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Lobular breast cancer is the second most prevalent breast cancer subtype, but clinical trials have not focused on these patients. The GELATO study reveals the feasibility of trials that are specific for this difficult to treat cancer and indicates that patients with lobular breast cancer can benefit from immunotherapy using PD-L1 blockade.
Clinical utility of T cell engagers (TCEs) in cancer immunotherapy for solid tumors is hampered by on-target off-tumor activity and dose-limiting adverse events. A study now proposes a solution to tackle these challenges through the design and preclinical characterization of extended half-life TCEs that are conditionally activated in the tumor microenvironment.
Although targeting cancer cells on the basis of tissue-specific expression of key factors is an important strategy in precision oncology, few such therapies exist. Chemical screening now identifies YC-1 as a tissue-specific anti-cancer compound that is activated in the liver by the sulfotransferase enzyme SULT1A1.
Saur and colleagues provide an overview of single-cell analyses in pancreatic cancer and discuss their implications for our understanding of heterogeneity and plasticity in the tumor and its microenvironment.
A study of the immune microenvironment of estrogen receptor-positive (ER+) invasive ductal carcinoma (IDC) and invasive lobular carcinoma (ILC) identifies pro-tumor and anti-tumor macrophages as key players that can potentially influence disease outcome.
Transactivation hubs and related biomolecular condensates are emerging as relevant molecular players in cancer biology. A new study now links PD-L1 upregulation on the cancer cell surface and IRF1–KAT8 transactivation hubs at PD-L1 loci. Therapeutic targeting of these hubs holds potential to unleash antitumor immunity.
Speiser and colleagues review the latest advances in understanding of the biological roles of CD4+ T cells in cancer immunology and applications for immunotherapy.
Shaw and colleagues discuss the oncogenic roles of ALK in lung cancer, targeting approaches and the mechanisms underlying acquired resistance to ALK-directed therapy.
High-fat diet and the secretome of breast tumors prime distant organs for metastasis formation. During lung priming, alveolar type II cells increase the release of palmitate, which is oxidized to acetyl-CoA by metastasizing breast cancer cells, where the increased acetylation of the NF-κB subunit p65 activates a pro-metastatic transcriptional program.
Using an unbiased algorithm based on kinase–phosphorylation site interactions that is applicable to any proteomic dataset, we identified and experimentally validated two protein kinases (PKCδ and DNA-PKcs) as the master kinases that drive two functional subtypes of glioblastoma multiforme and are potential therapeutic targets of other cancer subtypes.
Somatic mutations in cancer genomes are caused by multiple mutational processes, each generating characteristic mutational signatures. Our systematic mutational signature analysis of single base substitutions and small insertions and deletions in pediatric cancers indicates that the contribution of signatures of homologous recombination repair defect is limited and identifies a leukemia-specific signature.
Patients with blood cancer have fewer antibodies after SARS-CoV-2 vaccination — but recent work shows that these antibodies seem to bind to viral spike protein more strongly than those in matched controls. In addition, another study finds that convalescent or vaccinee plasma might improve COVID-19 outcomes in those with blood cancer.
Acute myeloid leukemia (AML) is a heterogeneous disease with poor prognosis and treatment options. A new study reveals a unique inflammatory signature in pediatric and adult AML malignant cells that is associated with the infiltration of atypical B cells in the bone marrow microenvironment, which adds an independent layer of prognostic information.
Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of mortality worldwide. Integrative analysis of the genome, transcriptome and proteome of PDAC tissues, also known as proteogenomic analysis, provides insight into the biology of this cancer and is a resource for therapeutic discovery.
Modulation of T cell immune checkpoints combined with inhibition of chemokine receptors on myeloid-derived suppressor cells can reprogram the highly suppressive tumor immune microenvironment of pancreatic ductal adenocarcinoma (PDAC), and generates durable complete responses in a PDAC mouse model. These results provide a testable clinical regimen for human PDAC.
