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CAR T cells developed to target Cadherin-17 (CDH17) eradicate neuroendocrine and gastrointestinal tumors in preclinical models, yet show no toxicity to normal tissues that also express CDH17.
Nature Cancer and the Nature journals are raising the standards on reporting on sex and gender in research. Starting this June, authors will be prompted to provide details on how sex and gender were considered in study design.
As guidelines, therapies and literature on cancer variants expand, the lack of consensus variant interpretations impedes clinical applications. CIViC is a public-domain, crowd-sourced and adaptable knowledgebase of evidence for the clinical interpretation of variants in cancer, designed to reduce barriers to knowledge sharing and alleviate the variant-interpretation bottleneck.
Patients with cancer are known to be at increased risk of infection and severe complications from COVID-19, with vaccination being key for their protection. A prospective study now evaluates the effect of vaccination against COVID-19 on the immune response mounted by patients with lymphoma.
Acute myeloid leukemia (AML) is characterized by distinct genetic and molecular alterations, including rearrangements in the mixed lineage leukemia (MLL) gene. A study now presents a therapeutic strategy for MLL-rearranged (MLL-r) AML that exploits a unique co-dependency on IKAROS and MENIN.
The lethality of prostate cancer is driven by its progression to a castration-resistant state. A new study identifies gremlin 1 (GREM1) as an agonist of fibroblast growth factor receptor 1 (FGFR1) that drives such progression when androgen receptor (AR) signaling is low, nominating GREM1 as a therapeutic target for prostate cancer with low AR activity.
The transcription factor IKAROS is essential to maintaining a leukemogenic gene-expression profile mediated by transcription factors encoded by HOXA@ and MEIS1 in MLL1-rearranged (MLL-r) acute myeloid leukemia. Pharmacological degradation of IKAROS increases the effectiveness of inhibitors of the MLL1–MENIN protein–protein interaction, which leads to more-robust disruption of leukemogenic transcriptional networks and enhanced therapeutic benefit in preclinical models.
People with lymphoma have immune defects that compromise the immune response to vaccination. A prospective observational study of 457 people with lymphoma showed improvement in antibody and T cell responses after the third vaccine dose except in those who received anti-CD20 antibody therapy within a year prior to vaccination.
Stanley and Abdel-Wahab review the latest insights into the biological mechanisms of RNA splicing dysregulation in cancer and the emerging landscape of therapeutic opportunities in this field.
Pramesh and colleagues report a study on the risk factors and outcomes in a large cohort of patients with cancer infected with SARS-CoV-2 from a tertiary care cancer center in India.
Lim and colleagues present the UK PROSECO study where they assess humoral and cellular immune responses to one, two and three doses of vaccination against SARS-CoV-2 in patients with B-cell malignancies in a prospective observational study.
Zhu and colleagues identify GREMLIN1 as an FGFR1 ligand that promotes plasticity and castration resistance in prostate cancer through regulation of MAPK signaling, and show that anti-GREMLIN1 antibody therapy synergizes with androgen deprivation.
Hua and colleagues develop CAR T cells targeting CDH17 and show that they are effective at suppressing tumor growth in mouse and human models of neuroendocrine and gastrointestinal solid tumors, without damaging healthy tissues in preclinical models.
Armstrong and colleagues discover that combined targeting of IKAROS and MENIN is a therapeutic strategy for acute myeloid leukemia through disruption of essential leukemogenic transcriptional programs.
Ji and colleagues demonstrate that metabolic reprogramming in SCLC underlies chemotherapy resistance, resulting in an actionable dependency on the mevalonate pathway in tumor cells, which can be targeted using statins to revert chemoresistance.
Agnihotri and colleagues show that loss of the MAT2A enzyme of the methionine cycle induces a global depletion of H3K36me3 and extends survival in glioma models, representing a potential therapeutic vulnerability.