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Article ; Online: Correction: Restoring PUMA induction overcomes KRAS-mediated resistance to anti-EGFR antibodies in colorectal cancer.

Knickelbein, Kyle / Tong, Jingshan / Chen, Dongshi / Wang, Yi-Jun / Misale, Sandra / Bardelli, Alberto / Yu, Jian / Zhang, Lin

Oncogene

2023 Volume 42, Issue 23, Page(s) 1957

Language	English
Publishing date	2023-05-16
Publishing country	England
Document type	Published Erratum
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-023-02682-x
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Article ; Online: Inhibition of multiple CDKs potentiates colon cancer chemotherapy via p73-mediated DR5 induction.

Tong, Jingshan / Tan, Xiao / Hao, Suisui / Ermine, Kaylee / Lu, Xinyan / Liu, Zhaojin / Jha, Anupma / Yu, Jian / Zhang, Lin

Oncogene

2023 Volume 42, Issue 12, Page(s) 869–880

Abstract: Targeting cyclin-dependent kinases (CDKs) has recently emerged as a promising therapeutic approach against cancer. However, the anticancer mechanisms of different CDK inhibitors (CDKIs) are not well understood. Our recent study revealed that selective ... ...

Abstract	Targeting cyclin-dependent kinases (CDKs) has recently emerged as a promising therapeutic approach against cancer. However, the anticancer mechanisms of different CDK inhibitors (CDKIs) are not well understood. Our recent study revealed that selective CDK4/6 inhibitors sensitize colorectal cancer (CRC) cells to therapy-induced apoptosis by inducing Death Receptor 5 (DR5) via the p53 family member p73. In this study, we investigated if this pathway is involved in anticancer effects of different CDKIs. We found that less-selective CDKIs, including flavopiridol, roscovitine, dinaciclib, and SNS-032, induced DR5 via p73-mediated transcriptional activation. The induction of DR5 by these CDKIs was mediated by dephosphorylation of p73 at Threonine 86 and p73 nuclear translocation. Knockdown of a common target of these CDKIs, including CDK1, 2, or 9, recapitulated p73-mediated DR5 induction. CDKIs strongly synergized with 5-fluorouracil (5-FU), the most commonly used CRC chemotherapy agent, in vitro and in vivo to promote growth suppression and apoptosis, which required DR5 and p73. Together, these findings indicate p73-mediated DR5 induction as a potential tumor suppressive mechanism and a critical target engaged by different CDKIs in potentiating therapy-induced apoptosis in CRC cells. These findings help better understand the anticancer mechanisms of CDKIs and may help facilitate their clinical development and applications in CRC.
MeSH term(s)	Humans ; Cyclin-Dependent Kinases ; Cell Line, Tumor ; Colonic Neoplasms/drug therapy ; Colonic Neoplasms/genetics ; Colonic Neoplasms/metabolism ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Apoptosis ; Fluorouracil/pharmacology ; Fluorouracil/therapeutic use
Chemical Substances	Cyclin-Dependent Kinases (EC 2.7.11.22) ; Antineoplastic Agents ; Fluorouracil (U3P01618RT)
Language	English
Publishing date	2023-01-31
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-023-02598-6
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Article ; Online: Spatial and Temporal Variations in Extreme Precipitation and Temperature Events in the Beijing–Tianjin–Hebei Region of China over the Past Six Decades

Runze Tong / Wenchao Sun / Quan Han / Jingshan Yu / Zaifeng Tian

Sustainability, Vol 12, Iss 4, p

2020 Volume 1415

Abstract: Extreme weather events can cause a lot of damage in highly populated regions, such as in the Beijing−Tianjin−Hebei Region (BTHR) in northern China. To understand where and how extreme precipitation and temperature events are changing within the BTHR, ... ...

Abstract	Extreme weather events can cause a lot of damage in highly populated regions, such as in the Beijing−Tianjin−Hebei Region (BTHR) in northern China. To understand where and how extreme precipitation and temperature events are changing within the BTHR, data for 1959−2018 from 25 mereological stations were used to detect trends in the intensity, frequency, and duration of these events. The results showed that intensity, accumulated amount, the duration of extreme precipitation events, and the annual number of days with precipitation greater than 50 mm decreased on a regional scale over this 60-year period. Changes in extreme precipitation events at most stations were not statistically significant, although a few stations had a significant downward trend. The combined effects of the East Asian summer monsoon and rapid urbanization are possible reasons for these trends. Both the annual maximum and minimum temperature increased on a regional and local scale. The frequency of extreme hot and cold weather also, respectively, increased and decreased, with consistent patterns on a regional and local scale. However, the spatial changes of these trends were different, reflecting the effects of irrigation and urbanization on the regional surface energy balance. These findings are valuable to decisionmakers involved in disaster prevention in the BTHR and in other highly populated regions worldwide.
Keywords	beijing–tianjin–hebei region ; extreme temperature event ; extreme precipitation event ; temporal trends ; Environmental effects of industries and plants ; TD194-195 ; Renewable energy sources ; TJ807-830 ; Environmental sciences ; GE1-350
Subject code	910
Language	English
Publishing date	2020-02-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article: Dual inhibition of BET and HAT/p300 suppresses colorectal cancer via DR5- and p53/PUMA-mediated cell death.

Kuang, Chaoyuan / Tong, Jingshan / Ermine, Kaylee / Cai, Manbo / Dai, Fujun / Hao, Suisui / Giles, Francis / Huang, Yi / Yu, Jian / Zhang, Lin

Frontiers in oncology

2022 Volume 12, Page(s) 1018775

Abstract: Background: Colorectal cancer (CRC) frequently has a dysregulated epigenome causing aberrant up-regulation of oncogenes such as c-MYC. Bromodomain and extra-terminal domain (BET) proteins and histone acetyltransferases (HAT) are epigenetic regulatory ... ...

Abstract	Background: Colorectal cancer (CRC) frequently has a dysregulated epigenome causing aberrant up-regulation of oncogenes such as c-MYC. Bromodomain and extra-terminal domain (BET) proteins and histone acetyltransferases (HAT) are epigenetic regulatory proteins that create and maintain epigenetic states supporting oncogenesis. BET inhibitors and HAT inhibitors are currently being investigated as cancer therapeutics due to their ability to suppress cancer-promoting epigenetic modifiers. Due to the extensive molecular crosstalk between BET proteins and HAT proteins, we hypothesized that dual inhibition of BET and HAT could more potently inhibit CRC cells than inhibition of each individual protein. Methods: We investigated the activity and mechanisms of a dual BET and HAT inhibitor, NEO2734, in CRC cell lines and mouse xenografts. MTS, flow cytometry, and microscopy were used to assess cell viability. qPCR, Western blotting, and immunofluorescent staining were used to assess mechanisms of action. Results: We found that NEO2734 more potently suppresses CRC cell growth than first generation BET inhibitors, regardless of the status of common CRC driver mutations. We previously showed that BET inhibitors upregulate DR5 to induce extrinsic apoptosis. In the current study, we show that NEO2734 treatment induces CRC cell apoptosis Conclusions: Our study demonstrates NEO2734 potently suppresses CRC cells
Language	English
Publishing date	2022-10-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2022.1018775
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Article ; Online: BET protein degradation triggers DR5-mediated immunogenic cell death to suppress colorectal cancer and potentiate immune checkpoint blockade.

Tong, Jingshan / Tan, Xiao / Risnik, Denise / Gao, Man / Song, Xiangping / Ermine, Kaylee / Shen, Liangfang / Wang, Shaomeng / Yu, Jian / Zhang, Lin

Oncogene

2021 Volume 40, Issue 48, Page(s) 6566–6578

Abstract: Bromodomain and extra-terminal domain (BET) family proteins are epigenetic readers that play a critical role in oncogenesis by controlling the expression of oncogenes such as c-Myc. Targeting BET family proteins has recently emerged as a promising ... ...

Abstract	Bromodomain and extra-terminal domain (BET) family proteins are epigenetic readers that play a critical role in oncogenesis by controlling the expression of oncogenes such as c-Myc. Targeting BET family proteins has recently emerged as a promising anticancer strategy. However, the molecular mechanisms by which cancer cells respond to BET inhibition are not well understood. In this study, we found that inducing the degradation of BET proteins by the proteolysis targeting chimeras (PROTAC) approach potently suppressed the growth of colorectal cancer (CRC) including patient-derived tumors. Mechanistically, BET degradation transcriptionally activates Death Receptor 5 (DR5) to trigger immunogenic cell death (ICD) in CRC cells. Enhanced DR5 induction further sensitizes CRC cells with a mutation in Speckle-type POZ protein (SPOP). Furthermore, DR5 is indispensable for a striking antitumor effect of combining BET degradation and anti-PD-1 antibody, which was well tolerated in mice and almost eradicated syngeneic tumors. Our results demonstrate that BET degradation triggers DR5-mediated ICD to potently suppress CRC and potentiate immune checkpoint blockade. These results provide a rationale, mechanistic insights, and potential biomarkers for developing a precision CRC therapy by inducing BET protein degradation.
MeSH term(s)	Animals ; Apoptosis ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Cell Proliferation ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/immunology ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/pathology ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Immune Checkpoint Inhibitors/pharmacology ; Immunogenic Cell Death ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Proteins/genetics ; Proteins/metabolism ; Proteolysis ; Receptors, TNF-Related Apoptosis-Inducing Ligand/genetics ; Receptors, TNF-Related Apoptosis-Inducing Ligand/metabolism ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Chemical Substances	Biomarkers, Tumor ; Immune Checkpoint Inhibitors ; Proteins ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; TNFRSF10B protein, human ; bromodomain and extra-terminal domain protein, human
Language	English
Publishing date	2021-10-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-021-02041-8
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Article ; Online: Synthetical lethality of Werner helicase and mismatch repair deficiency is mediated by p53 and PUMA in colon cancer.

Hao, Suisui / Tong, Jingshan / Jha, Anupma / Risnik, Denise / Lizardo, Darleny / Lu, Xinyan / Goel, Ajay / Opresko, Patricia L / Yu, Jian / Zhang, Lin

Proceedings of the National Academy of Sciences of the United States of America

2022 Volume 119, Issue 51, Page(s) e2211775119

Abstract: Synthetic lethality is a powerful approach for targeting oncogenic drivers in cancer. Recent studies revealed that cancer cells with microsatellite instability (MSI) require Werner (WRN) helicase for survival; however, the underlying mechanism remains ... ...

Abstract	Synthetic lethality is a powerful approach for targeting oncogenic drivers in cancer. Recent studies revealed that cancer cells with microsatellite instability (MSI) require Werner (WRN) helicase for survival; however, the underlying mechanism remains unclear. In this study, we found that WRN depletion strongly induced p53 and its downstream apoptotic target PUMA in MSI colorectal cancer (CRC) cells. p53 or PUMA deletion abolished apoptosis induced by WRN depletion in MSI CRC cells. Importantly, correction of MSI abrogated the activation of p53/PUMA and cell killing, while induction of MSI led to sensitivity in isogenic CRC cells. Rare p53-mutant MSI CRC cells are resistant to WRN depletion due to lack of PUMA induction, which could be restored by wildtype (WT) p53 knock in or reconstitution. WRN depletion or treatment with the RecQ helicase inhibitor ML216 suppressed in vitro and in vivo growth of MSI CRCs in a p53/PUMA-dependent manner. ML216 treatment was efficacious in MSI CRC patient-derived xenografts. Interestingly,
MeSH term(s)	Humans ; Werner Syndrome Helicase/genetics ; Tumor Suppressor Protein p53/genetics ; Microsatellite Instability ; Colorectal Neoplasms/genetics ; RecQ Helicases/genetics ; Colonic Neoplasms
Chemical Substances	Werner Syndrome Helicase (EC 3.6.4.12) ; Tumor Suppressor Protein p53 ; RecQ Helicases (EC 3.6.4.12)
Language	English
Publishing date	2022-12-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2211775119
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Article ; Online: CDK4/6 Inhibition Suppresses p73 Phosphorylation and Activates DR5 to Potentiate Chemotherapy and Immune Checkpoint Blockade.

Tong, Jingshan / Tan, Xiao / Song, Xiangping / Gao, Man / Risnik, Denise / Hao, Suisui / Ermine, Kaylee / Wang, Peng / Li, Hua / Huang, Yi / Yu, Jian / Zhang, Lin

Cancer research

2022 Volume 82, Issue 7, Page(s) 1340–1352

Abstract: Targeting cyclin-dependent kinases 4 and 6 (CDK4/6) is a successful therapeutic approach against breast and other solid tumors. Inhibition of CDK4/6 halts cell cycle progression and promotes antitumor immunity. However, the mechanisms underlying the ... ...

Abstract	Targeting cyclin-dependent kinases 4 and 6 (CDK4/6) is a successful therapeutic approach against breast and other solid tumors. Inhibition of CDK4/6 halts cell cycle progression and promotes antitumor immunity. However, the mechanisms underlying the antitumor activity of CDK4/6 inhibitors are not fully understood. We found that CDK4/6 bind and phosphorylate the p53 family member p73 at threonine 86, which sequesters p73 in the cytoplasm. Inhibition of CDK4/6 led to dephosphorylation and nuclear translocation of p73, which transcriptionally activated death receptor 5 (DR5), a cytokine receptor and key component of the extrinsic apoptotic pathway. p73-mediated induction of DR5 by CDK4/6 inhibitors promoted immunogenic cell death of cancer cells. Deletion of DR5 in cancer cells in vitro and in vivo abrogated the potentiating effects of CDK4/6 inhibitors on immune cytokine TRAIL, 5-fluorouracil chemotherapy, and anti-PD-1 immunotherapy. Together, these results reveal a previously unrecognized consequence of CDK4/6 inhibition, which may be critical for potentiating the killing and immunogenic effects on cancer cells. Significance: This work demonstrates how inhibition of CDK4/6 sensitizes cancer cells to chemotherapy and immune checkpoint blockade and may provide a new molecular marker for improving CDK4/6-targeted cancer therapies. See related commentary by Frank, p. 1170.
MeSH term(s)	Apoptosis ; Cell Line, Tumor ; Cyclin-Dependent Kinase 4/antagonists & inhibitors ; Cyclin-Dependent Kinase 6/antagonists & inhibitors ; Fluorouracil/pharmacology ; Humans ; Immune Checkpoint Inhibitors ; Phosphorylation ; Receptors, TNF-Related Apoptosis-Inducing Ligand/metabolism ; TNF-Related Apoptosis-Inducing Ligand/pharmacology ; Tumor Protein p73/metabolism
Chemical Substances	Immune Checkpoint Inhibitors ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; TNF-Related Apoptosis-Inducing Ligand ; TP73 protein, human ; Tumor Protein p73 ; CDK4 protein, human (EC 2.7.11.22) ; CDK6 protein, human (EC 2.7.11.22) ; Cyclin-Dependent Kinase 4 (EC 2.7.11.22) ; Cyclin-Dependent Kinase 6 (EC 2.7.11.22) ; Fluorouracil (U3P01618RT)
Language	English
Publishing date	2022-02-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-21-3062
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Article: Determination of Transdermal Rate of Metallic Microneedle Array through an Impedance Measurements-Based Numerical Check Screening Algorithm.

Mo, Jingshan / Liu, Junqing / Huang, Shuang / Liang, Baoming / Huang, Xinshuo / Yang, Cheng / Chen, Meiwan / Liu, Jing / Zhang, Tong / Xie, Xi / Guo, Jun / Liu, Fanmao / Chen, Hui-Jiuan

Micromachines

2022 Volume 13, Issue 5

Abstract: Microneedle systems have been widely used in health monitoring, painless drug delivery, and medical cosmetology. Although many studies on microneedle materials, structures, and applications have been conducted, the applications of microneedles often ... ...

Abstract	Microneedle systems have been widely used in health monitoring, painless drug delivery, and medical cosmetology. Although many studies on microneedle materials, structures, and applications have been conducted, the applications of microneedles often suffered from issues of inconsistent penetration rates due to the complication of skin-microneedle interface. In this study, we demonstrated a methodology of determination of transdermal rate of metallic microneedle array through impedance measurements-based numerical check screening algorithm. Metallic sheet microneedle array sensors with different sizes were fabricated to evaluate different transdermal rates. In vitro sensing of hydrogen peroxide confirmed the effect of transdermal rate on the sensing outcomes. An FEM simulation model of a microneedle array revealed the monotonous relation between the transdermal state and test current. Accordingly, two methods were primely derived to calculate the transdermal rate from the test current. First, an exact logic method provided the number of unpenetrated tips per sheet, but it required more rigorous testing results. Second, a fuzzy logic method provided an approximate transdermal rate on adjacent areas, being more applicable and robust to errors. Real-time transdermal rate estimation may be essential for improving the performance of microneedle systems, and this study provides various fundaments toward that goal.
Language	English
Publishing date	2022-04-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2620864-7
ISSN	2072-666X
ISSN	2072-666X
DOI	10.3390/mi13050718
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Article ; Online: miR-126 reduces trastuzumab resistance by targeting PIK3R2 and regulating AKT/mTOR pathway in breast cancer cells.

Fu, Rao / Tong, Jing-Shan

Journal of cellular and molecular medicine

2020 Volume 24, Issue 13, Page(s) 7600–7608

Abstract: MicroRNAs (miRNAs) have been found to play a key role in drug resistance. In the current study, we aimed to explore the potential role of miR-126 in trastuzumab resistance in breast cancer cells. We found that the trastuzumab-resistant cell lines SKBR3/ ... ...

Abstract	MicroRNAs (miRNAs) have been found to play a key role in drug resistance. In the current study, we aimed to explore the potential role of miR-126 in trastuzumab resistance in breast cancer cells. We found that the trastuzumab-resistant cell lines SKBR3/TR and BT474/TR had low expression of miR-126 and increased ability to migrate and invade. The resistance, invasion and mobilization abilities of the cells resistant to trastuzumab were reduced by ectopic expression of miR-126 mimics. In comparison, inhibition of miR-126 in SKBR3 parental cells had the opposite effect of an increased resistance to trastuzumab as well as invasion and migration. It was also found that miR-126 directly targets PIK3R2 in breast cancer cells. PIK3R2-knockdown cells showed decreased resistance to trastuzumab, while overexpression of PIK3R2 increased trastuzumab resistance. In addition, our finding showed that overexpression of miR-126 reduced resistance to trastuzumab in the trastuzumab-resistant cells and that inhibition of the PIK3R2/PI3K/AKT/mTOR signalling pathway was involved in this effect. SKBR3/TR cells also showed increased sensitivity to trastuzumab mediated by miR-126 in vivo. In conclusion, the above findings demonstrated that overexpression of miR-126 or down-regulation of its target gene may be a potential approach to overcome trastuzumab resistance in breast cancer cells.
MeSH term(s)	Animals ; Base Sequence ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Movement/genetics ; Down-Regulation/drug effects ; Down-Regulation/genetics ; Drug Resistance, Neoplasm/genetics ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Mice, Nude ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Neoplasm Invasiveness ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction/drug effects ; TOR Serine-Threonine Kinases/metabolism ; Trastuzumab/pharmacology ; Trastuzumab/therapeutic use
Chemical Substances	MIRN126 microRNA, human ; MicroRNAs ; phosphoinositol-3 kinase regulatory subunit 2, human (EC 2.7.1.-) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Trastuzumab (P188ANX8CK)
Language	English
Publishing date	2020-05-15
Publishing country	England
Document type	Journal Article
ZDB-ID	2074559-X
ISSN	1582-4934 ; 1582-4934 ; 1582-1838
ISSN (online)	1582-4934
ISSN	1582-4934 ; 1582-1838
DOI	10.1111/jcmm.15396
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Article ; Online: Mcl-1 inhibition overcomes intrinsic and acquired regorafenib resistance in colorectal cancer.

Song, Xiangping / Shen, Lin / Tong, Jingshan / Kuang, Chaoyuan / Zeng, Shan / Schoen, Robert E / Yu, Jian / Pei, Haiping / Zhang, Lin

Theranostics

2020 Volume 10, Issue 18, Page(s) 8098–8110

Abstract: Intrinsic and acquired resistance to targeted therapies is a significant clinical problem in cancer. We previously showed that resistance to regorafenib, a multi-kinase inhibitor for treating colorectal cancer (CRC) patients, can be caused by mutations ... ...

Abstract	Intrinsic and acquired resistance to targeted therapies is a significant clinical problem in cancer. We previously showed that resistance to regorafenib, a multi-kinase inhibitor for treating colorectal cancer (CRC) patients, can be caused by mutations in the tumor suppressor Methods: Small-molecule Mcl-1 inhibitors were tested on CRC cells with knock-in (KI) of a non-degradable Mcl-1. Effects of Mcl-1 inhibitors on regorafenib sensitivity were determined in Results: We found that highly potent and specific Mcl-1 inhibitors such as S63845 overcame regorafenib resistance by restoring apoptosis in multiple regorafenib-resistant CRC models. Mcl-1 inhibition re-sensitized CRC tumors with intrinsic and acquired regorafenib resistance Conclusions: Our results demonstrate that Mcl-1 inhibitors can overcome intrinsic and acquired regorafenib resistance in CRCs by restoring apoptotic response.
MeSH term(s)	Aged ; Animals ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Biomarkers, Tumor/genetics ; Cell Line, Tumor ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/genetics ; Drug Synergism ; F-Box-WD Repeat-Containing Protein 7/genetics ; Female ; Gene Knock-In Techniques ; Humans ; Male ; Mice ; Mutation ; Myeloid Cell Leukemia Sequence 1 Protein/antagonists & inhibitors ; Myeloid Cell Leukemia Sequence 1 Protein/genetics ; Organoids ; Phenylurea Compounds/pharmacology ; Phenylurea Compounds/therapeutic use ; Precision Medicine/methods ; Primary Cell Culture ; Pyridines/pharmacology ; Pyridines/therapeutic use ; Pyrimidines/pharmacology ; Pyrimidines/therapeutic use ; Thiophenes/pharmacology ; Thiophenes/therapeutic use ; Xenograft Model Antitumor Assays
Chemical Substances	Biomarkers, Tumor ; F-Box-WD Repeat-Containing Protein 7 ; FBXW7 protein, human ; MCL1 protein, human ; Myeloid Cell Leukemia Sequence 1 Protein ; Phenylurea Compounds ; Pyridines ; Pyrimidines ; S63845 ; Thiophenes ; regorafenib (24T2A1DOYB)
Language	English
Publishing date	2020-07-09
Publishing country	Australia
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2592097-2
ISSN	1838-7640 ; 1838-7640
ISSN (online)	1838-7640
ISSN	1838-7640
DOI	10.7150/thno.45363
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