several drugs in late-stage development, a new era in anticancer immunotherapy is beginning.
The video takes an audio-visual journey through the different approaches that are being investigated to harness the immune system to treat cancer. CLICK HERE
As more chronic lymphocytic leukemia CLL treatments are approved, with many more in development, are researchers closer to hitting a “home run” in treating the disease? Patient advocate Dr. Brian Koffman met with CLL expert Dr. Thomas Kipps at ASCO 2014 to explore emerging therapies and the goal for patients to achieve deep remission.
Click here: https://www.youtube.com/watch?v=CYS78SbXjKA
Thanks to Patient Power!
Published on the August 7th (2014) in the journal of Genome Biology:
Accurate allele frequencies are important for measuring subclonal heterogeneity and
clonal evolution. Deep-targeted sequencing data can contain PCR duplicates, inflating perceived read depth. Here we adapted the Illumina TruSeq Custom Amplicon kit to include single molecule tagging (SMT) and show that SMT-identified duplicates arise from PCR. We demonstrate that retention of PCR duplicate reads can imply clonal evolution when none exists, while their removal effectively controls the false positive rate. Additionally, PCR duplicates alter estimates of subclonal heterogeneity in tumor samples. Our method simplifies PCR duplicate identification and emphasizes their removal in studies of tumor heterogeneity and clonal evolution.
Lenalidomide has demonstrated clinical activity in patients with chronic lymphocytic leukemia (CLL), even though it is not cytotoxic for primary CLL cells in vitro. We examined the direct effect of lenalidomide on CLL-cell proliferation induced by CD154-expressing accessory cells in media containing interleukin (IL)-4 and IL-10. Treatment with lenalidomide significantly inhibited CLL-cell proliferation, an effect that was associated with the p53-independent upregulation of the cyclin-dependent kinase inhibitor p21WAF1/Cip1 (p21). Silencing p21 with small interfering RNA (siRNA) impaired the capacity of lenalidomide to inhibit CLL-cell proliferation. Silencing cereblon (CRBN), a known molecular target of lenalidomide, impaired the capacity of lenalidomide to induce expression of p21, inhibit CD154-induced CLL-cell proliferation, or enhance the degradation of Ikaros family zinc finger proteins 1 and 3 (IKZF1 and IKZF3).
We isolated CLL cells from the blood of patients before and after short-term treatment with low-dose lenalidomide (5 mg per day) and found the leukemia cells also were induced to express p21 in vivo. These results indicate that lenalidomide can directly inhibit proliferation of CLL cells in a CRBN/p21-dependent, but p53-independent, manner at concentrations achievable in vivo, potentially contributing to the capacity of this drug to inhibit disease-progression in patients with CLL.