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Combination curcumin and (-)-epigallocatechin-3-gallate inhibits colorectal carcinoma microenvironment-induced angiogenesis by JAK/STAT3/IL-8 pathway.

Oncogenesis

Jin G, Yang Y, Liu K, Zhao J, Chen X, Liu H, Bai R, Li X, Jiang Y, Zhang X, Lu J, Dong Z.
PMID: 28967875
Oncogenesis. 2017 Oct 02;6(10):e384. doi: 10.1038/oncsis.2017.84.

Tumor microenvironment has a crucial role in cancer development and progression, whereas the mechanism of how it regulates angiogenesis is unclear. In this study, we simulated the colorectal carcinoma microenvironment by conditioned medium (CM) of colorectal carcinoma cell lines...

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Jin G, Yang Y, Liu K, et al. Combination curcumin and (-)-epigallocatechin-3-gallate inhibits colorectal carcinoma microenvironment-induced angiogenesis by JAK/STAT3/IL-8 pathway. Oncogenesis. 2017;6(10):e384doi: 10.1038/oncsis.2017.84.
Jin, G., Yang, Y., Liu, K., Zhao, J., Chen, X., Liu, H., Bai, R., Li, X., Jiang, Y., Zhang, X., Lu, J., & Dong, Z. (2017). Combination curcumin and (-)-epigallocatechin-3-gallate inhibits colorectal carcinoma microenvironment-induced angiogenesis by JAK/STAT3/IL-8 pathway. Oncogenesis, 6(10), e384. https://doi.org/10.1038/oncsis.2017.84
Jin, G, et al. "Combination curcumin and (-)-epigallocatechin-3-gallate inhibits colorectal carcinoma microenvironment-induced angiogenesis by JAK/STAT3/IL-8 pathway." Oncogenesis vol. 6,10 (2017): e384. doi: https://doi.org/10.1038/oncsis.2017.84
Jin G, Yang Y, Liu K, Zhao J, Chen X, Liu H, Bai R, Li X, Jiang Y, Zhang X, Lu J, Dong Z. Combination curcumin and (-)-epigallocatechin-3-gallate inhibits colorectal carcinoma microenvironment-induced angiogenesis by JAK/STAT3/IL-8 pathway. Oncogenesis. 2017 Oct 02;6(10):e384. doi: 10.1038/oncsis.2017.84. PMID: 28967875; PMCID: PMC5668882.
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p16 controls epithelial cell growth and suppresses carcinogenesis through mechanisms that do not require RB1 function.

Oncogenesis

Sen M, Akeno N, Reece A, Miller AL, Simpson DS, Wikenheiser-Brokamp KA.
PMID: 28414317
Oncogenesis. 2017 Apr 17;6(4):e320. doi: 10.1038/oncsis.2017.5.

The p16/RB1 tumor suppressor pathway is inactivated in the vast majority, if not all, human cancers. The current paradigm is that p16 and RB1 function in a linear pathway to suppress tumorigenesis; however p16 is preferentially lost in human...

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Sen M, Akeno N, Reece A, et al. p16 controls epithelial cell growth and suppresses carcinogenesis through mechanisms that do not require RB1 function. Oncogenesis. 2017;6(4):e320doi: 10.1038/oncsis.2017.5.
Sen, M., Akeno, N., Reece, A., Miller, A. L., Simpson, D. S., & Wikenheiser-Brokamp, K. A. (2017). p16 controls epithelial cell growth and suppresses carcinogenesis through mechanisms that do not require RB1 function. Oncogenesis, 6(4), e320. https://doi.org/10.1038/oncsis.2017.5
Sen, M, et al. "p16 controls epithelial cell growth and suppresses carcinogenesis through mechanisms that do not require RB1 function." Oncogenesis vol. 6,4 (2017): e320. doi: https://doi.org/10.1038/oncsis.2017.5
Sen M, Akeno N, Reece A, Miller AL, Simpson DS, Wikenheiser-Brokamp KA. p16 controls epithelial cell growth and suppresses carcinogenesis through mechanisms that do not require RB1 function. Oncogenesis. 2017 Apr 17;6(4):e320. doi: 10.1038/oncsis.2017.5. PMID: 28414317; PMCID: PMC5520502.
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Initial sites of hepadnavirus integration into host genome in human hepatocytes and in the woodchuck model of hepatitis B-associated hepatocellular carcinoma.

Oncogenesis

Chauhan R, Churchill ND, Mulrooney-Cousins PM, Michalak TI.
PMID: 28414318
Oncogenesis. 2017 Apr 17;6(4):e317. doi: 10.1038/oncsis.2017.22.

Hepatitis B virus (HBV) and the closely related woodchuck hepatitis virus (WHV) are potent carcinogens that trigger development of primary hepatocellular carcinoma (HCC). The initial sites of hepadnavirus-host genome integration, their diversity and kinetics of formation can be central...

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Chauhan R, Churchill ND, Mulrooney-Cousins PM, et al. Initial sites of hepadnavirus integration into host genome in human hepatocytes and in the woodchuck model of hepatitis B-associated hepatocellular carcinoma. Oncogenesis. 2017;6(4):e317doi: 10.1038/oncsis.2017.22.
Chauhan, R., Churchill, N. D., Mulrooney-Cousins, P. M., & Michalak, T. I. (2017). Initial sites of hepadnavirus integration into host genome in human hepatocytes and in the woodchuck model of hepatitis B-associated hepatocellular carcinoma. Oncogenesis, 6(4), e317. https://doi.org/10.1038/oncsis.2017.22
Chauhan, R, et al. "Initial sites of hepadnavirus integration into host genome in human hepatocytes and in the woodchuck model of hepatitis B-associated hepatocellular carcinoma." Oncogenesis vol. 6,4 (2017): e317. doi: https://doi.org/10.1038/oncsis.2017.22
Chauhan R, Churchill ND, Mulrooney-Cousins PM, Michalak TI. Initial sites of hepadnavirus integration into host genome in human hepatocytes and in the woodchuck model of hepatitis B-associated hepatocellular carcinoma. Oncogenesis. 2017 Apr 17;6(4):e317. doi: 10.1038/oncsis.2017.22. PMID: 28414318; PMCID: PMC5520499.
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DUOX1 silencing in lung cancer promotes EMT, cancer stem cell characteristics and invasive properties.

Oncogenesis

Little AC, Sham D, Hristova M, Danyal K, Heppner DE, Bauer RA, Sipsey LM, Habibovic A, van der Vliet A.
PMID: 27694834
Oncogenesis. 2016 Oct 03;5(10):e261. doi: 10.1038/oncsis.2016.61.

Dual oxidase 1 (DUOX1) is an oxidant-generating enzyme within the airway epithelium that participates in innate airway host defense and epithelial homeostasis. Recent studies indicate that DUOX1 is suppressed in lung cancers by epigenetic silencing, although the importance of...

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Little AC, Sham D, Hristova M, et al. DUOX1 silencing in lung cancer promotes EMT, cancer stem cell characteristics and invasive properties. Oncogenesis. 2016;5(10):e261doi: 10.1038/oncsis.2016.61.
Little, A. C., Sham, D., Hristova, M., Danyal, K., Heppner, D. E., Bauer, R. A., Sipsey, L. M., Habibovic, A., & van der Vliet, A. (2016). DUOX1 silencing in lung cancer promotes EMT, cancer stem cell characteristics and invasive properties. Oncogenesis, 5(10), e261. https://doi.org/10.1038/oncsis.2016.61
Little, A C, et al. "DUOX1 silencing in lung cancer promotes EMT, cancer stem cell characteristics and invasive properties." Oncogenesis vol. 5,10 (2016): e261. doi: https://doi.org/10.1038/oncsis.2016.61
Little AC, Sham D, Hristova M, Danyal K, Heppner DE, Bauer RA, Sipsey LM, Habibovic A, van der Vliet A. DUOX1 silencing in lung cancer promotes EMT, cancer stem cell characteristics and invasive properties. Oncogenesis. 2016 Oct 03;5(10):e261. doi: 10.1038/oncsis.2016.61. PMID: 27694834; PMCID: PMC5117847.
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Loss of LZAP inactivates p53 and regulates sensitivity of cells to DNA damage in a p53-dependent manner.

Oncogenesis

Wamsley JJ, Gary C, Biktasova A, Hajek M, Bellinger G, Virk R, Issaeva N, Yarbrough WG.
PMID: 28394357
Oncogenesis. 2017 Apr 10;6(4):e314. doi: 10.1038/oncsis.2017.12.

Chemotherapy and radiation, the two most common cancer therapies, exert their anticancer effects by causing damage to cellular DNA. However, systemic treatment damages DNA not only in cancer, but also in healthy cells, resulting in the progression of serious...

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Wamsley JJ, Gary C, Biktasova A, et al. Loss of LZAP inactivates p53 and regulates sensitivity of cells to DNA damage in a p53-dependent manner. Oncogenesis. 2017;6(4):e314doi: 10.1038/oncsis.2017.12.
Wamsley, J. J., Gary, C., Biktasova, A., Hajek, M., Bellinger, G., Virk, R., Issaeva, N., & Yarbrough, W. G. (2017). Loss of LZAP inactivates p53 and regulates sensitivity of cells to DNA damage in a p53-dependent manner. Oncogenesis, 6(4), e314. https://doi.org/10.1038/oncsis.2017.12
Wamsley, J J, et al. "Loss of LZAP inactivates p53 and regulates sensitivity of cells to DNA damage in a p53-dependent manner." Oncogenesis vol. 6,4 (2017): e314. doi: https://doi.org/10.1038/oncsis.2017.12
Wamsley JJ, Gary C, Biktasova A, Hajek M, Bellinger G, Virk R, Issaeva N, Yarbrough WG. Loss of LZAP inactivates p53 and regulates sensitivity of cells to DNA damage in a p53-dependent manner. Oncogenesis. 2017 Apr 10;6(4):e314. doi: 10.1038/oncsis.2017.12. PMID: 28394357; PMCID: PMC5520489.
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EMT Involved in Migration of Stem/Progenitor Cells for Pituitary Development and Regeneration.

Journal of clinical medicine

Yoshida S, Kato T, Kato Y.
PMID: 27058562
J Clin Med. 2016 Apr 06;5(4). doi: 10.3390/jcm5040043.

Epithelial-mesenchymal transition (EMT) and cell migration are important processes in embryonic development of many tissues as well as oncogenesis. The pituitary gland is a master endocrine tissue and recent studies indicate that Sox2-expressing stem/progenitor cells actively migrate and develop...

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Yoshida S, Kato T, Kato Y. EMT Involved in Migration of Stem/Progenitor Cells for Pituitary Development and Regeneration. J Clin Med. 2016;5(4)doi: 10.3390/jcm5040043.
Yoshida, S., Kato, T., & Kato, Y. (2016). EMT Involved in Migration of Stem/Progenitor Cells for Pituitary Development and Regeneration. Journal of clinical medicine, 5(4), . https://doi.org/10.3390/jcm5040043
Yoshida, Saishu, et al. "EMT Involved in Migration of Stem/Progenitor Cells for Pituitary Development and Regeneration." Journal of clinical medicine vol. 5,4 (2016). doi: https://doi.org/10.3390/jcm5040043
Yoshida S, Kato T, Kato Y. EMT Involved in Migration of Stem/Progenitor Cells for Pituitary Development and Regeneration. J Clin Med. 2016 Apr 06;5(4). doi: 10.3390/jcm5040043. PMID: 27058562; PMCID: PMC4850466.
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Blockade of sonic hedgehog signaling decreases viability and induces apoptosis in retinoblastoma cells: The key role of the PI3K/Akt pathway.

Oncology letters

Song Z, Du Y, Tao Y.
PMID: 28943916
Oncol Lett. 2017 Oct;14(4):4099-4105. doi: 10.3892/ol.2017.6701. Epub 2017 Aug 02.

Retinoblastoma (RB) is the most common type of malignant intraocular cancer in teenagers. One of the proteins abnormally expressed during oncogenesis of RB is sonic hedgehog (SHH), which possesses the capability to selectively activate transcription factors of different genes....

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Song Z, Du Y, Tao Y. Blockade of sonic hedgehog signaling decreases viability and induces apoptosis in retinoblastoma cells: The key role of the PI3K/Akt pathway. Oncol Lett. 2017;14(4):4099-4105doi: 10.3892/ol.2017.6701.
Song, Z., Du, Y., & Tao, Y. (2017). Blockade of sonic hedgehog signaling decreases viability and induces apoptosis in retinoblastoma cells: The key role of the PI3K/Akt pathway. Oncology letters, 14(4), 4099-4105. https://doi.org/10.3892/ol.2017.6701
Song, Zhidu, et al. "Blockade of sonic hedgehog signaling decreases viability and induces apoptosis in retinoblastoma cells: The key role of the PI3K/Akt pathway." Oncology letters vol. 14,4 (2017): 4099-4105. doi: https://doi.org/10.3892/ol.2017.6701
Song Z, Du Y, Tao Y. Blockade of sonic hedgehog signaling decreases viability and induces apoptosis in retinoblastoma cells: The key role of the PI3K/Akt pathway. Oncol Lett. 2017 Oct;14(4):4099-4105. doi: 10.3892/ol.2017.6701. Epub 2017 Aug 02. PMID: 28943916; PMCID: PMC5604099.
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PRAS40 promotes NF-κB transcriptional activity through association with p65.

Oncogenesis

Zhu G, Qi Q, Havel JJ, Li Z, Du Y, Zhang X, Fu H.
PMID: 28945219
Oncogenesis. 2017 Sep 25;6(9):e381. doi: 10.1038/oncsis.2017.80.

PRAS40 has been shown to have a crucial role in the repression of mammalian target of rapamycin (mTOR). Nonetheless, PRAS40 appears to have an oncogenic function in cancer cells. Whether PRAS40 mediates signaling independent of mTOR inhibition in cancer...

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Zhu G, Qi Q, Havel JJ, et al. PRAS40 promotes NF-κB transcriptional activity through association with p65. Oncogenesis. 2017;6(9):e381doi: 10.1038/oncsis.2017.80.
Zhu, G., Qi, Q., Havel, J. J., Li, Z., Du, Y., Zhang, X., & Fu, H. (2017). PRAS40 promotes NF-κB transcriptional activity through association with p65. Oncogenesis, 6(9), e381. https://doi.org/10.1038/oncsis.2017.80
Zhu, G, et al. "PRAS40 promotes NF-κB transcriptional activity through association with p65." Oncogenesis vol. 6,9 (2017): e381. doi: https://doi.org/10.1038/oncsis.2017.80
Zhu G, Qi Q, Havel JJ, Li Z, Du Y, Zhang X, Fu H. PRAS40 promotes NF-κB transcriptional activity through association with p65. Oncogenesis. 2017 Sep 25;6(9):e381. doi: 10.1038/oncsis.2017.80. PMID: 28945219; PMCID: PMC5623906.
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Formal modeling and analysis of the hexosamine biosynthetic pathway: role of O-linked N-acetylglucosamine transferase in oncogenesis and cancer progression.

PeerJ

Saeed MT, Ahmad J, Kanwal S, Holowatyj AN, Sheikh IA, Zafar Paracha R, Shafi A, Siddiqa A, Bibi Z, Khan M, Ali A.
PMID: 27703839
PeerJ. 2016 Sep 27;4:e2348. doi: 10.7717/peerj.2348. eCollection 2016.

The alteration of glucose metabolism, through increased uptake of glucose and glutamine addiction, is essential to cancer cell growth and invasion. Increased flux of glucose through the Hexosamine Biosynthetic Pathway (HBP) drives increased cellular O-GlcNAcylation (hyper-O-GlcNAcylation) and contributes to...

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Saeed MT, Ahmad J, Kanwal S, et al. Formal modeling and analysis of the hexosamine biosynthetic pathway: role of O-linked N-acetylglucosamine transferase in oncogenesis and cancer progression. PeerJ. 2016;4:e2348doi: 10.7717/peerj.2348.
Saeed, M. T., Ahmad, J., Kanwal, S., Holowatyj, A. N., Sheikh, I. A., Zafar Paracha, R., Shafi, A., Siddiqa, A., Bibi, Z., Khan, M., & Ali, A. (2016). Formal modeling and analysis of the hexosamine biosynthetic pathway: role of O-linked N-acetylglucosamine transferase in oncogenesis and cancer progression. PeerJ, 4e2348. https://doi.org/10.7717/peerj.2348
Saeed, Muhammad Tariq, et al. "Formal modeling and analysis of the hexosamine biosynthetic pathway: role of O-linked N-acetylglucosamine transferase in oncogenesis and cancer progression." PeerJ vol. 4 (2016): e2348. doi: https://doi.org/10.7717/peerj.2348
Saeed MT, Ahmad J, Kanwal S, Holowatyj AN, Sheikh IA, Zafar Paracha R, Shafi A, Siddiqa A, Bibi Z, Khan M, Ali A. Formal modeling and analysis of the hexosamine biosynthetic pathway: role of O-linked N-acetylglucosamine transferase in oncogenesis and cancer progression. PeerJ. 2016 Sep 27;4:e2348. doi: 10.7717/peerj.2348. eCollection 2016. PMID: 27703839; PMCID: PMC5047222.
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Etiopathogenesis of Differentiated Thyroid Carcinomas.

Open access Macedonian journal of medical sciences

Makazlieva T, Vaskova O, Majstorov V.
PMID: 27703585
Open Access Maced J Med Sci. 2016 Sep 15;4(3):517-522. doi: 10.3889/oamjms.2016.086. Epub 2016 Aug 02.

INTRODUCTION: Thyroid malignomas are a heterogeneous group of neoplasm consisting of most frequent differentiated encountered carcinomas, papillary and follicular thyroid carcinoma, then medullary thyroid carcinoma originating from neuroendocrine calcitonin-producing C-cells and rare forms of thyroid lymphomas arising from intrathyroidal...

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Makazlieva T, Vaskova O, Majstorov V. Etiopathogenesis of Differentiated Thyroid Carcinomas. Open Access Maced J Med Sci. 2016;4(3):517-522doi: 10.3889/oamjms.2016.086.
Makazlieva, T., Vaskova, O., & Majstorov, V. (2016). Etiopathogenesis of Differentiated Thyroid Carcinomas. Open access Macedonian journal of medical sciences, 4(3), 517-522. https://doi.org/10.3889/oamjms.2016.086
Makazlieva, Tanja, et al. "Etiopathogenesis of Differentiated Thyroid Carcinomas." Open access Macedonian journal of medical sciences vol. 4,3 (2016): 517-522. doi: https://doi.org/10.3889/oamjms.2016.086
Makazlieva T, Vaskova O, Majstorov V. Etiopathogenesis of Differentiated Thyroid Carcinomas. Open Access Maced J Med Sci. 2016 Sep 15;4(3):517-522. doi: 10.3889/oamjms.2016.086. Epub 2016 Aug 02. PMID: 27703585; PMCID: PMC5042645.
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Synthesis and Structure-Activity Relationship Study of 5a-Carbasugar Analogues of SL0101.

ACS medicinal chemistry letters

Li M, Li Y, Mrozowski RM, Sandusky ZM, Shan M, Song X, Wu B, Zhang Q, Lannigan DA, O'Doherty GA.
PMID: 25589938
ACS Med Chem Lett. 2014 Nov 26;6(1):95-9. doi: 10.1021/ml5004525. eCollection 2015 Jan 08.

The Ser/Thr protein kinase, RSK, is associated with oncogenesis, and therefore, there are ongoing efforts to develop RSK inhibitors that are suitable for use in vivo. SL0101 is a natural product that demonstrates selectivity for RSK inhibition. However, SL0101...

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Li M, Li Y, Mrozowski RM, et al. Synthesis and Structure-Activity Relationship Study of 5a-Carbasugar Analogues of SL0101. ACS Med Chem Lett. 2014;6(1):95-9doi: 10.1021/ml5004525.
Li, M., Li, Y., Mrozowski, R. M., Sandusky, Z. M., Shan, M., Song, X., Wu, B., Zhang, Q., Lannigan, D. A., & O'Doherty, G. A. (2015). Synthesis and Structure-Activity Relationship Study of 5a-Carbasugar Analogues of SL0101. ACS medicinal chemistry letters, 6(1), 95-9. https://doi.org/10.1021/ml5004525
Li, Mingzong, et al. "Synthesis and Structure-Activity Relationship Study of 5a-Carbasugar Analogues of SL0101." ACS medicinal chemistry letters vol. 6,1 (2015): 95-9. doi: https://doi.org/10.1021/ml5004525
Li M, Li Y, Mrozowski RM, Sandusky ZM, Shan M, Song X, Wu B, Zhang Q, Lannigan DA, O'Doherty GA. Synthesis and Structure-Activity Relationship Study of 5a-Carbasugar Analogues of SL0101. ACS Med Chem Lett. 2014 Nov 26;6(1):95-9. doi: 10.1021/ml5004525. eCollection 2015 Jan 08. PMID: 25589938; PMCID: PMC4291707.
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An Insight into the Increasing Role of LncRNAs in the Pathogenesis of Gliomas.

Frontiers in molecular neuroscience

Yan Y, Xu Z, Li Z, Sun L, Gong Z.
PMID: 28293170
Front Mol Neurosci. 2017 Feb 28;10:53. doi: 10.3389/fnmol.2017.00053. eCollection 2017.

Long non-coding RNAs (LncRNAs) are essential epigenetic regulators with critical roles in tumor initiation and malignant progression. However, the roles and mechanisms of aberrantly expressed lncRNAs in the pathogenesis of gliomas are not fully understood. With the development of...

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Yan Y, Xu Z, Li Z, et al. An Insight into the Increasing Role of LncRNAs in the Pathogenesis of Gliomas. Front Mol Neurosci. 2017;10:53doi: 10.3389/fnmol.2017.00053.
Yan, Y., Xu, Z., Li, Z., Sun, L., & Gong, Z. (2017). An Insight into the Increasing Role of LncRNAs in the Pathogenesis of Gliomas. Frontiers in molecular neuroscience, 1053. https://doi.org/10.3389/fnmol.2017.00053
Yan, Yuanliang, et al. "An Insight into the Increasing Role of LncRNAs in the Pathogenesis of Gliomas." Frontiers in molecular neuroscience vol. 10 (2017): 53. doi: https://doi.org/10.3389/fnmol.2017.00053
Yan Y, Xu Z, Li Z, Sun L, Gong Z. An Insight into the Increasing Role of LncRNAs in the Pathogenesis of Gliomas. Front Mol Neurosci. 2017 Feb 28;10:53. doi: 10.3389/fnmol.2017.00053. eCollection 2017. PMID: 28293170; PMCID: PMC5328963.
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Showing 1 to 12 of 3012 entries