ORCID Profile
0000-0002-6727-9507
Current Organisation
Peter MacCallum Cancer Centre
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Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1535-7163.22521234.V1
Abstract: Figure S3 shows extended correlation analysis in haematopoietic and lymphoid, breast and lung cancer cell lines
Publisher: Elsevier BV
Date: 07-2023
Publisher: Wiley
Date: 25-05-2022
DOI: 10.1111/ANS.17787
Abstract: Computed tomography (CT) is the first‐line staging imaging modality for pancreatic ductal adenocarcinoma (PDAC) which determines resectability and treatment pathways. Between January 2016 and December 2019, prospectively collated data from two Australian cancer centres was extracted from the PURPLE Pancreatic Cancer registry. Real‐world staging CTs and corresponding reports were blindly reviewed by a sub‐specialist radiologist and compared to initial reports. Of 131 patients assessed, 117 (89.3%) presented with symptoms, 74 (56.5%) CTs included slices ≤3 mm thickness and CT pancreas protocol was applied in 69 (52.7%) patients. Initial reports lacked synoptic reporting in 131 (100%), tumour identification in 2 (1.6%) and tumour measurement in 13 (9.9%) cases. Tumour‐vascular relationship reporting was missing in 69–109 (52.7–83.2%) for regarding the key arterial and venous structures that is required to assess resectability. Initial reports had no comment on venous thrombus or venous collaterals in 80 (61.1%) and 109 (83.2%) and lacked locoregional lymphadenopathy interpretation in 13 (9.9%) cases. Complete initial staging report was present in 72 (55.0%) patients. Sub‐specialist radiological review resulted in down‐staging in 16 (22.2%) and up‐staging in 1 (1.4%) patient. Staging discrepancies were mainly regarding metastatic disease (12, 70.6%) and tumour‐vascular relationship (5, 29.4%). Real‐world staging imaging in PDAC patients show low proportion of dedicated CT pancreas protocol, high proportion of incomplete staging reports and no synoptic reporting. The most common discrepancy between initial and sub‐specialist reporting was regarding metastases and tumour‐vascular relationship assessment resulting in sub‐specialist down‐staging in almost every fifth case.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1535-7163.22521225.V1
Abstract: Gene List from siRNA screen with APR-246 growth inhibition in H1299 p53-null (Sheet 1) and p53-R273H (Sheet 2)
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1535-7163.22521228.V1
Abstract: Figure S5 shows MYC directly regulates SLC7A11 levels and APR-246 sensitivity.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1535-7163.22521228
Abstract: Figure S5 shows MYC directly regulates SLC7A11 levels and APR-246 sensitivity.
Publisher: American Association for Cancer Research (AACR)
Date: 26-07-2021
DOI: 10.1158/1535-7163.MCT-21-0067
Abstract: APR-246 (eprenetapopt) is in clinical development with a focus on hematologic malignancies and is promoted as a mutant-p53 reactivation therapy. Currently, the detection of at least one TP53 mutation is an inclusion criterion for patient selection into most APR-246 clinical trials. Preliminary results from our phase Ib/II clinical trial investigating APR-246 combined with doublet chemotherapy [cisplatin and 5-fluorouracil (5-FU)] in metastatic esophageal cancer, together with previous preclinical studies, indicate that TP53 mutation status alone may not be a sufficient biomarker for APR-246 response. This study aims to identify a robust biomarker for response to APR-246. Correlation analysis of the PRIMA-1 activity (lead compound to APR-246) with mutational status, gene expression, protein expression, and metabolite abundance across over 700 cancer cell lines (CCL) was performed. Functional validation and a boutique siRNA screen of over 850 redox-related genes were also conducted. TP53 mutation status was not consistently predictive of response to APR-246. The expression of SLC7A11, the cystine/glutamate transporter, was identified as a superior determinant of response to APR-246. Genetic regulators of SLC7A11, including ATF4, MDM2, wild-type p53, and c-Myc, were confirmed to also regulate cancer-cell sensitivity to APR-246. In conclusion, SLC7A11 expression is a broadly applicable determinant of sensitivity to APR-246 across cancer and should be utilized as the key predictive biomarker to stratify patients for future clinical investigation of APR-246.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1535-7163.22521222.V1
Abstract: Supplemental Table 1, 2, 3. Supplemental Materials and Methods.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1535-7163.22521240.V1
Abstract: Figure S1 shows TP53 mutation alone is not predictive of cancer cell response to PRIMA-1.
Publisher: Springer Science and Business Media LLC
Date: 10-10-2023
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1535-7163.22521234
Abstract: Figure S3 shows extended correlation analysis in haematopoietic and lymphoid, breast and lung cancer cell lines
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1535-7163.22521225
Abstract: Gene List from siRNA screen with APR-246 growth inhibition in H1299 p53-null (Sheet 1) and p53-R273H (Sheet 2)
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1535-7163.22521237
Abstract: Figure S2 shows APR-246 and PX-12 activity correlate in CTRPv2 and their impact on mutant-p53 thermostability.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1535-7163.22521231
Abstract: Figure S4 shows the effects of p53 overexpression and repression on SLC7A11 mRNA expression.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1535-7163.22521222
Abstract: Supplemental Table 1, 2, 3. Supplemental Materials and Methods.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1535-7163.22521237.V1
Abstract: Figure S2 shows APR-246 and PX-12 activity correlate in CTRPv2 and their impact on mutant-p53 thermostability.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1535-7163.22521240
Abstract: Figure S1 shows TP53 mutation alone is not predictive of cancer cell response to PRIMA-1.
Publisher: American Association for Cancer Research (AACR)
Date: 03-04-2023
DOI: 10.1158/1535-7163.22521231.V1
Abstract: Figure S4 shows the effects of p53 overexpression and repression on SLC7A11 mRNA expression.
Publisher: Springer Science and Business Media LLC
Date: 20-04-2023
No related grants have been discovered for Hyun Soo Ko.