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Source: Clinical Cancer Research

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Total 104 results found since Jan 2013.

HIF2 inactivation and tumor suppression with a tumor-directed RNA-silencing drug in mice and humans
CONCLUSIONS: To our knowledge, this is the first example of functional inactivation of an oncoprotein and tumor suppression with a systemic, tumor-directed, RNA-silencing drug. These studies provide a proof-of-principle of HIF2α inhibition by RNA-targeting drugs in ccRCC and establish a paradigm for tumor-directed RNA-based therapeutics in cancer.PMID:36190432 | DOI:10.1158/1078-0432.CCR-22-0963
Source: Clinical Cancer Research - October 3, 2022 Category: Cancer & Oncology Authors: Yuanqing Ma Allison Joyce Olivia Brandenburg Faeze Saatchi Christina Stevens Vanina Toffessi Tcheuyap Alana Christie Quyen Do Oluwatomilade Fatunde Alyssa Macchiaroli So C Wong Layton Woolford Qurratulain Yousuf Jeffrey Miyata Deyssy Carrillo Oreoluwa Ona Source Type: research

The impact of PIK3R1 mutations and insulin-PI3K-glycolytic pathway regulation in prostate cancer
CONCLUSIONS: Our findings describe a novel genomic feature in metastatic prostate cancer and suggest that PIK3R1 alteration may be a key event for insulin-PI3K-glycolytic pathway regulation in prostate cancer.PMID:35670774 | DOI:10.1158/1078-0432.CCR-21-4272
Source: Clinical Cancer Research - June 7, 2022 Category: Cancer & Oncology Authors: Goutam Chakraborty Subhiksha Nandakumar Rahim Hirani Bastien Nguyen Konrad H Stopsack Christoph Kreitzer Sai Harisha Rajanala Romina Ghale Ying Z Mazzu Naga Vara Kishore Pillarsetty Gwo-Shu Mary Lee Howard I Scher Michael J Morris Tiffany Traina Pedram Ra Source Type: research

Targeting podoplanin for the treatment of osteosarcoma
CONCLUSIONS: Targeting PDPN with a neutralizing antibody against PDPN-CLEC-2 without ADCC and CDC is a novel therapeutic strategy for PDPN-positive OS.PMID:35381070 | DOI:10.1158/1078-0432.CCR-21-4509
Source: Clinical Cancer Research - April 5, 2022 Category: Cancer & Oncology Authors: Ai Takemoto Satoshi Takagi Takao Ukaji Nobuhiko Gyobu Mamoru Kakino Miho Takami Asami Kobayashi Marie Lebel Tokuichi Kawaguchi Minoru Sugawara Kazue Tsuji-Takayama Kenji Ichihara Yuki Funauchi Keisuke Ae Seiichi Matsumoto Yoshiya Sugiura Kengo Takeuchi Te Source Type: research

KRAS inhibitor-resistance in < em > MET < /em > -amplified < em > KRAS < /em > < sup > G12C < /sup > non-small cell lung cancer induced by RAS- and non-RAS-mediated cell signaling mechanisms
CONCLUSIONS: MET amplification leads to the development of resistance to KRAS G12C inhibitors in NSCLC. Dual blockade of MET and KRAS G12C could be a treatment option for MET amplified, KRAS G12C-mutated NSCLC.PMID:34365406 | DOI:10.1158/1078-0432.CCR-21-0856
Source: Clinical Cancer Research - August 8, 2021 Category: Cancer & Oncology Authors: Shinichiro Suzuki Kimio Yonesaka Takeshi Teramura Toshiyuki Takehara Ryoji Kato Hitomi Sakai Koji Haratani Junko Tanizaki Hisato Kawakami Hidetoshi Hayashi Kazuko Sakai Kazuto Nishio Kazuhiko Nakagawa Source Type: research

Nuclear FGFR1 regulates gene transcription and promotes antiestrogen resistance in ER+ breast cancer
CONCLUSIONS: These data suggest nuclear FGFR1 contributes to endocrine resistance by modulating gene transcription in ER+ breast cancer. Nuclear FGFR1 activity was unaffected by FGFR TKIs, thus supporting the development of treatment strategies to inhibit nuclear FGFR1 in ER+/FGFR1 overexpressing breast cancer.PMID:34011560 | DOI:10.1158/1078-0432.CCR-20-3905
Source: Clinical Cancer Research - May 20, 2021 Category: Cancer & Oncology Authors: Alberto Servetto Rahul Kollipara Luigi Formisano Chang-Ching Lin Kyung-Min Lee Dhivya R Sudhan Paula I Gonzalez-Ericsson Sumanta Chatterjee Angel Guerrero-Zotano Saurabh Mendiratta Hiroaki Akamatsu Nicholas James Roberto Bianco Ariella B Hanker Ralf Kittl Source Type: research

Alterations in BAP1 are Associated with Cisplatin Resistance Through Inhibition of Apoptosis in Malignant Pleural Mesothelioma (MPM).
CONCLUSIONS: Alterations in BAP1 in MPM were a negative predictor for response to chemotherapy and could possibly be used as a companion biomarker for treatment decision. PMID: 33547197 [PubMed - as supplied by publisher]
Source: Clinical Cancer Research - February 5, 2021 Category: Cancer & Oncology Authors: Oehl K, Vrugt B, Wagner U, Kirschner MB, Meerang M, Weder W, Felley-Bosco E, Wollscheid B, Bankov K, Demes MC, Opitz I, Wild PJ Tags: Clin Cancer Res Source Type: research

Steroid sulfatase stimulates intracrine androgen synthesis and is a therapeutic target for advanced prostate cancer.
CONCLUSIONS: These studies suggest that STS drives intracrine androgen synthesis and prostate cancer proliferation. Targeting STS represents a therapeutic strategy to treat CRPC and improve second generation anti-androgen therapy. PMID: 32928794 [PubMed - as supplied by publisher]
Source: Clinical Cancer Research - September 13, 2020 Category: Cancer & Oncology Authors: Gao AC, Armstrong CM, Liu C, Liu L, Yang JC, Lou W, Zhao R, Ning S, Lombard AP, Zhao J, D'Abronzo LS, Evans CP, Li PK Tags: Clin Cancer Res Source Type: research

Chemerin reactivates PTEN and suppresses PD-L1 in tumor cells via modulation of a novel CMKLR1-mediated signaling cascade.
CONCLUSIONS: Collectively, our data show a novel link between chemerin, PTEN and PD-L1 in human tumor cells, that may have a role in improving T cell-mediated immunotherapies. PMID: 32605911 [PubMed - as supplied by publisher]
Source: Clinical Cancer Research - June 29, 2020 Category: Cancer & Oncology Authors: Rennier KR, Shin WJ, Krug E, Virdi GS, Pachynski RK Tags: Clin Cancer Res Source Type: research

Identification of FES as a novel radiosensitizing target in human cancers.
CONCLUSIONS: We uncovered that inhibition of FES could be a potential strategy for inducing radiosensitization in cancer. Our results provide the basis for developing novel radiosensitizers. PMID: 31573955 [PubMed - as supplied by publisher]
Source: Clinical Cancer Research - September 30, 2019 Category: Cancer & Oncology Authors: Kim BH, Kim YJ, Kim MH, Na YR, Jung D, Seok SH, Kim J, Kim HJ Tags: Clin Cancer Res Source Type: research

Glycogen Synthase Kinase-3 Inhibition Sensitizes Pancreatic Cancer Cells to Chemotherapy by Abrogating the TopBP1/ATR-Mediated DNA Damage Response.
Conclusions: These data identify a previously unknown role for GSK-3 kinases in the regulation of the TopBP1/ATR/Chk1 DNA damage response pathway. The data also support the inclusion of patients with PDAC in clinical studies of 9-ING-41 alone and in combination with gemcitabine. PMID: 31533931 [PubMed - as supplied by publisher]
Source: Clinical Cancer Research - September 17, 2019 Category: Cancer & Oncology Authors: Ding L, Madamsetty VS, Kiers S, Alekhina O, Ugolkov A, Dube J, Zhang Y, Zhang JS, Wang E, Dutta SK, Schmitt DM, Giles FJ, Kozikowski AP, Mazar AP, Mukhopadhyay D, Billadeau DD Tags: Clin Cancer Res Source Type: research