Elisa de Stanchina

This study identifies SLC25A28 as a synthetic lethal target in NER-deficient cancers, showing its loss impairs cell viability and increases oxidative stress.

Loss of extracellular matrix-integrin signaling switches off YAP/TEAD and lets prostate adenocarcinoma organoids turn neuroendocrine; LATS inhibition reverses it, and combined YAP, NOTCH and AR inhibition fully reprograms them.

This study identifies an IL-1β/IL-6 signaling circuit in the tumor microenvironment that drives prostate cancer progression from pre-invasive to invasive stages.

The paper identifies SMARCA4/STK11/KEAP1 triple mutant lung adenocarcinoma as a poor prognosis subset and links it to TGF-β pathway activation.

The paper introduces Suco and Compocyte to classify immune cells from 3,965 patients, identifying new macrophage and monocyte states and T cell memory erosion in metastases.

This study shows that coexisting PTEN and PIK3CA mutations in endometrial cancers hyperactivate mTORC1, making them sensitive to mTORC1 inhibitors but not PI3K or AKT inhibitors.

This study identifies RRASQ87L and RRAS2Q72L mutations as recurrent oncogenic drivers in lung cancer and shows sensitivity to the pan-RAS inhibitor RMC-6236.

This study shows mechanical confinement drives phenotype switching in melanoma via chromatin remodeling mediated by HMGB2.

This study shows that loss of MHC Class II in BRAF-mutant anaplastic thyroid cancers leads to resistance to MAPK inhibitors by reducing CD4+ T-cell activation.

The paper identifies ATR as a target for combination EZH2 epigenetic therapy in SMARCB1-deficient sarcomas, showing that EZH2 inhibition promotes DNA damage via PGBD5, and that ATR inhibition enhances therapeutic responses.

This paper identifies eIF4A as a key regulator of ER translation in breast cancer and shows that inhibiting eIF4A, either alone or with fulvestrant, suppresses ER expression and tumor growth in advanced ER+ breast cancer.

The paper shows that diet-induced insulin resistance results from increased PTEN expression, which inhibits PI3K signaling, and that PTEN and mTORC1 inhibitors can reverse this effect.

This study shows that BRAFV600E mutations inhibit cell migration and invasion through feedback inhibition of RAC1, requiring secondary mutations to overcome this block and enable tumorigenesis.

This study shows that RBM10 loss causes aberrant splicing of cytoskeletal and ECM genes, leading to RAC1 activation and metastatic fitness in thyroid cancer.

This study identifies TET2-mutant clonal hematopoiesis in thyroid cancer microenvironments and shows that TGFβ signaling from these macrophages mediates resistance to BRAF/MEK inhibition, with TGFβ inhibition restoring sensitivity.

This study evaluates CR-1-31-B's effects on neuroblastoma, showing reduced tumor growth and revealing translational inhibition of key dependencies and synergistic effects with CHK1 inhibition.