Abstract 29P
Background
Arising from the arachnoid villi cells, meningioma constitutes 35% of all the primary brain tumors. According to WHO, meningiomas can be classified into 3 grades i.e. WHO grade I (typical), WHO grade II (atypical), WHO grade III (anaplastic), further dividing them into 15 subtypes. Based solely on histology, nine of these subtypes comes under WHO grade I and three each in grade II and grade III. Though benign, 80% meningiomas can be treated by resection and chemotherapy thereafter. However, 20% recur and need further surgery, radiotherapy or another round of chemotherapy. Moreover, comorbidities like neurological and cognitive disorders can be caused by relatively indolent meningiomas. Impede cognition, in grade I patients further diminishes the life surviving conditions. Though, meningiomas are the most common intracranial tumors, occurrence of multiple meningioma (10% of the affected population) present another set of complications to deal with. Biomarkers as ‘targets’ may provide a better treatment and prognostic factors for these patients and their follow up routines.
Methods
Proteome studies that aim to decipher novel insights in the tumors provide a vast reservoir for likely molecular targets. However, non-availability of in depth proteomic re-searches in this field renders the treatment dubious. Herein, we present a proteome analysis of meningioma patients aimed to decipher the role of selected functional proteins which may serve to be target for therapies.
Results
The study presented here dwell on the proteins like adenylate kinase 2 (AK2), collagen type 1 alpha 1 (COL1A1)), plasminogen (PLG), found via mass spectrometry analysis. Simultaneously, cell sorting by FACS was used to support the mass spec findings.
Conclusions
Furthermore, these ‘protein markers’ might be targeted to identify another panel of proteins that can be screened in a large patient cohort using targeted proteomics.
Editorial acknowledgement
Clinical trial identification
Legal entity responsible for the study
Sir Ganga Ram Hospital.
Funding
Has not received any funding.
Disclosure
The author has declared no conflicts of interest.
Resources from the same session
31P - Identification of proteins associated with mRNA processing and maturation by quantitative proteomic analysis in Indian cervical cancer patients
Presenter: Amrita Mukherjee
Session: Cocktail & Poster Display session
Resources:
Abstract
32P - Expression of STAT3 and hypoxia markers in repeatedly resected glioma patients
Presenter: Katerina Dvorakova
Session: Cocktail & Poster Display session
Resources:
Abstract
33P - Unraveling the mechanisms of cisplatin resistance in bladder organoid by single cell RNA sequencing
Presenter: Tingting Xie
Session: Cocktail & Poster Display session
Resources:
Abstract
34P - Functional diagnostics and ex-vivo screening of erlotinib and nintedanib in non-small cell lung carcinoma: Implications for multidrug resistance and personalized therapy
Presenter: Jelena Dinić
Session: Cocktail & Poster Display session
Resources:
Abstract
35P - Enhancing efficacy of the MEK inhibitor trametinib in KRAS-mutated colorectal cancer cells
Presenter: Lee Ellis
Session: Cocktail & Poster Display session
Resources:
Abstract
36P - Comparison of pelitinib, tepotinib or docetaxel efficacy according to the copy number or gene alteration status of EGFR, MET, HRAS, KRAS and NRAS genes
Presenter: Dae Young Zang
Session: Cocktail & Poster Display session
Resources:
Abstract
37P - NET-mediated radio-resistance in early-stage non-small cell lung cancer
Presenter: Malcolm Ryan
Session: Cocktail & Poster Display session
Resources:
Abstract
39P - The use of antibiotics or proton pump inhibitors and the response to intravesical Bacillus Calmette Guérin therapy in non-muscle-invasive bladder cancer
Presenter: João Barbosa Martins
Session: Cocktail & Poster Display session
Resources:
Abstract
40P - YAP1 promotes sorafenib resistance by activation of TGFβ signaling pathway
Presenter: Chit Lai Chee
Session: Cocktail & Poster Display session
Resources:
Abstract
41P - HLA genotypes modify the age-related penetrance of BRCA1 pathogenic variants in breast cancer patients
Presenter: Ekaterina Kuligina
Session: Cocktail & Poster Display session
Resources:
Abstract