[1] Colao A and Savastano S: Medical treatment of prolactinomas. Nat Rev Endocrinol. 2001;7:267–278.
[2] Daly AF, Rixhon M, Adam C, Dempegioti A, Tichomirowa MA and Beckers A: High prevalence of pituitary adenomas: a cross-sectional study in the province of Liege, Belgium. J Clin Endocrinol Metab. 2006;91:4769–4775.
[3] Gillam MP, Molitch ME, Lombardi G and Colao A: Advances in the treatment of prolactinomas. Endocr Rev. 2006;27:485–534.
[4] Oh MC and Aghi MK: Dopamine agonist-resistant prolactinomas. J Neurosurg. 2011;114:1369-1379.
[5] Cuenda A and Rousseau S: p38 MAP-kinases pathway regulation, function and role in human diseases. Biochim Biophys Acta. 2007;1773:1358–1375.
[6] Remy G, Risco AM, Iñesta-Vaquera FA, González-Terán B, Sabio G, Davis RJ and Cuenda A: Differential activation of p38MAPK isoforms by MKK6 and MKK3. Cell Signal. 2010;22:660–667.
[7] Kang YJ, Chen J, Otsuka M, Mols J, Ren S, Wang Y and Han J: Macrophage deletion of p38alpha partially impairs lipopolysaccharide-induced cellular activation. J Immunol. 2008;180:5075–5082.
[8] Kim C, Sano Y, Todorova K, Carlson BA, Arpa L, Celada A, Lawrence T, Otsu K, Brissette JL, Arthur JS, et al: The kinase p38 alpha serves cell type-specific inflammatory functions in skin injury and coordinates proand anti-inflammatory gene expression. Nat Immunol. 2008; 9:1019–1027.
[9] Otsuka M, Kang YJ, Ren J, Jiang H, Wang Y, Omata M and Han J: Distinct effects of p38alpha deletion in myeloid lineage and gut epithelia in mouse models of inflammatory bowel disease. Gastroenterology. 2010;138:1255–1265.
[10] Hommes D, van den Blink B, Plasse T, Bartelsman J, Xu C, Macpherson B, Tytgat G, Peppelenbosch M and Van Deventer S: Inhibition of stress-activated MAP kinases induces clinical improvement in moderate to severe Crohn's disease. Gastroenterology. 2002;122:7–14.
[11] Hollenbach E, Neumann M, Vieth M, Roessner A, Malfertheiner P and Naumann M: Inhibition of p38 MAP kinase- and RICK/NF-kappaB-signaling suppresses inflammatory bowel disease. FASEB J. 2004;18:1550–1552.
[12] Schreiber S, Feagan B, D'Haens G, Colombel JF, Geboes K, Yurcov M, Isakov V, Golovenko O, Bernstein CN, Ludwig D, et al: Oral p38 mitogen-activated protein kinase inhibition with BIRB 796 for active Crohn's disease: a randomized, double-blind, placebo-controlled trial. Clin Gastroenterol Hepatol. 2006;4:325–334.
[13] ten Hove T, van den Blink B, Pronk I, Drillenburg P, Peppelenbosch MP and van Deventer SJ: Dichotomal role of inhibition of p38 MAPK with SB 203580 in experimental colitis. Gut. 2002;50:507–512.
[14] Heaney AP, Horwitz GA, Wang Z, Singson R and Melmed S: Early involvement of estrogen-induced pituitary tumor transforming gene and fibroblast growth factor expression in prolactinoma pathogenesis. Nat Med. 1999;5:1317-1721.
[15] Cristina C, García-Tornadú I, Díaz-Torga G, Rubinstein M, Low MJ, Becú- Villalobos D: Dopaminergic D2 receptor knockout mouse: an animal model of prolactinoma. Front Horm Res. 2006;35:50-63.
[16] Seruggia D, Montoliu L:The new CRISPR-Cas system: RNA-guided genome engineering to efficiently produce any desired genetic alteration in animals. Transgenic Res. 2014;23:707-716.
[17] Kelly MA, Rubinstein M, Asa SL, Zhang G, Saez C, Bunzow JR, Allen RG, Hnasko R, Ben-Jonathan N, Grandy DK, et al: Pituitary lactotroph hyperplasia and chronic hyperprolactinemia in dopamine D2 receptor-deficient mice. Neuron. 1997;19: 103-113.
[18] Otsuka M, Kang YJ, Ren J, Jiang H, Wang Y, Omata M and Han J: Distinct effects of p38alpha deletion in myeloid lineage and gut epithelia in mouse models of inflammatory bowel disease. Gastroenterology. 2010;138:1255-1265.
[19] Wong A, Eloy JA, Couldwell WT and Liu JK. Update on prolactinomas. Part 2: Treatment and management strategies. J Clin Neurosci. 2015;22:1568-1574.
[20] Vroonen L, Jaffrain-Rea ML, Petrossians P, Tamagno G, Chanson P, Vilar L, Borson-Chazot F, Naves LA, Brue T, Gatta B, et al: Prolactinomas resistant to standard doses of cabergoline: a multicenter study of 92 patients. Eur J Endocrinol. 2012;167:651-662.
[21] Burotto M, Chiou VL, Lee JM and Kohn EC: The MAPK pathway across different malignancies: A new perspective. Cancer. 2014;120:3446–3456.
[22] Iyoda K, Sasaki Y, Horimoto M, Toyama T, Yakushijin T, Sakakibara M, Takehara T, Fujimoto J, Hori M, Wands JR, et al: Involvement of the p38 mitogen-activated protein kinase cascade in hepatocellular carcinoma. Cancer.2003; 97:3017-3026.
[23] Tsai PW, Shiah SG, Lin MT, Wu CW and Kuo ML: Up-regulation of vascular endothelial growth factor C in breast cancer cells by heregulin-beta 1. A critical role of p38/nuclear factor-kappa B signaling pathway. J Biol Chem. 2003;278:5750-5959.
[24] Suarez-Cuervo C, Merrell MA, Watson L, Harris KW, Rosenthal EL, Väänänen HK and Selander KS: Breast cancer cells with inhibition of p38alpha have decreased MMP-9 activity and exhibit decreased bone metastasis in mice. Clin Exp Metastasis. 2004;21:525-533.
[25] Greenberg AK, Basu S, Hu J, Yie TA, Tchou-Wong KM, Rom WN and Lee TC: Selective p38 activation in human non-small cell lung cancer. Am J Respir Cell Mol Biol. 2002;26:558-564.
[26] Kumar B, Sinclair J, Khandrika L, Koul S, Wilson S and Koul HK: Differential effects of MAPKs signaling on the growth of invasive bladder cancer cells. Int J Oncol. 2009;34:1557-1564.
[27] Kumar B, Koul S, Petersen J, Khandrika L, Hwa JS, Meacham RB, Wilson S and Koul HK: p38 mitogenactivated protein kinase-driven MAPKAPK2 regulates invasion of bladder cancer by modulation of MMP-2 and MMP-9 activity. Cancer Res. 2010;70:832-841.
[28] Park JI, Lee MG, Cho K, Park BJ, Chae KS, Byun DS, Ryu BK, Park YK and Chi SG: Transforming growth factor-beta1 activates interleukin-6 expression in prostate cancer cells through the synergistic collaboration of the Smad2, p38-NF-kappaB, JNK, and Ras signaling pathways. Oncogene. 2003;22:4314-4332.
[29] Khandrika L, Lieberman R, Koul S, Kumar B, Maroni P, Chandhoke R, Meacham RB and Koul HK: Hypoxia-associated p38 mitogen-activated protein kinase-mediated androgen receptor activation and increased HIF-1alpha levels contribute to emergence of an aggressive phenotype in prostate cancer. Oncogene. 2009;28:1248-1260.
[30] Maroni PD, Koul S, Meacham RB and Koul HK: Mitogen activated protein kinase signal transduction pathways in the prostate. Cell Commun Signal. 2004;2: 5.
[31] Liu RY, Fan C, Liu G, Olashaw NE and Zuckerman KS: Activation of p38 mitogen-activated protein kinase is required for tumor necrosis factor-alpha-supported proliferation of leukemia and lymphoma cell lines. J Biol Chem. 2000;275:21086- 21093.
[32] Elenitoba-Johnson KS, Jenson SD, Abbott RT, Palais RA, Bohling SD, Lin Z, Tripp S, Shami PJ, Wang LY, Coupland RW, et al: Involvement of multiple signaling pathways in follicular lymphoma transformation: p38-mitogen-activated protein kinase as a target for therapy. Proc Natl Acad Sci U S A. 2003;100:7259-7264.
[33] Lin Z, Crockett DK, Jenson SD, Lim MS and Elenitoba-Johnson KS: Quantitative proteomic and transcriptional analysis of the response to the p38 mitogen-activated protein kinase inhibitor SB203580 in transformed follicular lymphoma cells. Mol Cell Proteomics. 2004;3:820-833.