SYST-28 FUNCTIONAL MAPPING REVEALS WIDESPREAD REMODELLING AND A NOVEL TARGETABLE PTP4A2-ROBO1 SIGNALING AXIS AT GLIOBLASTOMA RECURRENCE

نویسندگان

چکیده

Abstract Resistance to genotoxic therapies and tumor recurrence are hallmarks of glioblastoma (GBM), an aggressive brain tumor. Here, we explore the functional drivers post-treatment recurrent GBM. By conducting genome-wide CRISPR-Cas9 screens in patient-derived GBM models, uncover distinct genetic dependencies cells that were absent their patient-matched primary predecessors, accompanied by increased mutational burden differential transcript protein expression. These analyses map a multilayered response drive recurrence, identifying tyrosine phosphatase 4A2 (PTP4A2) as novel modulator self-renewal, proliferation tumorigenicity at recurrence. Mechanistically, perturbation or small molecule inhibition PTP4A2 represses axon guidance activity through dephosphorylation axis with roundabout receptor 1 (ROBO1), exploiting dependency on ROBO signaling. Roundabout (ROBO1) is involved axonal during neurodevelopment aberrant ROBO1 signaling associated higher was highly expressed surface malignant treatment-refractory initiating (BTICs) rGBM, metastasis (BM) medulloblastoma (MB). Importantly, engineered anti-ROBO1 single-domain antibodies also mimic effects inhibition. We therefore developed validated second-generation CAR-T against ROBO1, which demonstrated upregulation activation markers, enhanced cytokine release, markedly proliferation, induction potent specific cell death compared untransduced all three cancers. findings further vivo MB BM where showed significant reduction increase survival treated mice. conclude reprogramming drives dependence multi-targetable PTP4A2-ROBO1

برای دانلود باید عضویت طلایی داشته باشید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

A novel tool to analyze MRI recurrence patterns in glioblastoma.

At least 10% of glioblastoma relapses occur at distant and even contralateral locations. This disseminated growth limits surgical intervention and contributes to neurological morbidity. Preclinical data pointed toward a role for temozolomide (TMZ) in reducing radiotherapy-induced glioma cell invasiveness. Our objective was to develop and validate a new analysis tool of MRI data to examine the c...

متن کامل

Phosphoproteome of Human Glioblastoma Initiating Cells Reveals Novel Signaling Regulators Encoded by the Transcriptome

BACKGROUND Glioblastoma is one of the most aggressive tumors with poor prognosis. Although various studies have been performed so far, there are not effective treatments for patients with glioblastoma. METHODOLOGY/PRINCIPAL FINDINGS In order to systematically elucidate the aberrant signaling machinery activated in this malignant brain tumor, we investigated phosphoproteome dynamics of gliobla...

متن کامل

Lifting Up the HAT: Synthetic Lethal Screening Reveals a Novel Vulnerability at the CBP-p300 Axis.

Cancer genotype-specific synthetic lethal vulnerabilities represent promising therapeutic targets. In this issue of Cancer Discovery, Ogiwara and colleagues uncover a synthetic lethal relationship between two histone acetyl transferase paralogs, CBP and p300, highlighting that cancer cells deficient in CBP are uniquely sensitized to genetic and chemical inhibition of p300.

متن کامل

Beta Adrenergic Signaling: A Targetable Regulator of Angiosarcoma and Hemangiosarcoma

Human angiosarcomas and canine hemangiosarcomas are highly aggressive cancers thought to arise from cells of vascular origin. The pathological features, morphological organization, and clinical behavior of canine hemangiosarcomas are virtually indistinct from those of human angiosarcomas. Overall survival with current standard-of-care approaches remains dismal for both humans and dogs, and each...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

ژورنال

عنوان ژورنال: Neuro-oncology advances

سال: 2023

ISSN: ['2632-2498']

DOI: https://doi.org/10.1093/noajnl/vdad070.130