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Inflammatory bowel disease, colorectal cancer and type 2 diabetes mellitus: The links.

BBA clinical

Jurjus A, Eid A, Al Kattar S, Zeenny MN, Gerges-Geagea A, Haydar H, Hilal A, Oueidat D, Matar M, Tawilah J, Hussein IH, Schembri-Wismayer P, Cappello F, Tomasello G, Leone A, Jurjus RA.
PMID: 27051585
BBA Clin. 2015 Nov 05;5:16-24. doi: 10.1016/j.bbacli.2015.11.002. eCollection 2016 Jun.

The co-occurrence of the three disease entities, inflammatory bowel disease (IBD), colorectal cancer (CRC), type 2diabetes mellitus (T2DM) along with inflammation and dismicrobism has been frequently reported. Some authors have even suggested that dysbiosis could be the link through...

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Jurjus A, Eid A, Al Kattar S, et al. Inflammatory bowel disease, colorectal cancer and type 2 diabetes mellitus: The links. BBA Clin. 2015;5:16-24doi: 10.1016/j.bbacli.2015.11.002.
Jurjus, A., Eid, A., Al Kattar, S., Zeenny, M. N., Gerges-Geagea, A., Haydar, H., Hilal, A., Oueidat, D., Matar, M., Tawilah, J., Hussein, I. H., Schembri-Wismayer, P., Cappello, F., Tomasello, G., Leone, A., & Jurjus, R. A. (2016). Inflammatory bowel disease, colorectal cancer and type 2 diabetes mellitus: The links. BBA clinical, 516-24. https://doi.org/10.1016/j.bbacli.2015.11.002
Jurjus, Abdo, et al. "Inflammatory bowel disease, colorectal cancer and type 2 diabetes mellitus: The links." BBA clinical vol. 5 (2016): 16-24. doi: https://doi.org/10.1016/j.bbacli.2015.11.002
Jurjus A, Eid A, Al Kattar S, Zeenny MN, Gerges-Geagea A, Haydar H, Hilal A, Oueidat D, Matar M, Tawilah J, Hussein IH, Schembri-Wismayer P, Cappello F, Tomasello G, Leone A, Jurjus RA. Inflammatory bowel disease, colorectal cancer and type 2 diabetes mellitus: The links. BBA Clin. 2015 Nov 05;5:16-24. doi: 10.1016/j.bbacli.2015.11.002. eCollection 2016 Jun. PMID: 27051585; PMCID: PMC4802401.
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Functional Defects in Type 3 Innate Lymphoid Cells and Classical Monocytes in a Patient with Hyper-IgE Syndrome.

Immune network

Chang Y, Kang SY, Kim J, Kang HR, Kim HY.
PMID: 29093656
Immune Netw. 2017 Oct;17(5):352-364. doi: 10.4110/in.2017.17.5.352. Epub 2017 Oct 25.

Hyper-IgE syndrome (HIES) is a very rare primary immune deficiency characterized by elevated serum IgE levels, recurrent bacterial infections, chronic dermatitis, and connective tissue abnormalities. Autosomal dominant (AD) HIES involves a mutation in signal transducer and activator of transcription...

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Chang Y, Kang SY, Kim J, et al. Functional Defects in Type 3 Innate Lymphoid Cells and Classical Monocytes in a Patient with Hyper-IgE Syndrome. Immune Netw. 2017;17(5):352-364doi: 10.4110/in.2017.17.5.352.
Chang, Y., Kang, S. Y., Kim, J., Kang, H. R., & Kim, H. Y. (2017). Functional Defects in Type 3 Innate Lymphoid Cells and Classical Monocytes in a Patient with Hyper-IgE Syndrome. Immune network, 17(5), 352-364. https://doi.org/10.4110/in.2017.17.5.352
Chang, Yuna, et al. "Functional Defects in Type 3 Innate Lymphoid Cells and Classical Monocytes in a Patient with Hyper-IgE Syndrome." Immune network vol. 17,5 (2017): 352-364. doi: https://doi.org/10.4110/in.2017.17.5.352
Chang Y, Kang SY, Kim J, Kang HR, Kim HY. Functional Defects in Type 3 Innate Lymphoid Cells and Classical Monocytes in a Patient with Hyper-IgE Syndrome. Immune Netw. 2017 Oct;17(5):352-364. doi: 10.4110/in.2017.17.5.352. Epub 2017 Oct 25. PMID: 29093656; PMCID: PMC5662784.
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Regulation of Natural Killer Cell Function by STAT3.

Frontiers in immunology

Cacalano NA.
PMID: 27148255
Front Immunol. 2016 Apr 11;7:128. doi: 10.3389/fimmu.2016.00128. eCollection 2016.

Natural killer (NK) cells, key members of a distinct hematopoietic lineage, innate lymphoid cells, are not only critical effectors that mediate cytotoxicity toward tumor and virally infected cells but also regulate inflammation, antigen presentation, and the adaptive immune response....

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Cacalano NA. Regulation of Natural Killer Cell Function by STAT3. Front Immunol. 2016;7:128doi: 10.3389/fimmu.2016.00128.
Cacalano, N. A. (2016). Regulation of Natural Killer Cell Function by STAT3. Frontiers in immunology, 7128. https://doi.org/10.3389/fimmu.2016.00128
Cacalano, Nicholas A. "Regulation of Natural Killer Cell Function by STAT3." Frontiers in immunology vol. 7 (2016): 128. doi: https://doi.org/10.3389/fimmu.2016.00128
Cacalano NA. Regulation of Natural Killer Cell Function by STAT3. Front Immunol. 2016 Apr 11;7:128. doi: 10.3389/fimmu.2016.00128. eCollection 2016. PMID: 27148255; PMCID: PMC4827001.
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Tyrosine 23 Phosphorylation of Annexin A2 Promotes Proliferation, Invasion, and Stat3 Phosphorylation in the Nucleus of Human Breast Cancer SK-BR-3 Cells.

Cancer biology & medicine

Wang YQ, Zhang F, Tian R, Ji W, Zhou Y, Sun XM, Liu Y, Wang ZY, Niu RF.
PMID: 23691485
Cancer Biol Med. 2012 Dec;9(4):248-53. doi: 10.7497/j.issn.2095-3941.2012.04.005.

OBJECTIVE: To investigate the role of tyrosine 23 (Tyr23) phosphorylation of Annexin A2 (Anxa2) in regulating the proliferation and invasion of human breast cancer SK-BR-3 cells.METHODS: A panel of lentivirus plasmids expressing Anxa2-wide type (Ana2-WT), Anxa2-Y23A, and Anxa2-Y23D was...

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Wang YQ, Zhang F, Tian R, et al. Tyrosine 23 Phosphorylation of Annexin A2 Promotes Proliferation, Invasion, and Stat3 Phosphorylation in the Nucleus of Human Breast Cancer SK-BR-3 Cells. Cancer Biol Med. 2012;9(4):248-53doi: 10.7497/j.issn.2095-3941.2012.04.005.
Wang, Y. Q., Zhang, F., Tian, R., Ji, W., Zhou, Y., Sun, X. M., Liu, Y., Wang, Z. Y., & Niu, R. F. (2012). Tyrosine 23 Phosphorylation of Annexin A2 Promotes Proliferation, Invasion, and Stat3 Phosphorylation in the Nucleus of Human Breast Cancer SK-BR-3 Cells. Cancer biology & medicine, 9(4), 248-53. https://doi.org/10.7497/j.issn.2095-3941.2012.04.005
Wang, Yu-Qing, et al. "Tyrosine 23 Phosphorylation of Annexin A2 Promotes Proliferation, Invasion, and Stat3 Phosphorylation in the Nucleus of Human Breast Cancer SK-BR-3 Cells." Cancer biology & medicine vol. 9,4 (2012): 248-53. doi: https://doi.org/10.7497/j.issn.2095-3941.2012.04.005
Wang YQ, Zhang F, Tian R, Ji W, Zhou Y, Sun XM, Liu Y, Wang ZY, Niu RF. Tyrosine 23 Phosphorylation of Annexin A2 Promotes Proliferation, Invasion, and Stat3 Phosphorylation in the Nucleus of Human Breast Cancer SK-BR-3 Cells. Cancer Biol Med. 2012 Dec;9(4):248-53. doi: 10.7497/j.issn.2095-3941.2012.04.005. PMID: 23691485; PMCID: PMC3643677.
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How should we define STAT3 as an oncogene and as a potential target for therapy?.

JAK-STAT

Sellier H, Rébillard A, Guette C, Barré B, Coqueret O.
PMID: 24069560
JAKSTAT. 2013 Jul 01;2(3):e24716. doi: 10.4161/jkst.24716. Epub 2013 Apr 16.

Aberrant activation of the STAT3 transcription factor has been reported in a large group of tumors and a strong biological basis now defines this protein as an oncogenic driver. Consequently, STAT3 is considered to be a promising target in...

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Sellier H, Rébillard A, Guette C, et al. How should we define STAT3 as an oncogene and as a potential target for therapy?. JAKSTAT. 2013;2(3):e24716doi: 10.4161/jkst.24716.
Sellier, H., Rébillard, A., Guette, C., Barré, B., & Coqueret, O. (2013). How should we define STAT3 as an oncogene and as a potential target for therapy?. JAK-STAT, 2(3), e24716. https://doi.org/10.4161/jkst.24716
Sellier, Hélène, et al. "How should we define STAT3 as an oncogene and as a potential target for therapy?." JAK-STAT vol. 2,3 (2013): e24716. doi: https://doi.org/10.4161/jkst.24716
Sellier H, Rébillard A, Guette C, Barré B, Coqueret O. How should we define STAT3 as an oncogene and as a potential target for therapy?. JAKSTAT. 2013 Jul 01;2(3):e24716. doi: 10.4161/jkst.24716. Epub 2013 Apr 16. PMID: 24069560; PMCID: PMC3772112.
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STAT3 is Overactivated in Gastric Cancer Stem-Like Cells.

Cell journal

Hajimoradi M, Mohammad Hassan Z, Ebrahimi M, Soleimani M, Bakhshi M, Firouzi J, Samani FS.
PMID: 26862521
Cell J. 2016;17(4):617-28. doi: 10.22074/cellj.2016.3834. Epub 2016 Jan 17.

OBJECTIVE: Gastric cancer (GC) is widely associated with chronic inflammation. The pro inflammatory microenvironment provides conditions that disrupt stem/progenitor cell proliferation and differentiation. The signal transducer and activator of transcrip- tion-3 (STAT3) signaling pathway is involved in inflammation and...

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Hajimoradi M, Mohammad Hassan Z, Ebrahimi M, et al. STAT3 is Overactivated in Gastric Cancer Stem-Like Cells. Cell J. 2016;17(4):617-28doi: 10.22074/cellj.2016.3834.
Hajimoradi, M., Mohammad Hassan, Z., Ebrahimi, M., Soleimani, M., Bakhshi, M., Firouzi, J., & Samani, F. S. (2016). STAT3 is Overactivated in Gastric Cancer Stem-Like Cells. Cell journal, 17(4), 617-28. https://doi.org/10.22074/cellj.2016.3834
Hajimoradi, Monireh, et al. "STAT3 is Overactivated in Gastric Cancer Stem-Like Cells." Cell journal vol. 17,4 (2016): 617-28. doi: https://doi.org/10.22074/cellj.2016.3834
Hajimoradi M, Mohammad Hassan Z, Ebrahimi M, Soleimani M, Bakhshi M, Firouzi J, Samani FS. STAT3 is Overactivated in Gastric Cancer Stem-Like Cells. Cell J. 2016;17(4):617-28. doi: 10.22074/cellj.2016.3834. Epub 2016 Jan 17. PMID: 26862521; PMCID: PMC4746412.
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Anti-Migration and Anti-Invasion Effects of Curcumin via Suppression of Fascin Expression in Glioblastoma Cells.

Brain tumor research and treatment

Park KS, Yoon SY, Park SH, Hwang JH.
PMID: 31062527
Brain Tumor Res Treat. 2019 Apr;7(1):16-24. doi: 10.14791/btrt.2019.7.e28.

BACKGROUND: The natural compound curcumin was known to inhibit migration and invasion of glioblastoma (GBM) cells. Fascin, a kind of actin-binding proteins, is correlated with migration and invasion of GBM cells. The purpose of this study was to investigate...

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Park KS, Yoon SY, Park SH, et al. Anti-Migration and Anti-Invasion Effects of Curcumin via Suppression of Fascin Expression in Glioblastoma Cells. Brain Tumor Res Treat. 2019;7(1):16-24doi: 10.14791/btrt.2019.7.e28.
Park, K. S., Yoon, S. Y., Park, S. H., & Hwang, J. H. (2019). Anti-Migration and Anti-Invasion Effects of Curcumin via Suppression of Fascin Expression in Glioblastoma Cells. Brain tumor research and treatment, 7(1), 16-24. https://doi.org/10.14791/btrt.2019.7.e28
Park, Ki Su, et al. "Anti-Migration and Anti-Invasion Effects of Curcumin via Suppression of Fascin Expression in Glioblastoma Cells." Brain tumor research and treatment vol. 7,1 (2019): 16-24. doi: https://doi.org/10.14791/btrt.2019.7.e28
Park KS, Yoon SY, Park SH, Hwang JH. Anti-Migration and Anti-Invasion Effects of Curcumin via Suppression of Fascin Expression in Glioblastoma Cells. Brain Tumor Res Treat. 2019 Apr;7(1):16-24. doi: 10.14791/btrt.2019.7.e28. PMID: 31062527; PMCID: PMC6504753.
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TLR9 expression in chronic lymphocytic leukemia identifies a promigratory subpopulation and novel therapeutic target.

Blood

Kennedy E, Coulter E, Halliwell E, Profitos-Peleja N, Walsby E, Clark B, Phillips EH, Burley TA, Mitchell S, Devereux S, Fegan CD, Jones CI, Johnston R, Chevassut T, Schulz R, Seiffert M, Agathanggelou A, Oldreive C, Davies N, Stankovic T, Liloglou T, Pepper C, Pepper AGS.
PMID: 33512408
Blood. 2021 Jun 03;137(22):3064-3078. doi: 10.1182/blood.2020005964.

Chronic lymphocytic leukemia (CLL) remains incurable despite B-cell receptor-targeted inhibitors revolutionizing treatment. This suggests that other signaling molecules are involved in disease escape mechanisms and resistance. Toll-like receptor 9 (TLR9) is a promising candidate that is activated by unmethylated...

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Kennedy E, Coulter E, Halliwell E, et al. TLR9 expression in chronic lymphocytic leukemia identifies a promigratory subpopulation and novel therapeutic target. Blood. 2021;137(22):3064-3078doi: 10.1182/blood.2020005964.
Kennedy, E., Coulter, E., Halliwell, E., Profitos-Peleja, N., Walsby, E., Clark, B., Phillips, E. H., Burley, T. A., Mitchell, S., Devereux, S., Fegan, C. D., Jones, C. I., Johnston, R., Chevassut, T., Schulz, R., Seiffert, M., Agathanggelou, A., Oldreive, C., Davies, N., Stankovic, T., Liloglou, T., Pepper, C., & Pepper, A. G. S. (2021). TLR9 expression in chronic lymphocytic leukemia identifies a promigratory subpopulation and novel therapeutic target. Blood, 137(22), 3064-3078. https://doi.org/10.1182/blood.2020005964
Kennedy, Emma, et al. "TLR9 expression in chronic lymphocytic leukemia identifies a promigratory subpopulation and novel therapeutic target." Blood vol. 137,22 (2021): 3064-3078. doi: https://doi.org/10.1182/blood.2020005964
Kennedy E, Coulter E, Halliwell E, Profitos-Peleja N, Walsby E, Clark B, Phillips EH, Burley TA, Mitchell S, Devereux S, Fegan CD, Jones CI, Johnston R, Chevassut T, Schulz R, Seiffert M, Agathanggelou A, Oldreive C, Davies N, Stankovic T, Liloglou T, Pepper C, Pepper AGS. TLR9 expression in chronic lymphocytic leukemia identifies a promigratory subpopulation and novel therapeutic target. Blood. 2021 Jun 03;137(22):3064-3078. doi: 10.1182/blood.2020005964. PMID: 33512408; PMCID: PMC8176769.
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Interleukin-10 and Small Molecule SHIP1 Allosteric Regulators Trigger Anti-inflammatory Effects through SHIP1/STAT3 Complexes.

iScience

Chamberlain TC, Cheung ST, Yoon JSJ, Ming-Lum A, Gardill BR, Shakibakho S, Dzananovic E, Ban F, Samiea A, Jawanda K, Priatel J, Krystal G, Ong CJ, Cherkasov A, Andersen RJ, McKenna SA, Van Petegem F, Mui AL.
PMID: 32823063
iScience. 2020 Aug 21;23(8):101433. doi: 10.1016/j.isci.2020.101433. Epub 2020 Aug 02.

The anti-inflammatory actions of interleukin-10 (IL10) are thought to be mediated primarily by the STAT3 transcription factor, but pro-inflammatory cytokines such as interleukin-6 (IL6) also act through STAT3. We now report that IL10, but not IL6 signaling, induces formation...

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Chamberlain TC, Cheung ST, Yoon JSJ, et al. Interleukin-10 and Small Molecule SHIP1 Allosteric Regulators Trigger Anti-inflammatory Effects through SHIP1/STAT3 Complexes. iScience. 2020;23(8):101433doi: 10.1016/j.isci.2020.101433.
Chamberlain, T. C., Cheung, S. T., Yoon, J. S. J., Ming-Lum, A., Gardill, B. R., Shakibakho, S., Dzananovic, E., Ban, F., Samiea, A., Jawanda, K., Priatel, J., Krystal, G., Ong, C. J., Cherkasov, A., Andersen, R. J., McKenna, S. A., Van Petegem, F., & Mui, A. L. (2020). Interleukin-10 and Small Molecule SHIP1 Allosteric Regulators Trigger Anti-inflammatory Effects through SHIP1/STAT3 Complexes. iScience, 23(8), 101433. https://doi.org/10.1016/j.isci.2020.101433
Chamberlain, Thomas C, et al. "Interleukin-10 and Small Molecule SHIP1 Allosteric Regulators Trigger Anti-inflammatory Effects through SHIP1/STAT3 Complexes." iScience vol. 23,8 (2020): 101433. doi: https://doi.org/10.1016/j.isci.2020.101433
Chamberlain TC, Cheung ST, Yoon JSJ, Ming-Lum A, Gardill BR, Shakibakho S, Dzananovic E, Ban F, Samiea A, Jawanda K, Priatel J, Krystal G, Ong CJ, Cherkasov A, Andersen RJ, McKenna SA, Van Petegem F, Mui AL. Interleukin-10 and Small Molecule SHIP1 Allosteric Regulators Trigger Anti-inflammatory Effects through SHIP1/STAT3 Complexes. iScience. 2020 Aug 21;23(8):101433. doi: 10.1016/j.isci.2020.101433. Epub 2020 Aug 02. PMID: 32823063; PMCID: PMC7452241.
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Neuroprotective potential of imatinib in global ischemia-reperfusion-induced cerebral injury: possible role of Janus-activated kinase 2/signal transducer and activator of transcription 3 and connexin 43.

The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology

Wang J, Bai T, Wang N, Li H, Guo X.
PMID: 31908570
Korean J Physiol Pharmacol. 2020 Jan;24(1):11-18. doi: 10.4196/kjpp.2020.24.1.11. Epub 2020 Dec 20.

The present study was aimed to explore the neuroprotective role of imatinib in global ischemia-reperfusion-induced cerebral injury along with possible mechanisms. Global ischemia was induced in mice by bilateral carotid artery occlusion for 20 min, which was followed by...

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Wang J, Bai T, Wang N, et al. Neuroprotective potential of imatinib in global ischemia-reperfusion-induced cerebral injury: possible role of Janus-activated kinase 2/signal transducer and activator of transcription 3 and connexin 43. Korean J Physiol Pharmacol. 2020;24(1):11-18doi: 10.4196/kjpp.2020.24.1.11.
Wang, J., Bai, T., Wang, N., Li, H., & Guo, X. (2020). Neuroprotective potential of imatinib in global ischemia-reperfusion-induced cerebral injury: possible role of Janus-activated kinase 2/signal transducer and activator of transcription 3 and connexin 43. The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, 24(1), 11-18. https://doi.org/10.4196/kjpp.2020.24.1.11
Wang, Jieying, et al. "Neuroprotective potential of imatinib in global ischemia-reperfusion-induced cerebral injury: possible role of Janus-activated kinase 2/signal transducer and activator of transcription 3 and connexin 43." The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology vol. 24,1 (2020): 11-18. doi: https://doi.org/10.4196/kjpp.2020.24.1.11
Wang J, Bai T, Wang N, Li H, Guo X. Neuroprotective potential of imatinib in global ischemia-reperfusion-induced cerebral injury: possible role of Janus-activated kinase 2/signal transducer and activator of transcription 3 and connexin 43. Korean J Physiol Pharmacol. 2020 Jan;24(1):11-18. doi: 10.4196/kjpp.2020.24.1.11. Epub 2020 Dec 20. PMID: 31908570; PMCID: PMC6940502.
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Anticancer Activity of Tubulosine through Suppression of Interleukin-6-Induced Janus Kinase 2/Signal Transducer and Activation of Transcription 3 Signaling.

Journal of breast cancer

Kim BH, Yi EH, Li YC, Park IC, Park JY, Ye SK.
PMID: 31598337
J Breast Cancer. 2019 Aug 02;22(3):362-374. doi: 10.4048/jbc.2019.22.e34. eCollection 2019 Sep.

PURPOSE: The chemical structure of tubulosine has been known since the mid-1960s. However, little is known about its biological and pharmacological functions. The aim of this study was to investigate the novel functions of tubulosine in cancer treatment, specifically...

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Kim BH, Yi EH, Li YC, et al. Anticancer Activity of Tubulosine through Suppression of Interleukin-6-Induced Janus Kinase 2/Signal Transducer and Activation of Transcription 3 Signaling. J Breast Cancer. 2019;22(3):362-374doi: 10.4048/jbc.2019.22.e34.
Kim, B. H., Yi, E. H., Li, Y. C., Park, I. C., Park, J. Y., & Ye, S. K. (2019). Anticancer Activity of Tubulosine through Suppression of Interleukin-6-Induced Janus Kinase 2/Signal Transducer and Activation of Transcription 3 Signaling. Journal of breast cancer, 22(3), 362-374. https://doi.org/10.4048/jbc.2019.22.e34
Kim, Byung-Hak, et al. "Anticancer Activity of Tubulosine through Suppression of Interleukin-6-Induced Janus Kinase 2/Signal Transducer and Activation of Transcription 3 Signaling." Journal of breast cancer vol. 22,3 (2019): 362-374. doi: https://doi.org/10.4048/jbc.2019.22.e34
Kim BH, Yi EH, Li YC, Park IC, Park JY, Ye SK. Anticancer Activity of Tubulosine through Suppression of Interleukin-6-Induced Janus Kinase 2/Signal Transducer and Activation of Transcription 3 Signaling. J Breast Cancer. 2019 Aug 02;22(3):362-374. doi: 10.4048/jbc.2019.22.e34. eCollection 2019 Sep. PMID: 31598337; PMCID: PMC6769386.
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T Cell-Specific Knockout of STAT3 Ameliorates Dextran Sulfate Sodium-Induced Colitis by Reducing the Inflammatory Response.

Immune network

Kwon SH, Seo EB, Lee SH, Cho CH, Kim SJ, Kim SJ, Kim HR, Ye SK.
PMID: 30181918
Immune Netw. 2018 Aug 21;18(4):e30. doi: 10.4110/in.2018.18.e30. eCollection 2018 Aug.

Signal transducer and activator of transcription 3 (STAT3) has a crucial role in various autoimmune disorders including, inflammatory bowel disease (IBD). Our previous study demonstrated that STAT3 activation by IL-6 in colonic epithelial cells exacerbates experimental ulcerative colitis. Activated...

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Kwon SH, Seo EB, Lee SH, et al. T Cell-Specific Knockout of STAT3 Ameliorates Dextran Sulfate Sodium-Induced Colitis by Reducing the Inflammatory Response. Immune Netw. 2018;18(4):e30doi: 10.4110/in.2018.18.e30.
Kwon, S. H., Seo, E. B., Lee, S. H., Cho, C. H., Kim, S. J., Kim, S. J., Kim, H. R., & Ye, S. K. (2018). T Cell-Specific Knockout of STAT3 Ameliorates Dextran Sulfate Sodium-Induced Colitis by Reducing the Inflammatory Response. Immune network, 18(4), e30. https://doi.org/10.4110/in.2018.18.e30
Kwon, Sun-Ho, et al. "T Cell-Specific Knockout of STAT3 Ameliorates Dextran Sulfate Sodium-Induced Colitis by Reducing the Inflammatory Response." Immune network vol. 18,4 (2018): e30. doi: https://doi.org/10.4110/in.2018.18.e30
Kwon SH, Seo EB, Lee SH, Cho CH, Kim SJ, Kim SJ, Kim HR, Ye SK. T Cell-Specific Knockout of STAT3 Ameliorates Dextran Sulfate Sodium-Induced Colitis by Reducing the Inflammatory Response. Immune Netw. 2018 Aug 21;18(4):e30. doi: 10.4110/in.2018.18.e30. eCollection 2018 Aug. PMID: 30181918; PMCID: PMC6117516.
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