AACR Hematologic Malignancies


Philadelphia; Photo by Ed Yakovich

The AACR conference Hematologic Malignancies: Translating Discoveries to Novel Therapies took place September 20-23, 2014, in Philadelphia, Pennsylvania.


Targeting drug resistance earlier

HT Staff Read Article
Published: 10/01/14

Drug release in a cancer cell
Credit: PNAS

A combination treatment strategy that takes tumor evolution into account could help us avoid drug resistance in hematologic malignancies, researchers say. Preclinical experiments suggest we can prevent resistance by starting secondary treatment prior to relapse. For example, a patient receiving dasatinib for acute lymphoblastic leukemia (ALL) could benefit from receiving crizotinib or foretinib during the early stages of clonal evolution. [Read Article]

Drug could treat a range of blood cancers

HT Staff Read Article
Published: 09/26/14

Multiple myeloma

A drug that targets the ribosome may be active in a broad range of hematologic malignancies, researchers say. The drug, CX-5461, inhibits the protein RNA polymerase I (Pol I), which is consistently upregulated in hematologic and other cancers. CX-5461 significantly prolonged survival in mouse models of refractory acute myeloid leukemia (AML) and multiple myeloma (MM). It also synergized with everolimus to extend survival in mice with B-cell lymphoma. [Read Article]

Method can detect drivers of AML

Jen Smith Read Article
Published: 09/25/14

AML in the bone marrow

Super-enhancer profiling can unearth biomarkers and therapeutic targets for acute myeloid leukemia (AML), according to research presented at the AACR conference Hematologic Malignancies: Translating Discoveries to Novel Therapies. Researchers used high-throughput ChIP sequencing to identify super-enhancer domains in a cohort of AML patients. And this revealed both known and previously unknown genes that are important for AML disease biology.  [Read Article]

Murine studies support use of TKIs in ALL subtype

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Published: 09/25/14

Lab mouse

Experiments in mice reinforce the idea that tyrosine kinase inhibitors (TKIs) can treat patients with Ph-like acute lymphoblastic leukemia (ALL). Investigators recently identified genomic alterations in Ph-like ALL that suggest these patients might respond to TKIs, and tests in a small number of patients supported this theory. Now, preclinical results show that kinase fusions in Ph-like ALL activate signaling pathways differently, and this affects sensitivity to TKIs. [Read Article]

ETBs prove effective against lymphoma and myeloma

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Published: 09/24/14

Researchers in the lab
Credit: Rhoda Baer

A pair of engineered toxin bodies (ETBs) can successfully treat Burkitt lymphoma and multiple myeloma, according to preclinical research presented at the AACR conference Hematologic Malignancies: Translating Discoveries to Novel Therapies. The ETBs, known as MT-4007 and MT-4007-D, work by targeting CD38. They greatly reduced tumor burden and improved survival in mouse models. And they were well-tolerated, even at the highest doses administered. [Read Article]

Drugs demonstrate inconsistent synergy in CLL, MCL

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Published: 09/24/14

Mantle cell lymphoma

The Bcl-2 inhibitor ABT-199 and the Bruton tyrosine kinase inhibitor ibrutinib can have a synergistic effect against mantle cell lymphoma (MCL) and chronic lymphocytic leukemia (CLL), preclinical data suggest. In one set of experiments with MCL and CLL samples, the drugs induced apoptosis at a much higher rate when used together than when used alone. However, in other experiments with CLL samples, ABT-199 and ibrutinib did not consistently display synergistic cytoxicity. [Read Article]


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