temozolomide and Invasiveness, Neoplasm studies

Research Excerpts

Excerpt	Relevance	Reference
"Temozolomide (TMZ) has been the standard-of-care chemotherapy for glioblastoma (GBM) patients for more than a decade."	9.34	Image-based metric of invasiveness predicts response to adjuvant temozolomide for primary glioblastoma. ( Bendok, BR; Doyle, T; Hawkins-Daarud, A; Hu, LS; Jackson, PR; Johnston, SK; Massey, SC; Mrugala, MM; Porter, AB; Sarkaria, JN; Singleton, KW; Swanson, KR; Vora, S; White, H; Whitmire, P, 2020)
" Eligible patients (newly diagnosed, histologically proven supratentorial glioblastoma, methylated MGMT promoter, and age ≥18 years) were stratified for prognostic Radiation Therapy Oncology Group recursive partitioning analysis class and geographic region and centrally randomised in a 1:1 ratio with interactive voice response system to receive temozolomide chemoradiotherapy with cilengitide 2000 mg intravenously twice weekly (cilengitide group) or temozolomide chemoradiotherapy alone (control group)."	9.19	Cilengitide combined with standard treatment for patients with newly diagnosed glioblastoma with methylated MGMT promoter (CENTRIC EORTC 26071-22072 study): a multicentre, randomised, open-label, phase 3 trial. ( Adamska, K; Aldape, KD; Brandes, AA; Erridge, SC; Gorlia, T; Grujicic, D; Gupta, T; Hau, P; Hegi, ME; Herrlinger, U; Hicking, C; Hong, YK; Kim, CY; Kortmann, RD; Lhermitte, B; Markivskyy, A; McBain, C; Nabors, LB; Nam, DH; Perry, J; Picard, M; Pietsch, T; Rao, N; Reardon, DA; Schnell, O; Shen, CC; Steinbach, JP; Stupp, R; Taphoorn, MJ; Tarnawski, R; Thurzo, L; Tonn, JC; van den Bent, MJ; Weller, M; Weyerbrock, A; Wick, W; Wiegel, T, 2014)
" CDC20 expression is increased in a variety of tumors and associated with temozolomide (TMZ) resistance in glioma cells."	8.02	Apcin inhibits the growth and invasion of glioblastoma cells and improves glioma sensitivity to temozolomide. ( Ding, Y; He, L; Pan, Y; Song, X; Yu, S; Zhang, C; Zheng, C, 2021)
"Temozolomide is a first line anti-tumor drug used for the treatment of patients with Glioblastoma multiforme (GBM)."	7.96	MicroRNA-128-3p Enhances the Chemosensitivity of Temozolomide in Glioblastoma by Targeting c-Met and EMT. ( Guan, F; Guo, R; Li, H; Li, M; Liu, X; Ma, S; Wu, J; Yang, B; Zhao, C, 2020)
"Glioma is a frequently diagnosed brain tumors and Temozolomide (TMZ) is a common chemotherapeutic drug for glioma."	7.91	MicroRNA-34a-5p suppresses tumorigenesis and progression of glioma and potentiates Temozolomide-induced cytotoxicity for glioma cells by targeting HMGA2. ( Fu, T; Gao, M; Ma, S; Zhao, S, 2019)
" In this study we aimed to evaluate the relationship of FBW7 with glioma pathology and prognosis, and examine its effect in glioma malignancies and temozolomide (TMZ)-based therapy."	7.88	FBW7 is associated with prognosis, inhibits malignancies and enhances temozolomide sensitivity in glioblastoma cells. ( Cui, Y; Feng, H; He, H; Ji, A; Li, J; Li, S; Lin, J; Lu, Y; Qiu, G; Song, C; Zou, Y, 2018)
"We showed that myricetin alone inhibited glioblastoma U-87 MG cell proliferation, migration and invasion, whereas combination of myricetin and temozolomide did not exhibit any synergistic effect."	7.88	A Multi-targeted Natural Flavonoid Myricetin Suppresses Lamellipodia and Focal Adhesions Formation and Impedes Glioblastoma Cell Invasiveness and Abnormal Motility. ( Chen, ZP; Li, WP; To, ST; Wang, G; Wang, J; Wu, CP; Zhao, HF; Zhou, XM, 2018)
"It has been reported that metformin acts synergistically with temozolomide (TMZ) to inhibit proliferation of glioma cells including glioblastoma multiforme (GBM)."	7.83	Metformin treatment reduces temozolomide resistance of glioblastoma cells. ( Kim, DH; Li, S; Liu, Y; Lu, G; Xue, H; Yang, SH; Zhu, JJ, 2016)
" The purpose of this study was determining the effects of HL156A, a newly designed biguanide with improved pharmacokinetics, on glioblastoma TSs (GMB TSs) and assess the feasibility of this drug as a new line of therapy against glioblastoma, alone or combined with a conventional therapeutic agent, temozolomide(TMZ)."	7.83	Inhibiting stemness and invasive properties of glioblastoma tumorsphere by combined treatment with temozolomide and a newly designed biguanide (HL156A). ( Chang, JH; Cheong, JH; Choi, J; Huh, YM; Jeon, JY; Kang, SG; Kim, EH; Kim, P; Kim, SH; Koh, I; Lee, JH; Lee, SJ; Park, J; Pollak, M; Shim, JK; Yook, JI; Yun, M, 2016)
"HIF-1α downregulation sensitizes U251 glioma cells to the temozolomide treatment via inhibiting MGMT expression and Notch1 pathway activation."	7.83	Downregulation of HIF-1a sensitizes U251 glioma cells to the temozolomide (TMZ) treatment. ( Huang, GH; Li, N; Lv, SQ; Ma, ZX; Sidlauskas, K; Tang, JH; Xiang, Y; Xu, QF; Zhang, EE, 2016)
"Despite multimodal treatment, glioblastoma (GBM) therapy with temozolomide (TMZ) remains inefficient due to chemoresistance."	7.81	The metalloprotease-disintegrin ADAM8 contributes to temozolomide chemoresistance and enhanced invasiveness of human glioblastoma cells. ( Bartsch, JW; Biniossek, ML; Carl, B; Conrad, C; Culmsee, C; Dolga, AM; Dong, F; Eibach, M; Koller, G; Nimsky, C; Schieber, S; Schilling, O; Schlomann, U; Strik, H, 2015)
"The frequent recurrence of glioblastoma multiforme (GBM) after standard treatment with temozolomide (TMZ) is a crucial issue to be solved in the clinical field."	7.80	YKL-40 downregulation is a key factor to overcome temozolomide resistance in a glioblastoma cell line. ( Akiyama, Y; Ashizawa, T; Hayashi, N; Iizuka, A; Komiyama, M; Kume, A; Mitsuya, K; Miyata, H; Nakasu, Y; Omiya, M; Oshita, C; Sugino, T; Yamaguchi, K, 2014)
" Recently, in a phase II trial in Brazil for the treatment of temozolomide (TMZ)-resistant malignant gliomas, POH was well tolerated when administered intranasally."	7.78	Perillyl alcohol for the treatment of temozolomide-resistant gliomas. ( Chen, TC; Cho, HY; Goldkorn, A; Hofman, FM; Jhaveri, N; Lee, DJ; Leong, MN; Louie, SG; Petasis, NA; Schönthal, AH; Torres, S; Tseng, J; Wang, W; Xu, T, 2012)
"Eight patients, five with pituitary carcinomas (three prolactin (PRL) and two ACTH) and three with aggressive pituitary tumors (one PRL and two ACTH), all treated with temozolomide administered orally for four to 24 cycles, were included in our French multicenter study."	7.76	Temozolomide treatment in aggressive pituitary tumors and pituitary carcinomas: a French multicenter experience. ( Assaker, R; Bernier, M; Borson-Chazot, F; Brue, T; Caron, P; Chabre, O; Chanson, P; Cornélius, A; Cortet-Rudelli, C; de Fraipont, F; Dufour, H; Figarella-Branger, D; François, P; Gaillard, S; Jouanneau, E; Muller, M; Passagia, JG; Raverot, G; Salenave, S; Sturm, N; Trouillas, J, 2010)
" In this study, the authors investigate the nature of the SP phenotype in 2 glioma cell lines, U87MG and T98G, and their response to temozolomide."	7.74	Characterization of a side population of astrocytoma cells in response to temozolomide. ( Ang, BT; Chong, KH; Chua, C; See, SJ; Tang, C; Wong, MC; Zaiden, N, 2008)
"Dasatinib inhibited growth of three of the five melanoma cell lines."	7.74	Preclinical evaluation of dasatinib, a potent Src kinase inhibitor, in melanoma cell lines. ( Clynes, M; Crown, J; Eustace, AJ; O'Donovan, N, 2008)
"Aggressive pituitary adenomas (APAs) are, by definition, resistant to optimal multimodality therapy."	5.62	Early Initiation of Temozolomide Therapy May Improve Response in Aggressive Pituitary Adenomas. ( Ahuja, CK; Bhansali, A; Das, L; Dhandapani, S; Dutta, P; Gupta, K; Gupta, N; Radotra, BD; Rai, A; Sood, R; Sreedharanunni, S; Tripathi, M; Vaiphei, K; Walia, R, 2021)
"Calpeptin is a chemical inhibitor of Calpain, which can inhibit this effect."	5.56	Calpain suppresses cell growth and invasion of glioblastoma multiforme by producing the cleavage of filamin A. ( Cai, L; Li, Q; Li, W; Lu, X; Su, Z; Tu, M; Wang, C; Zhu, Z, 2020)
"Glioma is one of the most aggressive forms of brain tumor and is hallmarked by high rate of mortality, metastasis and drug resistance."	5.56	Downregulation of hsa_circ_0000936 sensitizes resistant glioma cells to temozolomide by sponging miR-1294. ( Feng, H; Hua, L; Huang, L; Zhang, X, 2020)
"Glioma is the most common and lethal central nervous system tumors."	5.46	Down-Regulation of AQP4 Expression via p38 MAPK Signaling in Temozolomide-Induced Glioma Cells Growth Inhibition and Invasion Impairment. ( Chen, Y; Gao, F; Hou, J; Jiang, R; Kang, L; Li, Y; Liu, H; Liu, X; Yang, M; Yi, Y, 2017)
"Temozolomide (TMZ) has been showed to be an effective chemotherapeutic agent for glioblastoma treatment; however, the response rate is not satisfactory."	5.42	Synergistic Anti-Cancer Effects of Icariin and Temozolomide in Glioblastoma. ( Guo, H; Guo, M; Wang, Y; Yang, L, 2015)
"Gliomas account for more than 50% of all primary brain tumors."	5.36	Long-term temozolomide treatment induces marked amino metabolism modifications and an increase in TMZ sensitivity in Hs683 oligodendroglioma cells. ( Bontempi, G; Bruyère, C; Decaestecker, C; Dubois, J; Haibe-Kains, B; Kiss, R; Lamoral-Theys, D; Le Calvé, B; Le Mercier, M; Lefranc, F; Rynkowski, MA, 2010)
"Cilengitide is a cyclic peptide antagonist of integrins alphavbeta3 and alphavbeta5 that is currently being evaluated as a novel therapeutic agent for recurrent and newly diagnosed glioblastoma."	5.35	Cilengitide modulates attachment and viability of human glioma cells, but not sensitivity to irradiation or temozolomide in vitro. ( Adams, B; Maurer, GD; Stupp, R; Tabatabai, G; Tritschler, I; Weller, M; Wick, W, 2009)
"Temozolomide (TMZ) has been the standard-of-care chemotherapy for glioblastoma (GBM) patients for more than a decade."	5.34	Image-based metric of invasiveness predicts response to adjuvant temozolomide for primary glioblastoma. ( Bendok, BR; Doyle, T; Hawkins-Daarud, A; Hu, LS; Jackson, PR; Johnston, SK; Massey, SC; Mrugala, MM; Porter, AB; Sarkaria, JN; Singleton, KW; Swanson, KR; Vora, S; White, H; Whitmire, P, 2020)
"Temozolomide treatment of high-grade tv-a gliomas provided a 14-day growth delay compared with vehicle controls."	5.34	Magnetic resonance imaging determination of tumor grade and early response to temozolomide in a genetically engineered mouse model of glioma. ( Hambardzumyan, D; Holland, EC; Kreger, AR; Leopold, WR; McConville, P; Moody, JB; Rehemtulla, A; Ross, BD; Woolliscroft, MJ, 2007)
"Temozolomide is an alkylating cytostatic drug that finds increasing application in the treatment of melanoma, anaplastic astrocytoma and glioblastoma multiforme."	5.32	Temozolomide induces apoptosis and senescence in glioma cells cultured as multicellular spheroids. ( Arnold, H; Damasceno, R; Günther, W; Pawlak, E; Terzis, AJ, 2003)
"We evaluated patterns of tumor growth in patients with newly diagnosed MGMT-non-methylated glioblastoma who were assigned to undergo radiotherapy in conjunction with bevacizumab/irinotecan (BEV/IRI) or standard temozolomide (TMZ) within the randomized phase II GLARIUS trial."	5.27	Tumor growth patterns of MGMT-non-methylated glioblastoma in the randomized GLARIUS trial. ( Bähr, O; Belka, C; Braun, C; Gerlach, R; Glas, M; Goldbrunner, R; Hänel, M; Hattingen, E; Hau, P; Herrlinger, U; Junold, N; Kebir, S; Kortmann, RD; Krex, D; Mack, F; Niessen, M; Proescholdt, M; Rohde, V; Sabel, M; Schäfer, N; Schaub, C; Schlegel, U; Schmidt-Graf, F; Steinbach, JP; Stuplich, M; Tzaridis, T; Vatter, H; Weyerbrock, A, 2018)
" Eligible patients (newly diagnosed, histologically proven supratentorial glioblastoma, methylated MGMT promoter, and age ≥18 years) were stratified for prognostic Radiation Therapy Oncology Group recursive partitioning analysis class and geographic region and centrally randomised in a 1:1 ratio with interactive voice response system to receive temozolomide chemoradiotherapy with cilengitide 2000 mg intravenously twice weekly (cilengitide group) or temozolomide chemoradiotherapy alone (control group)."	5.19	Cilengitide combined with standard treatment for patients with newly diagnosed glioblastoma with methylated MGMT promoter (CENTRIC EORTC 26071-22072 study): a multicentre, randomised, open-label, phase 3 trial. ( Adamska, K; Aldape, KD; Brandes, AA; Erridge, SC; Gorlia, T; Grujicic, D; Gupta, T; Hau, P; Hegi, ME; Herrlinger, U; Hicking, C; Hong, YK; Kim, CY; Kortmann, RD; Lhermitte, B; Markivskyy, A; McBain, C; Nabors, LB; Nam, DH; Perry, J; Picard, M; Pietsch, T; Rao, N; Reardon, DA; Schnell, O; Shen, CC; Steinbach, JP; Stupp, R; Taphoorn, MJ; Tarnawski, R; Thurzo, L; Tonn, JC; van den Bent, MJ; Weller, M; Weyerbrock, A; Wick, W; Wiegel, T, 2014)
" CDC20 expression is increased in a variety of tumors and associated with temozolomide (TMZ) resistance in glioma cells."	4.02	Apcin inhibits the growth and invasion of glioblastoma cells and improves glioma sensitivity to temozolomide. ( Ding, Y; He, L; Pan, Y; Song, X; Yu, S; Zhang, C; Zheng, C, 2021)
"Temozolomide is a first line anti-tumor drug used for the treatment of patients with Glioblastoma multiforme (GBM)."	3.96	MicroRNA-128-3p Enhances the Chemosensitivity of Temozolomide in Glioblastoma by Targeting c-Met and EMT. ( Guan, F; Guo, R; Li, H; Li, M; Liu, X; Ma, S; Wu, J; Yang, B; Zhao, C, 2020)
"Glioma is the most common primary malignant tumour in the brain; temozolomide (TMZ) is the most prevalent chemotherapeutic drug currently used to combat this cancer."	3.96	LINC00470 promotes tumour proliferation and invasion, and attenuates chemosensitivity through the LINC00470/miR-134/Myc/ABCC1 axis in glioma. ( Li, Y; Liu, Q; Long, W; Pan, Y; Qin, C; Su, J; Wang, J; Wang, X; Wu, C; Xiao, K; Xiao, Q, 2020)
"Glioma is a frequently diagnosed brain tumors and Temozolomide (TMZ) is a common chemotherapeutic drug for glioma."	3.91	MicroRNA-34a-5p suppresses tumorigenesis and progression of glioma and potentiates Temozolomide-induced cytotoxicity for glioma cells by targeting HMGA2. ( Fu, T; Gao, M; Ma, S; Zhao, S, 2019)
"To collect outcome data in a large cohort of patients with aggressive pituitary tumours (APT)/carcinomas (PC) and specifically report effects of temozolomide (TMZ) treatment."	3.88	Treatment of aggressive pituitary tumours and carcinomas: results of a European Society of Endocrinology (ESE) survey 2016. ( Burman, P; Dekkers, OM; McCormack, A; Petersenn, S; Popovic, V; Raverot, G; Trouillas, J, 2018)
" In this study we aimed to evaluate the relationship of FBW7 with glioma pathology and prognosis, and examine its effect in glioma malignancies and temozolomide (TMZ)-based therapy."	3.88	FBW7 is associated with prognosis, inhibits malignancies and enhances temozolomide sensitivity in glioblastoma cells. ( Cui, Y; Feng, H; He, H; Ji, A; Li, J; Li, S; Lin, J; Lu, Y; Qiu, G; Song, C; Zou, Y, 2018)
"We showed that myricetin alone inhibited glioblastoma U-87 MG cell proliferation, migration and invasion, whereas combination of myricetin and temozolomide did not exhibit any synergistic effect."	3.88	A Multi-targeted Natural Flavonoid Myricetin Suppresses Lamellipodia and Focal Adhesions Formation and Impedes Glioblastoma Cell Invasiveness and Abnormal Motility. ( Chen, ZP; Li, WP; To, ST; Wang, G; Wang, J; Wu, CP; Zhao, HF; Zhou, XM, 2018)
"Evaluate survival of patients diagnosed with glioblastoma multiforme (GBM) managed with adjuvant intensity modulated radiation therapy and temozolomide since the introduction of the European Organisation for Research and Treatment of Cancer and National Cancer Institute of Canada Clinical Trials Group (EORTC-NCIC) protocol."	3.88	Survival improvements with adjuvant therapy in patients with glioblastoma. ( Back, MF; Brazier, D; Cook, R; Guo, L; Jayamanne, D; Kastelan, M; Schembri, G; Teo, C; Wheeler, H, 2018)
"Mean CBF1 expression is significantly increased in isocitrate dehydrogenase 1 (IDH1) R132H mutant glioblastoma and serves as prognostic marker for prolonged overall survival in brain tumours, particularly after therapy with temozolomide."	3.85	CBF1 is clinically prognostic and serves as a target to block cellular invasion and chemoresistance of EMT-like glioblastoma cells. ( Herrera-Rios, D; Hoerbelt, T; Jiang, T; Kahlert, UD; Koch, K; Li, G; Maciaczyk, D; Maciaczyk, J; Marquardt, V; Ouwens, DM; Pauck, D; Picard, D; Remke, M; Steiger, HJ; Zhang, W; Zhao, L, 2017)
" The purpose of this study was determining the effects of HL156A, a newly designed biguanide with improved pharmacokinetics, on glioblastoma TSs (GMB TSs) and assess the feasibility of this drug as a new line of therapy against glioblastoma, alone or combined with a conventional therapeutic agent, temozolomide(TMZ)."	3.83	Inhibiting stemness and invasive properties of glioblastoma tumorsphere by combined treatment with temozolomide and a newly designed biguanide (HL156A). ( Chang, JH; Cheong, JH; Choi, J; Huh, YM; Jeon, JY; Kang, SG; Kim, EH; Kim, P; Kim, SH; Koh, I; Lee, JH; Lee, SJ; Park, J; Pollak, M; Shim, JK; Yook, JI; Yun, M, 2016)
"It has been reported that metformin acts synergistically with temozolomide (TMZ) to inhibit proliferation of glioma cells including glioblastoma multiforme (GBM)."	3.83	Metformin treatment reduces temozolomide resistance of glioblastoma cells. ( Kim, DH; Li, S; Liu, Y; Lu, G; Xue, H; Yang, SH; Zhu, JJ, 2016)
" Then, knockdown of hnRNP A2/B1 expression induced by RNA interference (RNAi) method was used to analyze the role of hnRNP A2/B1 in glioblastoma cell viability, adhesion, migration, invasion, and chemoresistance for temozolomide (TMZ)."	3.83	Effects of hnRNP A2/B1 Knockdown on Inhibition of Glioblastoma Cell Invasion, Growth and Survival. ( Chen, S; Cheng, Y; Deng, J; Liang, P; Wang, F; Xie, Z; Xu, Z; Zhai, X; Zhang, Q; Zhao, H, 2016)
"HIF-1α downregulation sensitizes U251 glioma cells to the temozolomide treatment via inhibiting MGMT expression and Notch1 pathway activation."	3.83	Downregulation of HIF-1a sensitizes U251 glioma cells to the temozolomide (TMZ) treatment. ( Huang, GH; Li, N; Lv, SQ; Ma, ZX; Sidlauskas, K; Tang, JH; Xiang, Y; Xu, QF; Zhang, EE, 2016)
"Despite multimodal treatment, glioblastoma (GBM) therapy with temozolomide (TMZ) remains inefficient due to chemoresistance."	3.81	The metalloprotease-disintegrin ADAM8 contributes to temozolomide chemoresistance and enhanced invasiveness of human glioblastoma cells. ( Bartsch, JW; Biniossek, ML; Carl, B; Conrad, C; Culmsee, C; Dolga, AM; Dong, F; Eibach, M; Koller, G; Nimsky, C; Schieber, S; Schilling, O; Schlomann, U; Strik, H, 2015)
"Temozolomide (TMZ) is a promising chemotherapeutic agent for treating glioblastomas."	3.81	PI3K inhibitor combined with miR-125b inhibitor sensitize TMZ-induced anti-glioma stem cancer effects through inactivation of Wnt/β-catenin signaling pathway. ( Fei, X; Shi, L; Wang, Z; You, Y, 2015)
"The frequent recurrence of glioblastoma multiforme (GBM) after standard treatment with temozolomide (TMZ) is a crucial issue to be solved in the clinical field."	3.80	YKL-40 downregulation is a key factor to overcome temozolomide resistance in a glioblastoma cell line. ( Akiyama, Y; Ashizawa, T; Hayashi, N; Iizuka, A; Komiyama, M; Kume, A; Mitsuya, K; Miyata, H; Nakasu, Y; Omiya, M; Oshita, C; Sugino, T; Yamaguchi, K, 2014)
" Recently, in a phase II trial in Brazil for the treatment of temozolomide (TMZ)-resistant malignant gliomas, POH was well tolerated when administered intranasally."	3.78	Perillyl alcohol for the treatment of temozolomide-resistant gliomas. ( Chen, TC; Cho, HY; Goldkorn, A; Hofman, FM; Jhaveri, N; Lee, DJ; Leong, MN; Louie, SG; Petasis, NA; Schönthal, AH; Torres, S; Tseng, J; Wang, W; Xu, T, 2012)
"Autophagy was measured in tumor biopsies obtained from metastatic melanoma patients enrolled on a phase II trial of temozolomide and sorafenib and correlated to clinical outcome."	3.77	Measurements of tumor cell autophagy predict invasiveness, resistance to chemotherapy, and survival in melanoma. ( Amaravadi, RK; Li, LZ; Lum, JJ; Ma, XH; McAfee, QW; Nathanson, KL; Piao, S; Wang, D, 2011)
"Eight patients, five with pituitary carcinomas (three prolactin (PRL) and two ACTH) and three with aggressive pituitary tumors (one PRL and two ACTH), all treated with temozolomide administered orally for four to 24 cycles, were included in our French multicenter study."	3.76	Temozolomide treatment in aggressive pituitary tumors and pituitary carcinomas: a French multicenter experience. ( Assaker, R; Bernier, M; Borson-Chazot, F; Brue, T; Caron, P; Chabre, O; Chanson, P; Cornélius, A; Cortet-Rudelli, C; de Fraipont, F; Dufour, H; Figarella-Branger, D; François, P; Gaillard, S; Jouanneau, E; Muller, M; Passagia, JG; Raverot, G; Salenave, S; Sturm, N; Trouillas, J, 2010)
"The effects of folate supplementations were analyzed on the global DNA methylation status, the methylation status of DNA repeat element, the sensitivity of temozolomide-induced apoptosis, and the proliferation index of glioma cells."	3.75	Folate supplementation limits the aggressiveness of glioma via the remethylation of DNA repeats element and genes governing apoptosis and proliferation. ( Campion, L; Cartron, PF; Charbord, J; Debien, E; Hervouet, E; Menanteau, J; Vallette, FM, 2009)
" In this study, the authors investigate the nature of the SP phenotype in 2 glioma cell lines, U87MG and T98G, and their response to temozolomide."	3.74	Characterization of a side population of astrocytoma cells in response to temozolomide. ( Ang, BT; Chong, KH; Chua, C; See, SJ; Tang, C; Wong, MC; Zaiden, N, 2008)
"Dasatinib inhibited growth of three of the five melanoma cell lines."	3.74	Preclinical evaluation of dasatinib, a potent Src kinase inhibitor, in melanoma cell lines. ( Clynes, M; Crown, J; Eustace, AJ; O'Donovan, N, 2008)
"Aggressive pituitary adenomas, defined from a clinical perspective, have earlier and more frequent recurrences and can be resistant to conventional treatments."	2.50	Aggressive pituitary adenomas--diagnosis and emerging treatments. ( Cusimano, MD; Di Ieva, A; Kovacs, K; Rotondo, F; Syro, LV, 2014)
"Prolactinomas are relatively unique among primary brain tumors in that medical treatment alone using dopamine agonists carries a high probability of disease control or even radiographic and endocrine remission, and thus has replaced surgery as the first line of therapy."	2.47	Dopamine agonist-resistant prolactinomas. ( Aghi, MK; Oh, MC, 2011)
"Aggressive pituitary adenomas (APAs) are, by definition, resistant to optimal multimodality therapy."	1.62	Early Initiation of Temozolomide Therapy May Improve Response in Aggressive Pituitary Adenomas. ( Ahuja, CK; Bhansali, A; Das, L; Dhandapani, S; Dutta, P; Gupta, K; Gupta, N; Radotra, BD; Rai, A; Sood, R; Sreedharanunni, S; Tripathi, M; Vaiphei, K; Walia, R, 2021)
"Cell invasion and metastasis were measured by cell invasion assays."	1.56	Relationship between CYP17A1-Mediated DNA Demethylation and Proliferation, Invasion and Metastasis of Glioma Cells. ( Lv, W; Meng, L; Zhou, Y, 2020)
"Calpeptin is a chemical inhibitor of Calpain, which can inhibit this effect."	1.56	Calpain suppresses cell growth and invasion of glioblastoma multiforme by producing the cleavage of filamin A. ( Cai, L; Li, Q; Li, W; Lu, X; Su, Z; Tu, M; Wang, C; Zhu, Z, 2020)
"Trametinib has a strong anti-proliferative effect on established GB cell lines, stem cell-like cells and their differentiated progeny and while it does not enhance anti-proliferative and cell death-inducing properties of the standard treatment, i."	1.56	The limitations of targeting MEK signalling in Glioblastoma therapy. ( Debatin, KM; Hadzalic, A; Halatsch, ME; Karpel-Massler, G; Payer, C; Schuster, A; Selvasaravanan, KD; Siegelin, MD; Strobel, H; Westhoff, MA; Wiederspohn, N, 2020)
"Glioma is one of the most aggressive forms of brain tumor and is hallmarked by high rate of mortality, metastasis and drug resistance."	1.56	Downregulation of hsa_circ_0000936 sensitizes resistant glioma cells to temozolomide by sponging miR-1294. ( Feng, H; Hua, L; Huang, L; Zhang, X, 2020)
"Temozolomide (TMZ) is an oral chemotherapy drug constituting the backbone of chemotherapy regimens utilized as first-line treatment of GBM."	1.56	LncRNA NEAT1 promotes malignant phenotypes and TMZ resistance in glioblastoma stem cells by regulating let-7g-5p/MAP3K1 axis. ( Bi, CL; Fang, JS; Lan, S; Liu, JF; Yang, ZY; Zhang, MY, 2020)
"Glioblastoma is the most common and lethal adult brain tumor."	1.51	SOX3 can promote the malignant behavior of glioblastoma cells. ( Aldaz, P; Anastasov, N; Atkinson, MJ; Drakulic, D; Garcia, I; Garros-Regulez, L; Marjanovic Vicentic, J; Matheu, A; Nikolic, I; Puskas, N; Raicevic, S; Sampron, N; Stevanovic, M; Tasic, G; Vukovic, V, 2019)
"Glioblastoma is the worst and most common primary brain tumor."	1.51	CD73 Downregulation Decreases In Vitro and In Vivo Glioblastoma Growth. ( Azambuja, JH; Battastini, AMO; Beckenkamp, LR; Braganhol, E; de Oliveira, FH; Fernandes, MC; Figueiró, F; Gelsleichter, NE; Iser, IC; Scholl, JN; Sévigny, J; Spanevello, RM; Stefani, MA; Teixeira, HF; Wink, MR, 2019)
"OBJECTIVE Glioblastoma is the most common primary central nervous system tumor in adults."	1.48	Enhancement of invadopodia activity in glioma cells by sublethal doses of irradiation and temozolomide. ( Kaye, AH; Luwor, RB; Mao, L; Morokoff, AP; Paradiso, L; Stylli, SS; Whitehead, CA, 2018)
"Glioma is the most common and lethal central nervous system tumors."	1.46	Down-Regulation of AQP4 Expression via p38 MAPK Signaling in Temozolomide-Induced Glioma Cells Growth Inhibition and Invasion Impairment. ( Chen, Y; Gao, F; Hou, J; Jiang, R; Kang, L; Li, Y; Liu, H; Liu, X; Yang, M; Yi, Y, 2017)
"Temozolomide (TMZ) is an oral alkylating agent that has been used over the past 8 years to treat aggressive pituitary tumors resistant to conventional therapy."	1.43	Temozolomide for aggressive ACTH pituitary tumors: failure of a second course of treatment. ( Aller, J; Campderá, M; Estrada, J; Lilienfeld, H; Magallón, R; Martín, P; Palacios, N; Saucedo, G, 2016)
"Pituitary adenomas are classified as typical or atypical, invasive or noninvasive, and aggressive or nonaggressive based on pathological features, radiological findings, and clinical behavior."	1.43	Refractory pituitary adenoma: a novel classification for pituitary tumors. ( Bao, X; Dai, C; Deng, K; Feng, M; Lian, W; Liu, X; Ma, S; Ma, W; Sun, B; Wang, R; Wang, Y; Xing, B; Yao, Y; Zhong, D, 2016)
"Temozolomide (TMZ) has been showed to be an effective chemotherapeutic agent for glioblastoma treatment; however, the response rate is not satisfactory."	1.42	Synergistic Anti-Cancer Effects of Icariin and Temozolomide in Glioblastoma. ( Guo, H; Guo, M; Wang, Y; Yang, L, 2015)
"Glioma is one of the most aggressive and lethal human brain tumors."	1.40	MiR-124 governs glioma growth and angiogenesis and enhances chemosensitivity by targeting R-Ras and N-Ras. ( Chen, Q; Jiang, BH; Jiang, C; Jiang, T; Kang, C; Li, C; Li, H; Liu, LZ; Liu, N; Liu, X; Qian, X; Shi, Z; Wang, L; Wang, X; You, Y, 2014)
"Glioblastoma are highly aggressive brain tumors with poor prognosis."	1.40	Suppressor of fused (Sufu) represses Gli1 transcription and nuclear accumulation, inhibits glioma cell proliferation, invasion and vasculogenic mimicry, improving glioma chemo-sensitivity and prognosis. ( Cai, J; Chang, L; Chen, L; Cui, Y; Dou, Z; Du, W; Jiang, C; Liu, X; Liu, Y; Wang, G; Wang, H; Wang, X; Yi, L; Zhang, P, 2014)
"Optic pathway oligodendrogliomas are a rare form of pediatric intracranial tumor."	1.40	Case of pediatric optic pathway oligodendroglioma presenting widespread invasion and dissemination in the cerebrospinal fluid. ( Asano, K; Ito, E; Katayama, K; Komori, T; Ohkuma, H; Sasaki, S; Sato, T; Terui, K, 2014)
"Invasive pituitary adenomas (PAs) are generally refractory to conventional therapy and salvage treatment with temozolomide (TMZ)."	1.39	Pyrimethamine sensitizes pituitary adenomas cells to temozolomide through cathepsin B-dependent and caspase-dependent apoptotic pathways. ( Bao, X; Cai, F; Dai, C; Deng, K; Feng, M; Guo, K; Jiao, Y; Junji, W; Lian, W; Liu, X; Ma, S; Wang, R; Wei, Z; Xing, B; Yang, Y; Yao, Y; Zhang, B, 2013)
"The case of a patient with recurrent esthesioneuroblastoma complicated by ectopic adrenocorticotropic hormone production is presented, including the workup and management of this uncommon complication of an uncommon disease."	1.36	Esthesioneuroblastoma (Olfactory Neuroblastoma) with Ectopic ACTH Syndrome: a multidisciplinary case presentation from the Joan Karnell cancer center of Pennsylvania Hospital. ( Benito, M; Mintzer, DM; Nagamine, M; Newman, J; Zheng, S, 2010)
"Gliomas account for more than 50% of all primary brain tumors."	1.36	Long-term temozolomide treatment induces marked amino metabolism modifications and an increase in TMZ sensitivity in Hs683 oligodendroglioma cells. ( Bontempi, G; Bruyère, C; Decaestecker, C; Dubois, J; Haibe-Kains, B; Kiss, R; Lamoral-Theys, D; Le Calvé, B; Le Mercier, M; Lefranc, F; Rynkowski, MA, 2010)
"Glioblastoma multiforme is the most commonly diagnosed malignant primary brain tumour in adults."	1.36	Inhibition of metalloproteinases derived from tumours: new insights in the treatment of human glioblastoma. ( Bendinelli, S; Casalini, F; Costa, B; Da Pozzo, E; Da Settimo, F; Gabelloni, P; Martini, C; Nuti, E; Orlandini, E; Rossello, A, 2010)
"Cilengitide is a cyclic peptide antagonist of integrins alphavbeta3 and alphavbeta5 that is currently being evaluated as a novel therapeutic agent for recurrent and newly diagnosed glioblastoma."	1.35	Cilengitide modulates attachment and viability of human glioma cells, but not sensitivity to irradiation or temozolomide in vitro. ( Adams, B; Maurer, GD; Stupp, R; Tabatabai, G; Tritschler, I; Weller, M; Wick, W, 2009)
"The multidisciplinary up to date treatment for glioblastoma patients combined maximal surgical removal of the tumor with postoperative radiotherapy and concomitant chemotherapy with temozolomide."	1.35	[The sodium pump could constitute a new target to combat glioblastomas]. ( Kiss, R; Lefranc, F; Mijatovic, T, 2008)
"Temozolomide treatment of high-grade tv-a gliomas provided a 14-day growth delay compared with vehicle controls."	1.34	Magnetic resonance imaging determination of tumor grade and early response to temozolomide in a genetically engineered mouse model of glioma. ( Hambardzumyan, D; Holland, EC; Kreger, AR; Leopold, WR; McConville, P; Moody, JB; Rehemtulla, A; Ross, BD; Woolliscroft, MJ, 2007)
"Temozolomide is an alkylating cytostatic drug that finds increasing application in the treatment of melanoma, anaplastic astrocytoma and glioblastoma multiforme."	1.32	Temozolomide induces apoptosis and senescence in glioma cells cultured as multicellular spheroids. ( Arnold, H; Damasceno, R; Günther, W; Pawlak, E; Terzis, AJ, 2003)

Research

Studies (109)

Authors

Clinical Trials (4)

Trial Overview

Trial Outcomes

Area Under the Plasma Concentration Curve From Time 0 to 6 Hours (AUC [0-6]) After Dose

Timeframe	Studies, this research(%)	All Research%
pre-1990	0 (0.00)	18.7374
1990's	0 (0.00)	18.2507
2000's	16 (14.68)	29.6817
2010's	75 (68.81)	24.3611
2020's	18 (16.51)	2.80

Authors	Studies
Pai, FC	1
Huang, HW	1
Tsai, YL	1
Tsai, WC	1
Cheng, YC	1
Chang, HH	1
Chen, Y	3
Ding, Y	1
Zhang, C	1
He, L	1
Song, X	1
Zheng, C	1
Pan, Y	2
Yu, S	1
Mirallas, O	1
Filippi-Arriaga, F	1
Hernandez Hernandez, I	1
Aubanell, A	1
Chaachou, A	1
Garcia-Alvarez, A	1
Hernando, J	1
Martínez-Saez, E	1
Biagetti, B	1
Capdevila, J	1
Xu, J	1
Song, J	1
Xiao, M	1
Wang, C	2
Zhang, Q	3
Yuan, X	1
Tian, S	1
Das, L	1
Gupta, N	1
Dutta, P	1
Walia, R	1
Vaiphei, K	1
Rai, A	1
Radotra, BD	1
Gupta, K	1
Sreedharanunni, S	1
Ahuja, CK	1
Bhansali, A	1
Tripathi, M	1
Sood, R	1
Dhandapani, S	1
Cai, L	1
Li, Q	1
Li, W	1
Tu, M	1
Zhu, Z	1
Su, Z	1
Lu, X	1
Burman, P	2
Lamb, L	1
McCormack, A	2
Massey, SC	1
White, H	1
Whitmire, P	1
Doyle, T	1
Johnston, SK	1
Singleton, KW	1
Jackson, PR	1
Hawkins-Daarud, A	1
Bendok, BR	1
Porter, AB	1
Vora, S	1
Sarkaria, JN	1
Hu, LS	1
Mrugala, MM	1
Swanson, KR	1
Selvasaravanan, KD	1
Wiederspohn, N	1
Hadzalic, A	1
Strobel, H	1
Payer, C	1
Schuster, A	1
Karpel-Massler, G	1
Siegelin, MD	1
Halatsch, ME	1
Debatin, KM	1
Westhoff, MA	1
Ngo, MT	1
Karvelis, E	1
Harley, BAC	1
Zhao, C	1
Guo, R	1
Guan, F	1
Ma, S	4
Li, M	3
Wu, J	1
Liu, X	7
Li, H	3
Yang, B	1
Pinto, F	1
Costa, ÂM	1
Andrade, RP	1
Reis, RM	1
Wu, C	1
Su, J	2
Long, W	1
Qin, C	1
Wang, X	4
Xiao, K	1
Li, Y	3
Xiao, Q	1
Wang, J	4
Liu, Q	1
Hua, L	1
Huang, L	1
Zhang, X	2
Feng, H	2
Bi, CL	1
Liu, JF	1
Zhang, MY	1
Lan, S	1
Yang, ZY	1
Fang, JS	1
Zhu, Y	1
Wang, H	4
Fei, M	1
Tang, T	1
Niu, W	1
Zhang, L	4
Meng, L	1
Lv, W	1
Zhou, Y	1
Yuan, Q	1
Yang, W	2
Zhang, S	2
Li, T	1
Zuo, M	1
Zhou, X	2
Li, J	2
Xia, X	1
Chen, M	1
Liu, Y	6
Silginer, M	1
Weller, M	4
Stupp, R	3
Roth, P	1
Lasolle, H	1
Cortet, C	1
Castinetti, F	1
Cloix, L	1
Caron, P	2
Delemer, B	1
Desailloud, R	1
Jublanc, C	1
Lebrun-Frenay, C	1
Sadoul, JL	1
Taillandier, L	1
Batisse-Lignier, M	1
Bonnet, F	1
Bourcigaux, N	1
Bresson, D	1
Chabre, O	2
Chanson, P	2
Garcia, C	1
Haissaguerre, M	1
Reznik, Y	1
Borot, S	1
Villa, C	1
Vasiljevic, A	1
Gaillard, S	2
Jouanneau, E	2
Assié, G	1
Raverot, G	3
Lan, T	2
Zhang, Z	3
Zhang, M	2
Qu, Y	2
Zhao, Z	3
Fan, X	2
Zhan, Q	2
Song, Y	2
Yu, C	2
Gao, F	1
Jiang, R	1
Liu, H	2
Hou, J	1
Yi, Y	1
Kang, L	1
Yang, M	1
Maciaczyk, D	1
Picard, D	1
Zhao, L	1
Koch, K	1
Herrera-Rios, D	1
Li, G	2
Marquardt, V	1
Pauck, D	1
Hoerbelt, T	1
Zhang, W	1
Ouwens, DM	1
Remke, M	1
Jiang, T	2
Steiger, HJ	1
Maciaczyk, J	1
Kahlert, UD	1
Zhang, ZH	1
Fan, XY	1
Zhao, ZT	1
Song, YM	1
Yu, CJ	1
Wang, L	2
Hou, Y	1
Yin, X	1
Zheng, N	1
Yan, J	1
Xia, J	1
Wang, Z	3
Jayamanne, D	1
Wheeler, H	1
Cook, R	1
Teo, C	1
Brazier, D	1
Schembri, G	1
Kastelan, M	1
Guo, L	1
Back, MF	1
Mao, L	1
Whitehead, CA	1
Paradiso, L	1
Kaye, AH	1
Morokoff, AP	1
Luwor, RB	1
Stylli, SS	1
Dekkers, OM	1
Petersenn, S	1
Popovic, V	1
Trouillas, J	2
Lin, J	1
Ji, A	1
Qiu, G	1
Li, S	3
Zou, Y	1
Cui, Y	2
Song, C	1
He, H	1
Lu, Y	2
Schaub, C	1
Kebir, S	1
Junold, N	1
Hattingen, E	1
Schäfer, N	1
Steinbach, JP	2
Weyerbrock, A	2
Hau, P	2
Goldbrunner, R	1
Niessen, M	1
Mack, F	1
Stuplich, M	1
Tzaridis, T	1
Bähr, O	1
Kortmann, RD	2
Schlegel, U	1
Schmidt-Graf, F	1
Rohde, V	2
Braun, C	1
Hänel, M	1
Sabel, M	1
Gerlach, R	1
Krex, D	1
Belka, C	1
Vatter, H	1
Proescholdt, M	1
Herrlinger, U	2
Glas, M	1
Zhao, HF	1
Wang, G	2
Wu, CP	1
Zhou, XM	1
Chen, ZP	1
To, ST	1
Li, WP	1
Azambuja, JH	1
Gelsleichter, NE	1
Beckenkamp, LR	1
Iser, IC	1
Fernandes, MC	1
Figueiró, F	1
Battastini, AMO	1
Scholl, JN	1
de Oliveira, FH	1
Spanevello, RM	1
Sévigny, J	1
Wink, MR	1
Stefani, MA	1
Teixeira, HF	1
Braganhol, E	1
Marjanovic Vicentic, J	1
Drakulic, D	1
Garcia, I	1
Vukovic, V	1
Aldaz, P	1
Puskas, N	1
Nikolic, I	1
Tasic, G	1
Raicevic, S	1
Garros-Regulez, L	1
Sampron, N	1
Atkinson, MJ	1
Anastasov, N	1
Matheu, A	1
Stevanovic, M	1
Eisemann, T	1
Costa, B	2
Harter, PN	1
Wick, W	5
Mittelbronn, M	1
Angel, P	1
Peterziel, H	1
Sachkova, A	1
Sperling, S	1
Mielke, D	1
Schatlo, B	1
Ninkovic, M	1
Fu, T	1
Zhao, S	1
Gao, M	1
Jeong, H	1
Park, J	2
Shim, JK	2
Lee, JE	1
Kim, NH	1
Kim, HS	1
Chang, JH	2
Yook, JI	2
Kang, SG	2
Li, C	3
Yan, JL	1
Torheim, T	1
McLean, MA	1
Boonzaier, NR	1
Zou, J	1
Huang, Y	1
Yuan, J	1
van Dijken, BRJ	1
Matys, T	1
Markowetz, F	1
Price, SJ	1
Wang, B	2
Wu, ZH	1
Lou, PY	1
Chai, C	1
Han, SY	1
Ning, JF	1
Yu, L	1
Gui, S	1
Qiu, X	1
Zhang, G	1
Pan, J	1
Fan, J	1
Qi, S	1
Qiu, B	1
Yang, S	1
Liu, J	2
Wang, T	1
Li, X	1
You, C	1
Dai, C	2
Zhang, B	1
Guo, K	1
Cai, F	1
Yang, Y	1
Yao, Y	2
Feng, M	2
Bao, X	2
Deng, K	2
Jiao, Y	2
Wei, Z	1
Junji, W	1
Xing, B	2
Lian, W	2
Wang, R	2
Loftus, JC	1
Dhruv, H	1
Tuncali, S	1
Kloss, J	1
Yang, Z	1
Schumacher, CA	1
Cao, B	1
Williams, BO	1
Eschbacher, JM	1
Ross, JT	1
Tran, NL	1
Siebzehnrubl, FA	1
Silver, DJ	1
Tugertimur, B	1
Deleyrolle, LP	1
Siebzehnrubl, D	1
Sarkisian, MR	1
Devers, KG	1
Yachnis, AT	1
Kupper, MD	1
Neal, D	1
Nabilsi, NH	1
Kladde, MP	1
Suslov, O	1
Brabletz, S	1
Brabletz, T	1
Reynolds, BA	1
Steindler, DA	1
Wan, Y	1
Sun, G	1
Shi, L	2
Katayama, K	1
Asano, K	1
Ohkuma, H	1
Terui, K	1
Sasaki, S	1
Sato, T	1
Ito, E	1
Komori, T	1
Ren, X	1
Cheng, Y	3
Allen, JE	1
Zhang, Y	2
Yuan, Y	1
Huang, SY	1
Berg, A	1
Webb, BS	1
Connor, J	1
Liu, CG	1
Lu, Z	1
El-Deiry, WS	1
Yang, JM	1
Ashizawa, T	2
Akiyama, Y	2
Miyata, H	2
Iizuka, A	2
Komiyama, M	2
Kume, A	2
Omiya, M	2
Sugino, T	2
Asai, A	1
Hayashi, N	2
Mitsuya, K	2
Nakasu, Y	2
Yamaguchi, K	2
Di Ieva, A	2
Rotondo, F	2
Syro, LV	2
Cusimano, MD	2
Kovacs, K	2
Oshita, C	1
Shi, Z	1
Chen, Q	1
Qian, X	1
Jiang, C	2
Kang, C	1
Liu, LZ	1
You, Y	3
Liu, N	1
Jiang, BH	1
Han, S	1
Li, Z	1
Master, LM	1
Master, ZW	1
Wu, A	1
Hegi, ME	1
Gorlia, T	1
Erridge, SC	1
Perry, J	1
Hong, YK	1
Aldape, KD	1
Lhermitte, B	1
Pietsch, T	1
Grujicic, D	1
Tarnawski, R	1
Nam, DH	1
Taphoorn, MJ	1
Shen, CC	1
Rao, N	1
Thurzo, L	1
Gupta, T	1
Adamska, K	1
McBain, C	1
Brandes, AA	1
Tonn, JC	1
Schnell, O	1
Wiegel, T	1
Kim, CY	1
Nabors, LB	1
Reardon, DA	1
van den Bent, MJ	1
Hicking, C	1
Markivskyy, A	1
Picard, M	1
Tezcan, G	1
Tunca, B	1
Bekar, A	1
Yalcin, M	1
Sahin, S	1
Budak, F	1
Cecener, G	1
Egeli, U	1
Demir, C	1
Guvenc, G	1
Yilmaz, G	1

Trial	Phase	Enrollment	Study Type	Start Date	Status
Use of TTFields in Germany in Routine Clinical Care Study PROgram - Daily Activity, Sleep and Neurocognitive Functioning in Newly Diagnosed Glioblastoma Patients Study[NCT04717739]		500 participants (Anticipated)	Observational	2021-12-30	Recruiting
A Modified Ketogenic, Anti-Inflammatory Diet for Patients With High-Grade Gliomas[NCT05373381]		10 participants (Anticipated)	Interventional	2022-05-18	Recruiting
Cilengitide for Subjects With Newly Diagnosed Glioblastoma and Methylated MGMT Gene Promoter - A Multicenter, Open-label, Controlled Phase III Study, Testing Cilengitide in Combination With Standard Treatment (Temozolomide With Concomitant Radiation Thera[NCT00689221]	Phase 3	545 participants (Actual)	Interventional	2008-09-30	Completed
Pre-operative Radiation Therapy (RT) and Temozolomide (TMZ) in Patients With Newly Diagnosed Glioblastoma. A Phase I Study. (PARADIGMA)[NCT03480867]	Phase 1	0 participants (Actual)	Interventional	2017-03-31	Withdrawn (stopped due to competing study was opened by the surgeon after this trial was opened)
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

The AUC (0-6) for cilengitide was calculated by non-compartmental analysis using the computer program WinNonlin, Version 6.2.1. (NCT00689221)
Timeframe: Day 1 of Week -1

EuroQol 5-Dimensions (EQ-5D) Questionnaire Index

Intervention	hour*ng/mL (Mean)
Cilengitide + Temozolomide + Radiotherapy	295171.2

The EuroQuol-5D (EQ-5D) questionnaire is a measure of health status that provides a simple descriptive profile and a single index value. The optional part of the questionnaire was not applied. The EQ-5D defines health in terms of mobility, self-care, usual activities, pain/discomfort and anxiety/depression. The 5 items are combined to generate health profiles. These profiles were converted to a continuous single index score using a one to one matching. The lowest possible score is -0.594 (death) and the highest is 1.00 (full health). (NCT00689221)
Timeframe: Up to 50 months

Maximum Observed Plasma Concentration (Cmax)

Intervention	units on a scale (Mean)
Cilengitide + Temozolomide + Radiotherapy	0.598
Temozolomide + Radiotherapy	0.623

The Cmax for cilengitide was calculated by non-compartmental analysis using the computer program WinNonlin, Version 6.2.1. (NCT00689221)
Timeframe: Day 1 of Week -1

Overall Survival (OS) Time

Intervention	nanogram per milliliter (ng/mL) (Mean)
Cilengitide + Temozolomide + Radiotherapy	167363.2

The OS time is defined as the time (in months) from randomization to death or last day known to be alive. Participants without event are censored at the last date known to be alive or at the clinical cut-off date, whatever is earlier. (NCT00689221)
Timeframe: Time from randomization to death or last day known to be alive, reported between day of first participant randomized, that is, Sep 2008 until cut-off date, (19 Nov 2012)

Time to Maximum Plasma Concentration (Tmax)

Intervention	Months (Median)
Cilengitide + Temozolomide + Radiotherapy	26.3
Temozolomide + Radiotherapy	26.3

The Tmax for cilengitide was calculated by non-compartmental analysis using the computer program WinNonlin, Version 6.2.1. (NCT00689221)
Timeframe: Day 1 of Week -1

European Organization for the Research and Treatment of Cancer Quality of Life Questionnaire Brain Module (EORTC QLQ-BN20) Sub-scale Scores

Intervention	hours (Mean)
Cilengitide + Temozolomide + Radiotherapy	1.029

The QLQ-BN20 is a questionnaire specifically designed as the QLQ-C30 supplement for the evaluation of quality of life in brain tumor participants. It includes 4 multi-item sub-scales: future uncertainty, visual disorder, motor dysfunction, communication deficits, and 7 single-item scales: headaches, seizures, drowsiness, itchy skin, hair loss, weakness of legs, and bladder control. All items are rated on a 4-point Likert-type scale ('1=not at all', '2=a little', '3=quite a bit' and '4=very much'), and are linearly transformed to a 0-100 scale, with higher scores indicating more severe symptoms. (NCT00689221)
Timeframe: Up to 50 months

European Organization for the Research and Treatment of Cancer Quality of Life Questionnaire Core 30 (EORTC QLQ-C30) Sub-scale Scores

Intervention	units on a scale (Mean)
	Future Uncertainty (n=68, 86)	Visual Disorder (n=68, 85)	Motor Dysfunction (n=68, 86)	Communication Deficit (n=68, 86)	Headaches (n=68, 86)	Seizures (n=68, 87)	Drowsiness (n=66, 87)	Itchy Skin (n=68, 86)	Hair Loss (n=66, 86)	Weakness of Legs (n=67, 85)	Bladder Control (n=67, 85)
Cilengitide + Temozolomide + Radiotherapy	44.49	12.99	27.45	26.14	25.98	9.31	38.38	9.80	13.13	24.38	19.40
Temozolomide + Radiotherapy	39.31	17.78	23.39	19.96	21.71	8.05	35.25	13.57	15.12	20.39	10.20

The EORTC QLQ-C30 is a questionnaire including following sub-scales: global health status, functional scales (physical functioning, role functioning, emotional functioning, cognitive functioning, and social activity), symptom scales (fatigue, nausea and vomiting, and pain) and single items (dyspnoea, insomnia, appetite loss, constipation, diarrhoea and financial difficulties). Scores are averaged for each scale and transformed to 0-100 scale; higher score indicates better quality of life on global health status and functional scales and worse quality of life on symptom scales and financial difficulty scale. (NCT00689221)
Timeframe: Up to 50 months

Number of Participants With Adverse Events (AEs), Serious AEs, Treatment-Related AEs, Treatment-Related Serious AEs, AEs Leading to Death, Treatment Related AEs Leading to Death, AEs of Grade 3 or 4 and Treatment Related AEs of Grade 3 or 4

Intervention	units on a scale (Mean)
	Global Health Status (n=71, 92)	Physical Functioning (n=71, 92)	Role Functioning (n=71, 92)	Emotional Functioning (n=71, 93)	Cognitive Functioning (n=70, 93)	Social Activity (n=71, 93)	Fatigue (n=71, 92)	Nausea and Vomiting (n=71, 93)	Pain (n=71, 93)	Dyspnoea (n=71, 92)	Insomnia (n=71, 91)	Appetite Loss (n=71, 92)	Constipation (n=71, 93)	Diarrhoea (n=70, 92)	Financial Difficulties (n=71, 93)
Cilengitide + Temozolomide + Radiotherapy	54.34	65.70	56.34	67.49	64.05	56.34	44.37	10.33	22.30	15.96	20.66	21.13	18.78	6.67	27.23
Temozolomide + Radiotherapy	55.43	67.46	56.34	67.00	65.41	62.72	39.73	7.71	24.37	13.04	20.51	15.94	13.98	4.35	22.94

An AE is defined as any new untoward medical occurrences/worsening of pre-existing medical condition without regard to possibility of causal relationship. Treatment-emergent AEs are the events between first dose of study drug and up to 28 days after last dose of study treatment. A Serious AE is an AE that resulted in any of the following outcomes: death; life threatening; persistent/significant disability/incapacity; initial or prolonged inpatient hospitalization; congenital anomaly/birth defect. Treatment-related AEs are the AEs which are suspected to be reasonably related to the study treatment (cilengitide, or radiotherapy, or temozolomide) as per investigator assessment. The severity of AEs was assessed according to the National Cancer Institute-Common Toxicity Criteria (NCI-CTCAE) (version 3.0): Grade 1=mild, Grade 2=moderate, Grade 3=severe, Grade 4=life threatening or disabling. Note: Death (Grade 5) was regarded as an outcome. (NCT00689221)
Timeframe: Time from first dose up to 28 days after last dose of study treatment, reported between day of first participant randomized, that is, Sep 2008 until cut-off date (19 Nov 2012)

Number of Participants With AEs Belonging to Standardized Medical Dictionary for Regulatory Activities (MedDRA) Queries (SMQs) Thromboembolic Events and Hemorrhage With NCI-CTC Toxicity Grade 3 or 4

Intervention	Participants (Number)
	AEs	Serious AEs	Treatment-related AEs	Treatment-Related Serious AEs	AEs leading to death	Treatment-related AEs leading to death	AEs with NCI-CTC toxicity Grade 3 or 4	Treatment-related AEs of Grade 3 or 4
Cilengitide + Temozolomide + Radiotherapy	261	138	229	55	11	3	169	100
Temozolomide + Radiotherapy	253	115	222	47	9	3	158	101

Thromboembolic events (standardized MedDRA query [SMQ]) Grade 3 or 4 AEs encompassed hemiparesis and cerebrovascular accident, pulmonary embolism, and deep vein thrombosis. Thromboembolic events (SMQ) of any grade and of Grade 3 or 4 were generally more frequent in the Cilengitide + Temozolomide/Radiotherapy group than in the Temozolomide/Radiotherapy group but were still in the expected range of this patient population The severity of AEs was assessed according to the National Cancer Institute-Common Toxicity Criteria (NCI-CTCAE) (version 3.0): Grade 1=mild, Grade 2=moderate, Grade 3=severe, Grade 4=life threatening or disabling. Note: Death (Grade 5) was regarded as an outcome. (NCT00689221)
Timeframe: Time from first dose up to 28 days after last dose of study treatment, reported between day of first participant randomized, that is, Sep 2008 until cut-off date (19 Nov 2012)

Number of Participants With Change From Baseline in Work Status at End of Study

Intervention	Participants (Number)
	SMQ:Thromboembolic events	SMQ: Hemorrhage
Cilengitide + Temozolomide + Radiotherapy	35	4
Temozolomide + Radiotherapy	23	4

Number of participants with change from baseline in work status (working full time [FT], part-time [PT], unemployed/retired [U/R]) at end of study (EOS) (up to cut-off date, [19 Nov 2012]) was reported. For the category 'part-time', the following sub-categories were defined: part-time due to basic disease (PT1); part-time not due to basic disease (PT2); part-time reason not known (PT3). (NCT00689221)
Timeframe: Baseline, End of study (up to cut-off date, [19 Nov 2012])

Progression Free Survival (PFS) Time - Investigator and Independent Read

Intervention	participants (Number)
	Baseline: FT, EOS: FT	Baseline: FT, EOS: PT1	Baseline: FT, EOS: PT2	Baseline: FT, EOS: PT3	Baseline: FT, EOS: U/R	Baseline: PT1, EOS: FT	Baseline: PT1, EOS: PT1	Baseline: PT1, EOS: PT2	Baseline: PT1, EOS: PT3	Baseline: PT1, EOS: U/R	Baseline: PT2, EOS: FT	Baseline: PT2, EOS: PT1	Baseline: PT2, EOS: PT2	Baseline: PT2, EOS: PT3	Baseline: PT2, EOS: U/R	Baseline: PT3, EOS: FT	Baseline: PT3, EOS: PT1	Baseline: PT3, EOS: PT2	Baseline: PT3, EOS: PT3	Baseline: PT3, EOS: U/R	Baseline: U/R, EOS: FT	Baseline: U/R, EOS: PT1	Baseline: U/R, EOS: PT2	Baseline: U/R, EOS: PT3	Baseline: U/R, EOS: U/R	Baseline: Missing, EOS: FT	Baseline: Missing, EOS: PT1	Baseline: Missing, EOS: PT2	Baseline: Missing, EOS: PT3	Baseline: Missing, EOS: U/R	Baseline: Missing, EOS: Missing
Cilengitide + Temozolomide + Radiotherapy	3	2	1	0	24	3	3	0	0	9	0	0	0	1	5	0	0	0	0	0	5	5	1	0	199	0	0	0	0	1	1
Temozolomide + Radiotherapy	6	1	0	0	22	2	1	0	0	12	1	0	0	0	4	0	0	0	0	0	8	7	1	0	191	0	0	0	0	1	1

"The PFS time is defined as the duration from randomization to either first observation of progressive disease (PD) or occurrence of death due to any cause. Investigator read is the assessment of all imaging by the treating physician at the local trial site and Independent Read is the assessment of all imaging centrally by an Independent Review Committee (IRC). Investigator's assessed progression according to MacDonald criteria and IRC by Response Assessment in Neuro-Oncology Working Group (RANO) criteria using Gadolinium-enhanced magnetic resonance imaging.~Investigator and IRC read: Progression is defined as greater than 25 percent increase in the sum of the product of the largest perpendicular diameters of enhancing tumor compared to the smallest prior sum, or Worsening of an evaluable lesion(s),or Marked increase in T2/FLAIR non-enhancing lesions (IRC only) or Any new lesion" (NCT00689221)
Timeframe: Time from randomization to disease progression, death or last tumor assessment, reported between day of first participant randomized, that is, Sep 2008 until cut-off date, (19 Nov 2012)

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Temozolomide therapy for aggressive pituitary tumours - current understanding and future perspectives. Reviews in endocrine & metabolic disorders, 2020, Volume: 21, Issue:2 Topics: Antineoplastic Agents, Alkylating; Humans; Neoplasm Invasiveness; Pituitary Neoplasms; Temozolomide	2020
Aggressive pituitary adenomas--diagnosis and emerging treatments. Nature reviews. Endocrinology, 2014, Volume: 10, Issue:7 Topics: Adenoma; Biomarkers, Tumor; Dacarbazine; Humans; Ki-67 Antigen; Neoplasm Invasiveness; Neovasculariz	2014
Treatment of invasive silent somatotroph pituitary adenoma with temozolomide. Report of a case and review of the literature. Endocrine pathology, 2015, Volume: 26, Issue:2 Topics: Adenoma; Adult; Antineoplastic Agents, Alkylating; Asymptomatic Diseases; Dacarbazine; Growth Hormon	2015
Dopamine agonist-resistant prolactinomas. Journal of neurosurgery, 2011, Volume: 114, Issue:5 Topics: Antineoplastic Agents, Alkylating; Cell Division; Dacarbazine; Dopamine Agonists; Drug Resistance, N	2011
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Image-based metric of invasiveness predicts response to adjuvant temozolomide for primary glioblastoma. PloS one, 2020, Volume: 15, Issue:3 Topics: Adolescent; Adult; Age Factors; Aged; Brain Neoplasms; DNA Methylation; DNA Modification Methylases;	2020
Tumor growth patterns of MGMT-non-methylated glioblastoma in the randomized GLARIUS trial. Journal of cancer research and clinical oncology, 2018, Volume: 144, Issue:8 Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Bevacizumab; Camptothecin; Cell Growth	2018
Cilengitide combined with standard treatment for patients with newly diagnosed glioblastoma with methylated MGMT promoter (CENTRIC EORTC 26071-22072 study): a multicentre, randomised, open-label, phase 3 trial. The Lancet. Oncology, 2014, Volume: 15, Issue:10 Topics: Aged; Antineoplastic Combined Chemotherapy Protocols; Brain Neoplasms; Confidence Intervals; Dacarba	2014
Cilengitide combined with standard treatment for patients with newly diagnosed glioblastoma with methylated MGMT promoter (CENTRIC EORTC 26071-22072 study): a multicentre, randomised, open-label, phase 3 trial. The Lancet. Oncology, 2014, Volume: 15, Issue:10 Topics: Aged; Antineoplastic Combined Chemotherapy Protocols; Brain Neoplasms; Confidence Intervals; Dacarba	2014
Cilengitide combined with standard treatment for patients with newly diagnosed glioblastoma with methylated MGMT promoter (CENTRIC EORTC 26071-22072 study): a multicentre, randomised, open-label, phase 3 trial. The Lancet. Oncology, 2014, Volume: 15, Issue:10 Topics: Aged; Antineoplastic Combined Chemotherapy Protocols; Brain Neoplasms; Confidence Intervals; Dacarba	2014
Cilengitide combined with standard treatment for patients with newly diagnosed glioblastoma with methylated MGMT promoter (CENTRIC EORTC 26071-22072 study): a multicentre, randomised, open-label, phase 3 trial. The Lancet. Oncology, 2014, Volume: 15, Issue:10 Topics: Aged; Antineoplastic Combined Chemotherapy Protocols; Brain Neoplasms; Confidence Intervals; Dacarba	2014
Invasive tumor cells and prognosis in a selected population of patients with glioblastoma multiforme. Cancer, 2008, Aug-15, Volume: 113, Issue:4 Topics: Aged; Brain Neoplasms; Combined Modality Therapy; Dacarbazine; Female; Glioblastoma; Humans; Male; M	2008

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Inhibition of FABP6 Reduces Tumor Cell Invasion and Angiogenesis through the Decrease in MMP-2 and VEGF in Human Glioblastoma Cells. Cells, 2021, 10-17, Volume: 10, Issue:10 Topics: Animals; Cell Line, Tumor; Cell Movement; Clone Cells; Disease Progression; Extracellular Matrix; Fa	2021
Apcin inhibits the growth and invasion of glioblastoma cells and improves glioma sensitivity to temozolomide. Bioengineered, 2021, Volume: 12, Issue:2 Topics: Antineoplastic Agents, Alkylating; Apoptosis; Brain Neoplasms; Carbamates; Cell Line, Tumor; Cell Pr	2021
Aggressive Pituitary Macroadenoma Treated With Capecitabine and Temozolomide Chemotherapy Combination in a Patient With Nelson's Syndrome: A Case Report. Frontiers in endocrinology, 2021, Volume: 12 Topics: Adenoma; Antineoplastic Combined Chemotherapy Protocols; Capecitabine; Humans; Male; Middle Aged; Ne	2021
RUNX1 (RUNX family transcription factor 1), a target of microRNA miR-128-3p, promotes temozolomide resistance in glioblastoma multiform by upregulating multidrug resistance-associated protein 1 (MRP1). Bioengineered, 2021, Volume: 12, Issue:2 Topics: Adult; Aged; Base Sequence; Cell Line, Tumor; Cell Movement; Cell Proliferation; Core Binding Factor	2021
Early Initiation of Temozolomide Therapy May Improve Response in Aggressive Pituitary Adenomas. Frontiers in endocrinology, 2021, Volume: 12 Topics: Adenoma; Adult; Cohort Studies; Early Medical Intervention; Female; Humans; India; Male; Middle Aged	2021
Calpain suppresses cell growth and invasion of glioblastoma multiforme by producing the cleavage of filamin A. International journal of clinical oncology, 2020, Volume: 25, Issue:6 Topics: Biomarkers, Tumor; Brain Neoplasms; Calpain; Cell Line, Tumor; Cell Movement; Cell Proliferation; Ce	2020
The limitations of targeting MEK signalling in Glioblastoma therapy. Scientific reports, 2020, 05-04, Volume: 10, Issue:1 Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Brain Neoplasms; Cell Adhesion; Cell Deat	2020
Multidimensional hydrogel models reveal endothelial network angiocrine signals increase glioblastoma cell number, invasion, and temozolomide resistance. Integrative biology : quantitative biosciences from nano to macro, 2020, 06-19, Volume: 12, Issue:6 Topics: Biocompatible Materials; Brain Neoplasms; Cell Count; Cell Line, Tumor; Cell Movement; Cell Prolifer	2020
MicroRNA-128-3p Enhances the Chemosensitivity of Temozolomide in Glioblastoma by Targeting c-Met and EMT. Scientific reports, 2020, 06-11, Volume: 10, Issue:1 Topics: Animals; Apoptosis; Brain Neoplasms; Cell Line, Tumor; Cell Proliferation; Drug Resistance, Neoplasm	2020
Brachyury Is Associated with Glioma Differentiation and Response to Temozolomide. Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2020, Volume: 17, Issue:4 Topics: Antineoplastic Agents, Alkylating; Brain Neoplasms; Cell Differentiation; Cell Line, Tumor; Cell Mov	2020
LINC00470 promotes tumour proliferation and invasion, and attenuates chemosensitivity through the LINC00470/miR-134/Myc/ABCC1 axis in glioma. Journal of cellular and molecular medicine, 2020, Volume: 24, Issue:20 Topics: Base Sequence; Brain Neoplasms; Cell Line, Tumor; Cell Proliferation; Gene Expression Regulation, Ne	2020
Downregulation of hsa_circ_0000936 sensitizes resistant glioma cells to temozolomide by sponging miR-1294. Journal of biosciences, 2020, Volume: 45 Topics: Antineoplastic Agents, Alkylating; Apoptosis; Base Pairing; Base Sequence; Brain Neoplasms; Cell Lin	2020
LncRNA NEAT1 promotes malignant phenotypes and TMZ resistance in glioblastoma stem cells by regulating let-7g-5p/MAP3K1 axis. Bioscience reports, 2020, 10-30, Volume: 40, Issue:10 Topics: Brain Neoplasms; Case-Control Studies; Cell Line, Tumor; Cell Movement; Cell Proliferation; Drug Res	2020
Smarcd1 Inhibits the Malignant Phenotypes of Human Glioblastoma Cells via Crosstalk with Notch1. Molecular neurobiology, 2021, Volume: 58, Issue:4 Topics: Animals; Apoptosis; Brain Neoplasms; Cell Cycle Checkpoints; Cell Line, Tumor; Cell Movement; Cell P	2021
Relationship between CYP17A1-Mediated DNA Demethylation and Proliferation, Invasion and Metastasis of Glioma Cells. Critical reviews in eukaryotic gene expression, 2020, Volume: 30, Issue:6 Topics: Apoptosis; Cell Line, Tumor; Cell Movement; Cell Proliferation; Dehydroepiandrosterone; DNA Demethyl	2020
Inhibition of mitochondrial carrier homolog 2 (MTCH2) suppresses tumor invasion and enhances sensitivity to temozolomide in malignant glioma. Molecular medicine (Cambridge, Mass.), 2021, 01-28, Volume: 27, Issue:1 Topics: Animals; Apoptosis; Brain Neoplasms; Cell Line, Tumor; Cell Movement; Drug Resistance, Neoplasm; Gen	2021
Biological activity of tumor-treating fields in preclinical glioma models. Cell death & disease, 2017, 04-20, Volume: 8, Issue:4 Topics: Apoptosis; Brain Neoplasms; Caspases; Cell Cycle; Cell Line, Tumor; Cell Movement; Cell Survival; Da	2017
Temozolomide treatment can improve overall survival in aggressive pituitary tumors and pituitary carcinomas. European journal of endocrinology, 2017, Volume: 176, Issue:6 Topics: ACTH-Secreting Pituitary Adenoma; Adult; Antineoplastic Agents, Alkylating; Carcinoma; Chemoradiothe	2017
Downregulation of β-arrestin 1 suppresses glioblastoma cell malignant progression vis inhibition of Src signaling. Experimental cell research, 2017, 08-01, Volume: 357, Issue:1 Topics: Animals; beta-Arrestin 1; Brain Neoplasms; Cell Line, Tumor; Cell Proliferation; Dacarbazine; Diseas	2017
Down-Regulation of AQP4 Expression via p38 MAPK Signaling in Temozolomide-Induced Glioma Cells Growth Inhibition and Invasion Impairment. Journal of cellular biochemistry, 2017, Volume: 118, Issue:12 Topics: Aquaporin 4; Cell Line, Tumor; Dacarbazine; Down-Regulation; Gene Expression Regulation, Neoplastic;	2017
CBF1 is clinically prognostic and serves as a target to block cellular invasion and chemoresistance of EMT-like glioblastoma cells. British journal of cancer, 2017, Jun-27, Volume: 117, Issue:1 Topics: Antineoplastic Agents, Alkylating; Blotting, Western; Brain Neoplasms; Cell Line, Tumor; Cell Surviv	2017
[RNA interference targeting DNA-PKcs inhibits glioma cells malignancies and enhances temozolomide sensitivity]. Zhonghua yi xue za zhi, 2017, Aug-15, Volume: 97, Issue:31 Topics: Cell Line, Tumor; Cell Proliferation; DNA; DNA-Activated Protein Kinase; Glioma; Humans; Neoplasm In	2017
MiR-26b reverses temozolomide resistance via targeting Wee1 in glioma cells. Cell cycle (Georgetown, Tex.), 2017, Oct-18, Volume: 16, Issue:20 Topics: Base Sequence; Biomarkers, Tumor; Cell Cycle Proteins; Cell Line, Tumor; Cell Movement; Dacarbazine;	2017
Survival improvements with adjuvant therapy in patients with glioblastoma. ANZ journal of surgery, 2018, Volume: 88, Issue:3 Topics: Adult; Aged; Analysis of Variance; Australia; Brain Neoplasms; Chemoradiotherapy, Adjuvant; Cohort S	2018
Enhancement of invadopodia activity in glioma cells by sublethal doses of irradiation and temozolomide. Journal of neurosurgery, 2018, Volume: 129, Issue:3 Topics: Brain Neoplasms; Cell Line, Tumor; Combined Modality Therapy; Dose-Response Relationship, Drug; Glio	2018
Treatment of aggressive pituitary tumours and carcinomas: results of a European Society of Endocrinology (ESE) survey 2016. European journal of endocrinology, 2018, Volume: 178, Issue:3 Topics: Adenoma; Adolescent; Adult; Aged; Antineoplastic Agents, Alkylating; Antineoplastic Combined Chemoth	2018
FBW7 is associated with prognosis, inhibits malignancies and enhances temozolomide sensitivity in glioblastoma cells. Cancer science, 2018, Volume: 109, Issue:4 Topics: Apoptosis; Aurora Kinase B; Cell Count; Cell Cycle Checkpoints; Cell Line, Tumor; Cell Movement; Cel	2018
A Multi-targeted Natural Flavonoid Myricetin Suppresses Lamellipodia and Focal Adhesions Formation and Impedes Glioblastoma Cell Invasiveness and Abnormal Motility. CNS & neurological disorders drug targets, 2018, Volume: 17, Issue:7 Topics: Antineoplastic Agents; Astrocytes; Cell Line, Tumor; Cell Movement; Cell Proliferation; Dose-Respons	2018
CD73 Downregulation Decreases In Vitro and In Vivo Glioblastoma Growth. Molecular neurobiology, 2019, Volume: 56, Issue:5 Topics: 5'-Nucleotidase; Adenosine; Animals; Biomarkers, Tumor; Brain Neoplasms; Cell Line, Tumor; Cell Move	2019
SOX3 can promote the malignant behavior of glioblastoma cells. Cellular oncology (Dordrecht), 2019, Volume: 42, Issue:1 Topics: Adult; Aged; Aged, 80 and over; Autophagy; Brain Neoplasms; Cell Line, Tumor; Cell Movement; Cell Pr	2019
Podoplanin expression is a prognostic biomarker but may be dispensable for the malignancy of glioblastoma. Neuro-oncology, 2019, 02-19, Volume: 21, Issue:3 Topics: Animals; Antineoplastic Agents, Alkylating; Apoptosis; Brain; Brain Neoplasms; Cell Line, Tumor; Cel	2019
Combined Applications of Repurposed Drugs and Their Detrimental Effects on Glioblastoma Cells. Anticancer research, 2019, Volume: 39, Issue:1 Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Cell Line, Tumor; Cell Proliferation; Cel	2019
MicroRNA-34a-5p suppresses tumorigenesis and progression of glioma and potentiates Temozolomide-induced cytotoxicity for glioma cells by targeting HMGA2. European journal of pharmacology, 2019, Jun-05, Volume: 852 Topics: Animals; Base Sequence; Carcinogenesis; Cell Line, Tumor; Cell Movement; Cell Proliferation; Disease	2019
Combined treatment with 2'-hydroxycinnamaldehyde and temozolomide suppresses glioblastoma tumorspheres by decreasing stemness and invasiveness. Journal of neuro-oncology, 2019, Volume: 143, Issue:1 Topics: Acrolein; Adenosine Triphosphate; Animals; Antineoplastic Agents; Benzoates; Cell Line, Tumor; Cell	2019
Low perfusion compartments in glioblastoma quantified by advanced magnetic resonance imaging and correlated with patient survival. Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 2019, Volume: 134 Topics: Adult; Aged; Chemoradiotherapy; Cohort Studies; Diffusion Magnetic Resonance Imaging; Female; Gliobl	2019
Human bone marrow-derived mesenchymal stem cell-secreted exosomes overexpressing microRNA-34a ameliorate glioblastoma development via down-regulating MYCN. Cellular oncology (Dordrecht), 2019, Volume: 42, Issue:6 Topics: Animals; Base Sequence; Cell Differentiation; Cell Line, Tumor; Cell Movement; Cell Proliferation; D	2019
Exosomes derived from microRNA-199a-overexpressing mesenchymal stem cells inhibit glioma progression by down-regulating AGAP2. Aging, 2019, 08-05, Volume: 11, Issue:15 Topics: Antineoplastic Agents, Alkylating; Apoptosis; Brain Neoplasms; Cell Line, Tumor; Cell Movement; Cell	2019
Cerebellar glioblastoma multiforme: a retrospective study of 28 patients at a single institution. The International journal of neuroscience, 2013, Volume: 123, Issue:10 Topics: Adolescent; Adult; Age Factors; Aged; Antineoplastic Agents; Antineoplastic Agents, Alkylating; Brai	2013
Pyrimethamine sensitizes pituitary adenomas cells to temozolomide through cathepsin B-dependent and caspase-dependent apoptotic pathways. International journal of cancer, 2013, Oct-15, Volume: 133, Issue:8 Topics: Animals; Antineoplastic Agents, Alkylating; Apoptosis; bcl-2-Associated X Protein; Caspase 3; Caspas	2013
TROY (TNFRSF19) promotes glioblastoma survival signaling and therapeutic resistance. Molecular cancer research : MCR, 2013, Volume: 11, Issue:8 Topics: Animals; Antineoplastic Agents; Apoptosis; Astrocytes; Cell Line, Tumor; Cell Movement; Cell Prolife	2013
The ZEB1 pathway links glioblastoma initiation, invasion and chemoresistance. EMBO molecular medicine, 2013, Volume: 5, Issue:8 Topics: Animals; Antineoplastic Agents; Brain Neoplasms; Cell Line, Tumor; Cell Survival; Dacarbazine; DNA M	2013
MicroRNA-125b inhibitor sensitizes human primary glioblastoma cells to chemotherapeutic drug temozolomide on invasion. In vitro cellular & developmental biology. Animal, 2013, Volume: 49, Issue:8 Topics: Cell Line, Tumor; Dacarbazine; Gene Expression Regulation, Neoplastic; Glioblastoma; Humans; In Vitr	2013
Case of pediatric optic pathway oligodendroglioma presenting widespread invasion and dissemination in the cerebrospinal fluid. Brain tumor pathology, 2014, Volume: 31, Issue:3 Topics: Antineoplastic Combined Chemotherapy Protocols; Carboplatin; Chemoradiotherapy, Adjuvant; Child; Dac	2014
The NFκB inhibitor, SN50, induces differentiation of glioma stem cells and suppresses their oncogenic phenotype. Cancer biology & therapy, 2014, Volume: 15, Issue:5 Topics: Animals; Antineoplastic Agents, Alkylating; Brain Neoplasms; Cell Differentiation; Dacarbazine; Drug	2014
Effect of the STAT3 inhibitor STX-0119 on the proliferation of a temozolomide-resistant glioblastoma cell line. International journal of oncology, 2014, Volume: 45, Issue:1 Topics: Animals; Antineoplastic Agents; Cell Line, Tumor; Dacarbazine; Drug Resistance, Neoplasm; Epithelial	2014
YKL-40 downregulation is a key factor to overcome temozolomide resistance in a glioblastoma cell line. Oncology reports, 2014, Volume: 32, Issue:1 Topics: Adipokines; Animals; Antigens, Neoplasm; Biomarkers, Tumor; Cell Line, Tumor; Chitinase-3-Like Prote	2014
MiR-124 governs glioma growth and angiogenesis and enhances chemosensitivity by targeting R-Ras and N-Ras. Neuro-oncology, 2014, Volume: 16, Issue:10 Topics: Animals; Apoptosis; Brain; Brain Neoplasms; Cell Line, Tumor; Cell Proliferation; Dacarbazine; Genes	2014
Exogenous IGFBP-2 promotes proliferation, invasion, and chemoresistance to temozolomide in glioma cells via the integrin β1-ERK pathway. British journal of cancer, 2014, Sep-23, Volume: 111, Issue:7 Topics: Antineoplastic Agents, Alkylating; Brain Neoplasms; Cell Line, Tumor; Cell Proliferation; Dacarbazin	2014
Ficus carica latex prevents invasion through induction of let-7d expression in GBM cell lines. Cellular and molecular neurobiology, 2015, Volume: 35, Issue:2 Topics: Antineoplastic Agents; Apoptosis; Brain Neoplasms; Cell Line, Tumor; Cell Proliferation; Cell Surviv	2015
Annexin A5 promotes invasion and chemoresistance to temozolomide in glioblastoma multiforme cells. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014, Volume: 35, Issue:12 Topics: Annexin A5; Antineoplastic Agents, Alkylating; Apoptosis; Brain Neoplasms; Cadherins; Cell Line, Tum	2014
Suppressor of fused (Sufu) represses Gli1 transcription and nuclear accumulation, inhibits glioma cell proliferation, invasion and vasculogenic mimicry, improving glioma chemo-sensitivity and prognosis. Oncotarget, 2014, Nov-30, Volume: 5, Issue:22 Topics: Adult; Animals; Brain Neoplasms; Cell Line, Tumor; Cell Nucleus; Cell Proliferation; Dacarbazine; Di	2014
Synergistic Anti-Cancer Effects of Icariin and Temozolomide in Glioblastoma. Cell biochemistry and biophysics, 2015, Volume: 71, Issue:3 Topics: Antineoplastic Agents; Apoptosis; Cell Line, Tumor; Cell Movement; Cell Proliferation; Dacarbazine;	2015
Effects of hnRNP A2/B1 Knockdown on Inhibition of Glioblastoma Cell Invasion, Growth and Survival. Molecular neurobiology, 2016, Volume: 53, Issue:2 Topics: Brain Neoplasms; Cell Adhesion; Cell Line, Tumor; Cell Proliferation; Cell Survival; Dacarbazine; Dr	2016
Glioma cell VEGFR-2 confers resistance to chemotherapeutic and antiangiogenic treatments in PTEN-deficient glioblastoma. Oncotarget, 2015, Oct-13, Volume: 6, Issue:31 Topics: Angiogenesis Inhibitors; Animals; Bevacizumab; Brain Neoplasms; Cell Line, Tumor; Cell Movement; Cel	2015
The metalloprotease-disintegrin ADAM8 contributes to temozolomide chemoresistance and enhanced invasiveness of human glioblastoma cells. Neuro-oncology, 2015, Volume: 17, Issue:11 Topics: ADAM Proteins; Antineoplastic Agents; Blotting, Western; Brain Neoplasms; Cell Separation; Cell Surv	2015
Resveratrol Inhibits the Invasion of Glioblastoma-Initiating Cells via Down-Regulation of the PI3K/Akt/NF-κB Signaling Pathway. Nutrients, 2015, Jun-02, Volume: 7, Issue:6 Topics: Animals; Cell Adhesion; Cell Line, Tumor; Cell Survival; Dacarbazine; Down-Regulation; Glioblastoma;	2015
PI3K inhibitor combined with miR-125b inhibitor sensitize TMZ-induced anti-glioma stem cancer effects through inactivation of Wnt/β-catenin signaling pathway. In vitro cellular & developmental biology. Animal, 2015, Volume: 51, Issue:10 Topics: Antineoplastic Agents, Alkylating; Apoptosis; beta Catenin; Cell Movement; Cell Survival; Chromones;	2015
HMGN5 blockade by siRNA enhances apoptosis, suppresses invasion and increases chemosensitivity to temozolomide in meningiomas. International journal of oncology, 2015, Volume: 47, Issue:4 Topics: Aged; Antineoplastic Agents; Apoptosis; Blotting, Western; Dacarbazine; Drug Resistance, Neoplasm; F	2015
BC3EE2,9B, a synthetic carbazole derivative, upregulates autophagy and synergistically sensitizes human GBM8901 glioblastoma cells to temozolomide. International journal of molecular medicine, 2015, Volume: 36, Issue:5 Topics: Antineoplastic Agents; Autophagy; Brain Neoplasms; Carbazoles; Cell Cycle Checkpoints; Cell Line, Tu	2015
Temozolomide for aggressive ACTH pituitary tumors: failure of a second course of treatment. Pituitary, 2016, Volume: 19, Issue:2 Topics: ACTH-Secreting Pituitary Adenoma; Adenoma; Adult; Antineoplastic Agents, Alkylating; Chemotherapy, A	2016
SRPX2 Enhances the Epithelial-Mesenchymal Transition and Temozolomide Resistance in Glioblastoma Cells. Cellular and molecular neurobiology, 2016, Volume: 36, Issue:7 Topics: Brain Neoplasms; Cell Line, Tumor; Cell Movement; Dacarbazine; Drug Resistance, Neoplasm; Epithelial	2016
A novel drug conjugate, NEO212, targeting proneural and mesenchymal subtypes of patient-derived glioma cancer stem cells. Cancer letters, 2016, Feb-28, Volume: 371, Issue:2 Topics: Animals; Antineoplastic Agents, Alkylating; Apoptosis; Biomarkers, Tumor; Brain Neoplasms; Dacarbazi	2016
Metronomic Doses of Temozolomide Enhance the Efficacy of Carbon Nanotube CpG Immunotherapy in an Invasive Glioma Model. PloS one, 2016, Volume: 11, Issue:2 Topics: Animals; Antineoplastic Agents; Brain Neoplasms; Cell Death; Cell Line, Tumor; Dacarbazine; Disease	2016
SPOCK1 is upregulated in recurrent glioblastoma and contributes to metastasis and Temozolomide resistance. Cell proliferation, 2016, Volume: 49, Issue:2 Topics: Antineoplastic Agents, Alkylating; Brain Neoplasms; Cell Line, Tumor; Cell Movement; Dacarbazine; Dr	2016
Downregulation of HIF-1a sensitizes U251 glioma cells to the temozolomide (TMZ) treatment. Experimental cell research, 2016, 05-01, Volume: 343, Issue:2 Topics: Apoptosis; Brain Neoplasms; Cell Differentiation; Cell Line, Tumor; Cell Movement; Cell Proliferatio	2016
miR-423-5p contributes to a malignant phenotype and temozolomide chemoresistance in glioblastomas. Neuro-oncology, 2017, Volume: 19, Issue:1 Topics: Animals; Antineoplastic Agents, Alkylating; Apoptosis; Brain Neoplasms; Cell Cycle Proteins; Cell Pr	2017
Targeting hyperactivated DNA-PKcs by KU0060648 inhibits glioma progression and enhances temozolomide therapy via suppression of AKT signaling. Oncotarget, 2016, Aug-23, Volume: 7, Issue:34 Topics: Animals; Antineoplastic Agents, Alkylating; Apoptosis; Brain Neoplasms; Cell Line, Tumor; Dacarbazin	2016
Reversibility of glioma stem cells' phenotypes explains their complex in vitro and in vivo behavior: Discovery of a novel neurosphere-specific enzyme, cGMP-dependent protein kinase 1, using the genomic landscape of human glioma stem cells as a discovery t Oncotarget, 2016, 09-27, Volume: 7, Issue:39 Topics: Animals; Apoptosis; Biomarkers, Tumor; Brain Neoplasms; Cell Line, Tumor; Cell Movement; Cell Prolif	2016
Inhibiting stemness and invasive properties of glioblastoma tumorsphere by combined treatment with temozolomide and a newly designed biguanide (HL156A). Oncotarget, 2016, 10-04, Volume: 7, Issue:40 Topics: Animals; Antineoplastic Agents, Alkylating; Apoptosis; Brain Neoplasms; Cell Proliferation; Dacarbaz	2016
MiRNA203 suppresses the expression of protumorigenic STAT1 in glioblastoma to inhibit tumorigenesis. Oncotarget, 2016, Dec-20, Volume: 7, Issue:51 Topics: Animals; Antineoplastic Agents; Apoptosis; Brain Neoplasms; Cell Line, Tumor; Cell Movement; Cell Pr	2016
A Novel Computer-Assisted Approach to evaluate Multicellular Tumor Spheroid Invasion Assay. Scientific reports, 2016, 10-12, Volume: 6 Topics: Algorithms; Animals; Computer Simulation; Dacarbazine; Enzyme Inhibitors; Glioblastoma; Glioma; High	2016
Metformin treatment reduces temozolomide resistance of glioblastoma cells. Oncotarget, 2016, Nov-29, Volume: 7, Issue:48 Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Brain Neoplasms; Cell Line, Tumor; Cell Mov	2016
Silencing of histone deacetylase 2 suppresses malignancy for proliferation, migration, and invasion of glioblastoma cells and enhances temozolomide sensitivity. Cancer chemotherapy and pharmacology, 2016, Volume: 78, Issue:6 Topics: Antineoplastic Agents, Alkylating; Brain Neoplasms; Cell Line, Tumor; Cell Movement; Cell Proliferat	2016
Refractory pituitary adenoma: a novel classification for pituitary tumors. Oncotarget, 2016, Dec-13, Volume: 7, Issue:50 Topics: Adenoma; Adult; Aged; Antineoplastic Agents, Alkylating; Biopsy; Cell Proliferation; Dacarbazine; Di	2016
MiR-433-3p suppresses cell growth and enhances chemosensitivity by targeting CREB in human glioma. Oncotarget, 2017, Jan-17, Volume: 8, Issue:3 Topics: 3' Untranslated Regions; Adult; Brain Neoplasms; Cell Line, Tumor; Cell Movement; Cell Proliferation	2017
The PI3K inhibitor GDC-0941 enhances radiosensitization and reduces chemoresistance to temozolomide in GBM cell lines. Neuroscience, 2017, 03-27, Volume: 346 Topics: Antineoplastic Agents; Antineoplastic Agents, Alkylating; Antineoplastic Combined Chemotherapy Proto	2017
Preclinical evaluation of dasatinib, a potent Src kinase inhibitor, in melanoma cell lines. Journal of translational medicine, 2008, Sep-29, Volume: 6 Topics: Antineoplastic Agents; Apoptosis; Benzenesulfonates; Blotting, Western; Cell Cycle; Cell Line, Tumor	2008
Characterization of a side population of astrocytoma cells in response to temozolomide. Journal of neurosurgery, 2008, Volume: 109, Issue:5 Topics: Animals; Antineoplastic Agents, Alkylating; Astrocytoma; ATP Binding Cassette Transporter, Subfamily	2008
Inhibition of PI3K-AKT-mTOR signaling sensitizes melanoma cells to cisplatin and temozolomide. The Journal of investigative dermatology, 2009, Volume: 129, Issue:6 Topics: Antineoplastic Agents, Alkylating; Apoptosis; Cell Line, Tumor; Cisplatin; Dacarbazine; Enzyme Inhib	2009
Pseudoprogression after radiotherapy with concurrent temozolomide for high-grade glioma: clinical observations and working recommendations. Surgical neurology, 2009, Volume: 72, Issue:4 Topics: Adult; Antineoplastic Agents, Alkylating; Brain Neoplasms; Combined Modality Therapy; Dacarbazine; D	2009
Editorial: on the road to multi-modal and pluri-disciplinary treatment of glioblastomas. Acta neurochirurgica, 2009, Volume: 151, Issue:2 Topics: Antineoplastic Agents, Alkylating; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Brain	2009
Cilengitide modulates attachment and viability of human glioma cells, but not sensitivity to irradiation or temozolomide in vitro. Neuro-oncology, 2009, Volume: 11, Issue:6 Topics: Animals; Antineoplastic Agents, Alkylating; bcl-X Protein; Brain Neoplasms; Cell Adhesion; Cell Move	2009
Folate supplementation limits the aggressiveness of glioma via the remethylation of DNA repeats element and genes governing apoptosis and proliferation. Clinical cancer research : an official journal of the American Association for Cancer Research, 2009, May-15, Volume: 15, Issue:10 Topics: Aged; Apoptosis; Apoptosis Regulatory Proteins; Becaplermin; Cell Line, Tumor; Cell Proliferation; D	2009
Temozolomide (Temodar®) and capecitabine (Xeloda®) treatment of an aggressive corticotroph pituitary tumor. Pituitary, 2011, Volume: 14, Issue:4 Topics: ACTH-Secreting Pituitary Adenoma; Adenoma; Antineoplastic Combined Chemotherapy Protocols; Capecitab	2011
Esthesioneuroblastoma (Olfactory Neuroblastoma) with Ectopic ACTH Syndrome: a multidisciplinary case presentation from the Joan Karnell cancer center of Pennsylvania Hospital. The oncologist, 2010, Volume: 15, Issue:1 Topics: ACTH Syndrome, Ectopic; Adrenocorticotropic Hormone; Anti-Inflammatory Agents; Antifungal Agents; An	2010
Long-term temozolomide treatment induces marked amino metabolism modifications and an increase in TMZ sensitivity in Hs683 oligodendroglioma cells. Neoplasia (New York, N.Y.), 2010, Volume: 12, Issue:1 Topics: Amino Acids; Animals; Antineoplastic Agents, Alkylating; Apoptosis; Blotting, Western; Brain Neoplas	2010
Bevacizumab is active as a single agent against recurrent malignant gliomas. Anticancer research, 2010, Volume: 30, Issue:2 Topics: Adult; Aged; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chem	2010
Inhibition of metalloproteinases derived from tumours: new insights in the treatment of human glioblastoma. Neuroscience, 2010, Jun-30, Volume: 168, Issue:2 Topics: Antineoplastic Agents; Brain Neoplasms; Cell Line, Tumor; Cell Proliferation; Cell Survival; Chemota	2010
Temozolomide treatment in aggressive pituitary tumors and pituitary carcinomas: a French multicenter experience. The Journal of clinical endocrinology and metabolism, 2010, Volume: 95, Issue:10 Topics: ACTH-Secreting Pituitary Adenoma; Adult; Antineoplastic Agents, Alkylating; Carcinoma; Dacarbazine;	2010
Measurements of tumor cell autophagy predict invasiveness, resistance to chemotherapy, and survival in melanoma. Clinical cancer research : an official journal of the American Association for Cancer Research, 2011, May-15, Volume: 17, Issue:10 Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Autophagy; Benzenesulfonates; Cell Count; C	2011
Perillyl alcohol for the treatment of temozolomide-resistant gliomas. Molecular cancer therapeutics, 2012, Volume: 11, Issue:11 Topics: Administration, Intranasal; Animals; Brain Neoplasms; Cell Death; Cell Line, Tumor; Cell Proliferati	2012
Increased xCT expression correlates with tumor invasion and outcome in patients with glioblastomas. Neurosurgery, 2013, Volume: 72, Issue:1 Topics: Adult; Age Factors; Aged; Aged, 80 and over; Amino Acid Transport System y+; Antineoplastic Agents,	2013
Knockdown of RLIP76 expression by RNA interference inhibits invasion, induces cell cycle arrest, and increases chemosensitivity to the anticancer drug temozolomide in glioma cells. Journal of neuro-oncology, 2013, Volume: 112, Issue:1 Topics: Antineoplastic Agents, Alkylating; ATP Binding Cassette Transporter, Subfamily B; ATP Binding Casset	2013
Temozolomide induces apoptosis and senescence in glioma cells cultured as multicellular spheroids. British journal of cancer, 2003, Feb-10, Volume: 88, Issue:3 Topics: Antineoplastic Agents, Alkylating; Apoptosis; Cell Division; Cell Movement; Cellular Senescence; Dac	2003
Gliomatosis cerebri: better definition, better treatment. Neurology, 2004, Jul-27, Volume: 63, Issue:2 Topics: Adolescent; Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Astrocyt	2004
Pro-invasive gene regulating effect of irradiation and combined temozolomide-radiation treatment on surviving human malignant glioma cells. European journal of pharmacology, 2006, Aug-07, Volume: 542, Issue:1-3 Topics: Antineoplastic Agents, Alkylating; Blotting, Western; Cell Line, Tumor; Cell Proliferation; Cell Sur	2006
Development of luciferase tagged brain tumour models in mice for chemotherapy intervention studies. European journal of cancer (Oxford, England : 1990), 2006, Volume: 42, Issue:18 Topics: Animals; Antineoplastic Agents, Alkylating; Blood-Brain Barrier; Brain Neoplasms; Cell Division; Cel	2006
Magnetic resonance imaging determination of tumor grade and early response to temozolomide in a genetically engineered mouse model of glioma. Clinical cancer research : an official journal of the American Association for Cancer Research, 2007, May-15, Volume: 13, Issue:10 Topics: Animals; Brain Neoplasms; Dacarbazine; Disease Models, Animal; Genetic Engineering; Glioma; Magnetic	2007
[The sodium pump could constitute a new target to combat glioblastomas]. Bulletin du cancer, 2008, Volume: 95, Issue:3 Topics: Animals; Antineoplastic Agents, Alkylating; Antineoplastic Agents, Phytogenic; Apoptosis; Autophagy;	2008
Prevention of irradiation-induced glioma cell invasion by temozolomide involves caspase 3 activity and cleavage of focal adhesion kinase. Cancer research, 2002, Mar-15, Volume: 62, Issue:6 Topics: 3T3 Cells; Animals; Antineoplastic Agents, Alkylating; Caspase 3; Caspases; Combined Modality Therap	2002

Intervention	Months (Median)
	PFS Time: Investigator read	PFS Time: Independent read
Cilengitide + Temozolomide + Radiotherapy	13.5	10.6
Temozolomide + Radiotherapy	10.7	7.9

temozolomide and Invasiveness, Neoplasm