Breakthrough in Leukemia Treatment Resistance
Researchers have uncovered the mechanism behind acute myeloid leukemia’s resistance to a class of drugs effective against other blood cancers, according to a new study from UC San Diego School of Medicine. The findings, published in Blood journal, reveal how AML cells activate backup systems to survive proteasome inhibitor treatment, which has long frustrated attempts to expand use of these medications beyond multiple myeloma.
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Understanding AML’s Evasion Tactics
Unlike multiple myeloma cells that succumb to proteasome inhibitors, AML cells rewire their internal networks to bypass treatment, sources indicate. The research team, led by Dr. Robert Signer, discovered that when proteasomes are blocked, AML cells activate alternative stress-response pathways regulated by the HSF1 gene or through autophagy processes.
“Imagine you’re driving down the highway and you hit construction, you just take an alternate route,” Signer explained in the report. “When AML cells hit the ‘construction’ of proteasome inhibitors, they do the same thing by rewiring their network to take an off-ramp and continue their way.”
Combination Therapy Shows Promise
By combining proteasome inhibitors with Lys05, a drug that impairs autophagy, the team successfully shut down AML’s primary escape route. Laboratory tests demonstrated that the dual approach slowed cancer cell growth and reduced disease colonization, analysts suggest. The treatment strategy also extended survival in preclinical models, offering new hope for addressing this aggressive leukemia that claims approximately 70% of patients within five years of diagnosis.
Dr. Kentson Lam, first author of the study, emphasized the significance of their mutation-agnostic approach: “We tested this method across a variety of AML cell lines and patient samples, and it worked across nearly all of them, regardless of their genetic mutations.” This broad effectiveness contrasts with current targeted therapies that only benefit small patient subgroups with specific mutations.
Broader Implications for Cancer Treatment
The research represents a shift toward targeting protein regulation pathways rather than specific genetic abnormalities. According to the report published in Blood journal, this approach could benefit a wider range of AML patients regardless of their cancer’s genetic profile.
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The team leveraged their expertise in stem cell biology—critical since AML originates from blood stem cells unlike multiple myeloma—to develop this innovative strategy. Building on previous research documented in PubMed studies, they are now working to identify additional drugs that could disable AML’s remaining backup survival mechanisms.
Future Directions and Clinical Translation
Researchers indicate they are actively pursuing combination therapies that could advance to clinical trials. The study’s success in overcoming treatment resistance comes amid broader industry developments in medical research and parallels related innovations in targeted therapies across medicine.
As the field progresses, experts note that market trends in pharmaceutical development increasingly favor combination approaches. Meanwhile, recent technology advances in drug discovery and related innovations in biomedical research continue to accelerate progress toward more effective cancer treatments.
“Targeting these protein pathways is a new approach to cancer treatment,” Signer concluded. “Our hope is that this research will improve treatment options for a wide range of AML patients. As scientists, that is our ultimate goal: to find new ways to treat disease to improve lives.”
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