Molecular Testing of Brain Tumor

Park, Shin Young; Won, Jae-Kyung; Kim, Seong Ik; Lee, Yujin; Kim, Seung Ki; Choi, Seung Hong

doi:10.4132/jptm.2017.03.08

Cited by 60 publications

(33 citation statements)

References 131 publications

(167 reference statements)

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“…Common therapeutic agents recommended were imatinib, sunitinib and pembrolizumab. The detected mutations and IHC scores observed in gliomas in this analysis are in keeping with previous studies [11][12][13] . xIDH1 , 2xMLH1, 2xATM, 1xABL, 1xALK, 1xAPC, 1xATR, 1xBRAF, 1xBRCA2, 1xCCND3, 1xCDKN1B, 1xCDKN2A, 1xEGFR, 1xERBB4, 1xFGFR3, 1xFGFR4, 1xIGF1R, 1xMRE11A, 1xMTOR, 1xNOTCH1, 1xPIK3CA, 1xPIK3R1, 1xPOLE, 1xPTCH, 1xPTPN11, 1xRAD51C, 1xRB, 1xSLX4, 1xSMAD4, 1xSMARCB1, 1xSTK11, The analysis presented in this study shows that molecular profiling from tumour samples of patients and subsequent identification of therapeutic options with highly advanced PBT appears feasible and safe, and consistent with previous work.…”

Section: Discussionsupporting

confidence: 91%

Applied Precision Cancer Medicine in Neuro-Oncology

Taghizadeh

Müllauer

Furtner

et al. 2019

Sci Rep

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Brain tumours that are refractory to treatment have a poor prognosis and constitute a major challenge in offering effective treatment strategies. By targeting molecular alterations, precision cancer medicine may be a viable option for the treatment of brain tumours. in this retrospective analysis of our PCM platform, we describe the molecular profiling of primary brain tumours from 50 patients. Tumour samples of the patients were examined by a 161-gene next-generation sequencing panel, immunohistochemistry, and fluorescence in situ hybridization (FISH). We identified 103 molecular aberrations in 36 (72%) of the 50 patients. The predominant mutations were TP53 (14.6%), IDH1 (9.7%) and PIK3CA (6.8%). No mutations were detected in 14 (28%) of the 50 patients. IHC demonstrated frequent overexpression of EGFR and mTOR, in 38 (76%) and 35 (70%) patients, respectively. Overexpression of PDGFRa and PDGFRb were less common and detected in 16 and four patients, respectively. For 35 patients a targeted therapy was recommended. In our database, the majority of patients displayed mutations, against which targeted therapy could be offered. Based on our observations, PCM may be a feasible novel treatment approach in neuro-oncology.

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Section: Discussionsupporting

confidence: 91%

Applied Precision Cancer Medicine in Neuro-Oncology

Taghizadeh

Müllauer

Furtner

et al. 2019

Sci Rep

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“…Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a phosphoinositide 3-phosphatase that can inhibit cellular proliferation, survival, growth, and differentiation in several types of neoplasm such as colon, breast, and lymphoid cell neoplasms [ 16 - 20 ]. Smad4 (DPC4) is a tumor suppressor gene that mediates the TGF-β signaling pathway, thus suppressing epithelial cell growth [ 21 ].…”

mentioning

confidence: 99%

The Smad4/PTEN Expression Pattern Predicts Clinical Outcomes in Colorectal Adenocarcinoma

Chung¹,

Wi²,

Kim³

et al. 2018

J Pathol Transl Med

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Background Smad4 and PTEN are prognostic indicators for various tumor types. Smad4 regulates tumor suppression, whereas PTEN inhibits cell proliferation. We analyzed and compared the performance of Smad4 and PTEN for predicting the prognosis of patients with colorectal adenocarcinoma. Methods Combined expression patterns based on Smad4+/– and PTEN+/– status were evaluated by immunostaining using a tissue microarray of colorectal adenocarcinoma. The relationships between the protein expression and clinicopathological variables were analyzed. Results Smad4–/PTEN– status was most frequently observed in metastatic adenocarcinoma, followed by primary adenocarcinoma and tubular adenoma (p<.001). When Smad4–/PTEN– and Smad4+/PTEN+ groups were compared, Smad4–/PTEN– status was associated with high N stage (p=.018) and defective mismatch repair proteins (p=.006). Significant differences in diseasefree survival and overall survival were observed among the three groups (Smad4+/PTEN+, Smad4–/PTEN+ or Smad4+/PTEN–, and Smad4–/PTEN–) (all p<.05). Conclusions Concurrent loss of Smad4 and PTEN may lead to more aggressive disease and poor prognosis in patients with colorectal adenocarcinoma compared to the loss of Smad4 or PTEN alone.

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“…It should be noted that the diagram only displays some of the classic pathways as an example to illustrate the pure additive mechanism between BA and JA and does not include all target pathways for these compounds. lymphoblastic leukemia [68] , and glioblastomas [69,70] ; PTEN is also reported to be related to nervous regeneration and repair [71][72][73] , and promotion of PTEN degradation may prevent hippocampal neuronal loss and memory impairment [74] . Thus, we speculate that apoptosis and cancer-related signaling pathways are unique targets of BA in treating cerebral ischemia, which are quite different from those of JA.…”

Section: Discussionmentioning

confidence: 99%

Pure mechanistic analysis of additive neuroprotective effects between baicalin and jasminoidin in ischemic stroke mice

Wang

Liu

et al. 2018

Acta Pharmacol Sin

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Both baicalin (BA) and jasminoidin (JA) are active ingredients in Chinese herb medicine Scutellaria baicalensis and Fructus gardeniae, respectively. They have been shown to exert additive neuroprotective action in ischemic stroke models. In this study we used transcriptome analysis to explore the pure therapeutic mechanisms of BA, JA and their combination (BJ) contributing to phenotype variation and reversal of pathological processes. Mice with middle cerebral artery obstruction were treated with BA, JA, their combination (BJ), or concha margaritifera (CM). Cerebral infarct volume was examined to determine the effect of these compounds on phenotype. Using the hippocampus microarray and ingenuity pathway analysis (IPA) software, we exacted the differentially expressed genes, networks, pathways, and functions in positive-phenotype groups (BA, JA and BJ) by comparing with the negative-phenotype group (CM). In the BA, JA, and BJ groups, a total of 7, 4, and 11 specific target molecules, 1, 1, and 4 networks, 51, 59, and 18 canonical pathways and 70, 53, and 64 biological functions, respectively, were identified. Pure therapeutic mechanisms of BA and JA were mainly overlapped in specific target molecules, functions and pathways, which were related to the nervous system, inﬂammation and immune response. The specific mechanisms of BA and JA were associated with apoptosis and cancer-related signaling and endocrine and hormone regulation, respectively. In the BJ group, novel target profiles distinct from mono-therapies were revealed, including 11 specific target molecules, 10 functions, and 10 pathways, the majority of which were related to a virus-mediated immune response. The pure additive effects between BA and JA were based on enhanced action in virus-mediated immune response. This pure mechanistic analysis may provide a clearer outline of the target profiles of multi-target compounds and combination therapies.

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Molecular Testing of Brain Tumor

Cited by 60 publications

References 131 publications

Applied Precision Cancer Medicine in Neuro-Oncology

Applied Precision Cancer Medicine in Neuro-Oncology

The Smad4/PTEN Expression Pattern Predicts Clinical Outcomes in Colorectal Adenocarcinoma

Pure mechanistic analysis of additive neuroprotective effects between baicalin and jasminoidin in ischemic stroke mice

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