Minimal residual disease (MRD) has become a central concept in modern oncology, reshaping how clinicians evaluate response, relapse risk and treatment precision. As increasingly sensitive technologies reveal traces of cancer that persist after therapy, MRD is emerging as both a biological challenge and a clinical opportunity, especially as new data illuminate its complexity across hematologic and solid tumors. This topic was addressed at the 2026 American Association for Cancer Research (AACR) annual meeting.
Incyte Corp. has developed and presented data for their CD70xCD3 bispecific antibody INCA-036873, which was designed to activate T cells and kill tumoral cells expressing CD70.
DNA polymerase θ (POLθ) plays a central role in microhomology-mediated end joining (MMEJ), an error-prone DSB repair pathway. Under normal conditions, MMEJ acts as a backup repair mechanism. However, in HRR-deficient tumors, reliance on POLlθ-driven MMEJ is markedly increased, making POLθ essential for cancer cell survival. Researchers from Astrazeneca plc reported the discovery and characterization of AZD-4956, a POLθ inhibitor that can be used in combination with PARP inhibitors and other DNA-damaging agents.
New Approach Methodologies (NAMs) for drug development are transforming biomedical research by replacing or complementing animal models. More than 90% of experimental compounds fail in clinical trials, underscoring the need for strategies that better capture human biology. Many of these techniques were showcased at the 2026 American Association for Cancer Research (AACR) annual meeting.
Cymirafen is a novel antibody-drug conjugate (ADC) from the University of California that targets leucine-rich repeat-containing G-protein coupled receptor 4 (LGR4)/LGR5/LGR6 and is composed of a potent cytotoxic payload, monomethyl auristatin E (MMAE), plus an Fc domain fused to the receptor binding domain of RSPO1.
Researchers from Cogent Biosciences Inc. presented the preclinical profile of CGT-1263, a pan-KRAS-directed compound that binds both ON and OFF KRAS conformations without affecting HRAS or NRAS.
Selective inhibition of Werner syndrome helicase (WRN) has been shown to trigger extensive DNA damage and cell death specifically in microsatellite instability-high (MSI-H) cancers, highlighting WRN as a tumor-selective target with potential for precision oncology approaches beyond immunotherapy. Researchers from Eikon Therapeutics Inc. presented the preclinical profile of EIK-1005, a WRN inhibitor.
Despite the success of immunotherapy, it is still limited due to the poor control of which T cells are activated and how strong and how long they are activated. Next-generation T-cell activators should address this limitation by engagement of selective T-cell subsets, allowing stronger control and durable responses. Ipsen SA has presented data regarding their T-cell activator IPN-01203, which is bispecific and selective for Vβ6 and Vβ10 (Vβ6/10) TCR-expressing T cells, alongside with IL-15 receptor coactivation.
When a tumor migrates and colonizes another tissue or organ, it can be identified as a metastasis, but its origin is not always clear. Now, a study based on machine learning has identified DNA-methylation patterns that reveal the type of tissue a cancer comes from when the primary tumor cannot be found. This technique could help guide more specific treatments for patients with cancers of unknown primary, who today often receive broad, nontargeted chemotherapy.
Recent evidence has pointed toward Werner syndrome helicase (WRN) as an attractive target for the management of microsatellite instability-high (MSI-H) tumors, including colorectal, gastric and endometrial cancer mainly.
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