sulfasalazine has been researched along with Brain Neoplasms in 22 studies
Sulfasalazine: A drug that is used in the management of inflammatory bowel diseases. Its activity is generally considered to lie in its metabolic breakdown product, 5-aminosalicylic acid (see MESALAMINE) released in the colon. (From Martindale, The Extra Pharmacopoeia, 30th ed, p907)
sulfasalazine : An azobenzene consisting of diphenyldiazene having a carboxy substituent at the 4-position, a hydroxy substituent at the 3-position and a 2-pyridylaminosulphonyl substituent at the 4'-position.
Brain Neoplasms: Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.
| Excerpt | Relevance | Reference |
|---|---|---|
| " A total of twenty patients with progressive malignant glioma despite surgery, radiation therapy and a first line of chemotherapy will be recruited and assigned to four dosage regimen of Sulfasalazine." | 9.12 | A phase 1-2, prospective, double blind, randomized study of the safety and efficacy of Sulfasalazine for the treatment of progressing malignant gliomas: study protocol of [ISRCTN45828668]. ( Albert, A; Bours, V; Chariot, A; Deprez, M; Martin, D; Robe, PA, 2006) |
| "Autocrine and paracrine factors, including glutamate and epidermal growth factor (EGF), are potent inducers of brain tumor cell invasion, a pathological hallmark of malignant gliomas." | 7.88 | Epidermal growth factor receptor promotes glioma progression by regulating xCT and GluN2B-containing N-methyl-d-aspartate-sensitive glutamate receptor signaling. ( Akashi, K; Baba, E; Hirata, Y; Kamenori, S; Mitsuishi, Y; Nagano, O; Okazaki, S; Sampetrean, O; Saya, H; Shintani, S; Suina, K; Takahashi, F; Takahashi, K; Tsuchihashi, K; Yamasaki, J, 2018) |
| " Food and Drug Administration and EMA-approved xCT inhibitor, sulfasalazine (SAS) in gliomas." | 7.83 | Sulfasalazine impacts on ferroptotic cell death and alleviates the tumor microenvironment and glioma-induced brain edema. ( Buchfelder, M; Dörfler, A; Engelhorn, T; Eyüpoglu, IY; Fan, Z; Ghoochani, A; Klucken, J; Minakaki, G; Rauh, M; Savaskan, N; Sehm, T, 2016) |
| "Glioblastoma multiforme is the most aggressive malignant primary brain tumor in adults." | 5.43 | Increased Expression of System xc- in Glioblastoma Confers an Altered Metabolic State and Temozolomide Resistance. ( Aboody, KS; Cassady, K; Cherryholmes, GA; Marinov, GK; Polewski, MD; Reveron-Thornton, RF, 2016) |
| "Celecoxib has been utilized with success in the treatment of several types of cancer, including gliomas." | 5.42 | Celecoxib and LLW-3-6 Reduce Survival of Human Glioma Cells Independently and Synergistically with Sulfasalazine. ( Winfield, LL; Yerokun, T, 2015) |
| "Glioblastomas, the most common primary brain cancers, respond poorly to current treatment modalities and carry a dismal prognosis." | 5.32 | In vitro and in vivo activity of the nuclear factor-kappaB inhibitor sulfasalazine in human glioblastomas. ( Bentires-Alj, M; Black, PM; Bonif, M; Bours, V; Deprez, M; Erkmen, K; Haddada, H; Jolois, O; Khac, MT; Merville, MP; Robe, PA; Rogister, B, 2004) |
| " A total of twenty patients with progressive malignant glioma despite surgery, radiation therapy and a first line of chemotherapy will be recruited and assigned to four dosage regimen of Sulfasalazine." | 5.12 | A phase 1-2, prospective, double blind, randomized study of the safety and efficacy of Sulfasalazine for the treatment of progressing malignant gliomas: study protocol of [ISRCTN45828668]. ( Albert, A; Bours, V; Chariot, A; Deprez, M; Martin, D; Robe, PA, 2006) |
| "Autocrine and paracrine factors, including glutamate and epidermal growth factor (EGF), are potent inducers of brain tumor cell invasion, a pathological hallmark of malignant gliomas." | 3.88 | Epidermal growth factor receptor promotes glioma progression by regulating xCT and GluN2B-containing N-methyl-d-aspartate-sensitive glutamate receptor signaling. ( Akashi, K; Baba, E; Hirata, Y; Kamenori, S; Mitsuishi, Y; Nagano, O; Okazaki, S; Sampetrean, O; Saya, H; Shintani, S; Suina, K; Takahashi, F; Takahashi, K; Tsuchihashi, K; Yamasaki, J, 2018) |
| " Food and Drug Administration and EMA-approved xCT inhibitor, sulfasalazine (SAS) in gliomas." | 3.83 | Sulfasalazine impacts on ferroptotic cell death and alleviates the tumor microenvironment and glioma-induced brain edema. ( Buchfelder, M; Dörfler, A; Engelhorn, T; Eyüpoglu, IY; Fan, Z; Ghoochani, A; Klucken, J; Minakaki, G; Rauh, M; Savaskan, N; Sehm, T, 2016) |
| " Sulfasalazine which is used clinically to treat Crohn's disease has emerged as a potential inhibitor of NF-kappaB and has shown promising results in two pre-clinical studies to target primary brain tumors, gliomas." | 3.75 | Sulfasalazine inhibits the growth of primary brain tumors independent of nuclear factor-kappaB. ( Chung, WJ; Sontheimer, H, 2009) |
| "Gliomas are primary brain tumors with still poor prognosis for the patients despite a combination of cytoreduction via surgery followed by a radio-chemotherapy." | 1.62 | Chemical hybridization of sulfasalazine and dihydroartemisinin promotes brain tumor cell death. ( Ackermann, A; Buchfelder, M; Çapcı, A; Savaskan, N; Tsogoeva, SB, 2021) |
| "Glioblastoma multiforme is the most aggressive malignant primary brain tumor in adults." | 1.43 | Increased Expression of System xc- in Glioblastoma Confers an Altered Metabolic State and Temozolomide Resistance. ( Aboody, KS; Cassady, K; Cherryholmes, GA; Marinov, GK; Polewski, MD; Reveron-Thornton, RF, 2016) |
| "Glioblastomas (GBMs) are aggressive brain tumors that always recur after radiotherapy." | 1.42 | Drug repurposing: sulfasalazine sensitizes gliomas to gamma knife radiosurgery by blocking cystine uptake through system Xc-, leading to glutathione depletion. ( Dodoo, E; Enger, PØ; Førde, HE; Heggdal, JI; Leiss, L; Netland, IA; Pedersen, PH; Selheim, F; Skeie, BS; Sleire, L; Wang, J, 2015) |
| "Malignant brain tumors are characterized by destructive growth and neuronal cell death making them one of the most devastating diseases." | 1.42 | Neurodegeneration and the Brain Tumor Microenvironment. [corrected]. ( Broggini, T; Buchfelder, M; Eyüpoglu, IY; Fan, Z; Savaskan, NE, 2015) |
| "Celecoxib has been utilized with success in the treatment of several types of cancer, including gliomas." | 1.42 | Celecoxib and LLW-3-6 Reduce Survival of Human Glioma Cells Independently and Synergistically with Sulfasalazine. ( Winfield, LL; Yerokun, T, 2015) |
| "Control of seizures in patients with gliomas is an essential component of clinical management; therefore, understanding the origin of seizures is vital." | 1.38 | Human glioma cells induce hyperexcitability in cortical networks. ( Buckingham, SC; Campbell, SL; Sontheimer, H, 2012) |
| "Sulfasalazine was able to reduce glutathione levels in tumor tissue and slow tumor growth in vivo in a commonly used intracranial xenograft animal model for human gliomas when administered by intraperitoneal injection." | 1.33 | Inhibition of cystine uptake disrupts the growth of primary brain tumors. ( Chung, WJ; Gillespie, GY; Gladson, CL; Hamza, H; Lyons, SA; Nelson, GM; Sontheimer, H, 2005) |
| "Glioblastomas, the most common primary brain cancers, respond poorly to current treatment modalities and carry a dismal prognosis." | 1.32 | In vitro and in vivo activity of the nuclear factor-kappaB inhibitor sulfasalazine in human glioblastomas. ( Bentires-Alj, M; Black, PM; Bonif, M; Bours, V; Deprez, M; Erkmen, K; Haddada, H; Jolois, O; Khac, MT; Merville, MP; Robe, PA; Rogister, B, 2004) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 6 (27.27) | 29.6817 |
| 2010's | 15 (68.18) | 24.3611 |
| 2020's | 1 (4.55) | 2.80 |
| Authors | Studies |
|---|---|
| Ackermann, A | 1 |
| Çapcı, A | 1 |
| Buchfelder, M | 3 |
| Tsogoeva, SB | 1 |
| Savaskan, N | 2 |
| Haryu, S | 1 |
| Saito, R | 1 |
| Jia, W | 1 |
| Shoji, T | 1 |
| Mano, Y | 1 |
| Sato, A | 1 |
| Kanamori, M | 1 |
| Sonoda, Y | 1 |
| Sampetrean, O | 3 |
| Saya, H | 3 |
| Tominaga, T | 1 |
| Garcia, CG | 1 |
| Kahn, SA | 1 |
| Geraldo, LHM | 1 |
| Romano, I | 1 |
| Domith, I | 1 |
| Silva, DCLE | 1 |
| Dos Santos Assunção, F | 1 |
| Ferreira, MJ | 1 |
| Portugal, CC | 1 |
| de Souza, JM | 1 |
| Romão, LF | 1 |
| Netto, ADP | 1 |
| Lima, FRS | 1 |
| Cossenza, M | 1 |
| Suina, K | 1 |
| Tsuchihashi, K | 2 |
| Yamasaki, J | 1 |
| Kamenori, S | 1 |
| Shintani, S | 1 |
| Hirata, Y | 1 |
| Okazaki, S | 2 |
| Baba, E | 2 |
| Akashi, K | 2 |
| Mitsuishi, Y | 1 |
| Takahashi, F | 1 |
| Takahashi, K | 1 |
| Nagano, O | 2 |
| Blecic, S | 1 |
| Rynkowski, M | 1 |
| De Witte, O | 1 |
| Lefranc, F | 1 |
| Chen, L | 1 |
| Li, X | 1 |
| Liu, L | 1 |
| Yu, B | 1 |
| Xue, Y | 1 |
| Liu, Y | 1 |
| Sleire, L | 1 |
| Skeie, BS | 1 |
| Netland, IA | 1 |
| Førde, HE | 1 |
| Dodoo, E | 1 |
| Selheim, F | 1 |
| Leiss, L | 1 |
| Heggdal, JI | 1 |
| Pedersen, PH | 1 |
| Wang, J | 1 |
| Enger, PØ | 1 |
| Thomas, AG | 1 |
| Sattler, R | 1 |
| Tendyke, K | 1 |
| Loiacono, KA | 1 |
| Hansen, H | 1 |
| Sahni, V | 1 |
| Hashizume, Y | 1 |
| Rojas, C | 1 |
| Slusher, BS | 1 |
| Savaskan, NE | 1 |
| Fan, Z | 2 |
| Broggini, T | 1 |
| Eyüpoglu, IY | 2 |
| Yerokun, T | 1 |
| Winfield, LL | 1 |
| Ohmura, M | 1 |
| Ishikawa, M | 1 |
| Onishi, N | 1 |
| Wakimoto, H | 1 |
| Yoshikawa, M | 1 |
| Seishima, R | 1 |
| Iwasaki, Y | 1 |
| Morikawa, T | 1 |
| Abe, S | 1 |
| Takao, A | 1 |
| Shimizu, M | 1 |
| Masuko, T | 1 |
| Nagane, M | 1 |
| Furnari, FB | 1 |
| Akiyama, T | 1 |
| Suematsu, M | 1 |
| Sehm, T | 1 |
| Ghoochani, A | 1 |
| Rauh, M | 1 |
| Engelhorn, T | 1 |
| Minakaki, G | 1 |
| Dörfler, A | 1 |
| Klucken, J | 1 |
| Polewski, MD | 1 |
| Reveron-Thornton, RF | 1 |
| Cherryholmes, GA | 1 |
| Marinov, GK | 1 |
| Cassady, K | 1 |
| Aboody, KS | 1 |
| Nawashiro, H | 1 |
| Chung, WJ | 3 |
| Sontheimer, H | 6 |
| Buckingham, SC | 2 |
| Campbell, SL | 2 |
| Haas, BR | 1 |
| Montana, V | 1 |
| Robel, S | 1 |
| Ogunrinu, T | 2 |
| Bridges, RJ | 1 |
| Robe, PA | 2 |
| Bentires-Alj, M | 1 |
| Bonif, M | 1 |
| Rogister, B | 1 |
| Deprez, M | 2 |
| Haddada, H | 1 |
| Khac, MT | 1 |
| Jolois, O | 1 |
| Erkmen, K | 1 |
| Merville, MP | 1 |
| Black, PM | 1 |
| Bours, V | 2 |
| Lyons, SA | 2 |
| Nelson, GM | 1 |
| Hamza, H | 1 |
| Gladson, CL | 1 |
| Gillespie, GY | 1 |
| Martin, D | 1 |
| Albert, A | 1 |
| Chariot, A | 1 |
| Weaver, AK | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Phase I Trial Combining Sulfasalazine and Gamma Knife Radiosurgery for Recurrent Glioblastoma[NCT04205357] | Phase 1 | 24 participants (Actual) | Interventional | 2020-03-01 | Completed | ||
| Role of Glutamate-mediate Excitotoxicity in Invasion and Progression Processes of Glioblastoma Multiforme[NCT05775458] | 50 participants (Anticipated) | Observational | 2020-06-01 | Recruiting | |||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
1 review available for sulfasalazine and Brain Neoplasms
| Article | Year |
|---|---|
[Glutamate and malignant gliomas, from epilepsia to biological aggressiveness: therapeutic implications].
Topics: Benzodiazepines; Brain Neoplasms; Cell Death; Cell Movement; Cell Proliferation; Dizocilpine Maleate | 2013 |
1 trial available for sulfasalazine and Brain Neoplasms
| Article | Year |
|---|---|
A phase 1-2, prospective, double blind, randomized study of the safety and efficacy of Sulfasalazine for the treatment of progressing malignant gliomas: study protocol of [ISRCTN45828668].
Topics: Administration, Oral; Adult; Aged; Anti-Inflammatory Agents, Non-Steroidal; Brain Neoplasms; Disease | 2006 |
20 other studies available for sulfasalazine and Brain Neoplasms
| Article | Year |
|---|---|
Chemical hybridization of sulfasalazine and dihydroartemisinin promotes brain tumor cell death.
Topics: Antineoplastic Agents; Artemisinins; Brain Neoplasms; Cell Cycle; Cell Death; Cell Line, Tumor; Glio | 2021 |
Convection-enhanced delivery of sulfasalazine prolongs survival in a glioma stem cell brain tumor model.
Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Antineoplastic Agents; Apoptosis; Brain Chemistry; | 2018 |
Combination Therapy with Sulfasalazine and Valproic Acid Promotes Human Glioblastoma Cell Death Through Imbalance of the Intracellular Oxidative Response.
Topics: Amino Acid Transport System y+; Animals; Ascorbic Acid; Brain Neoplasms; Cell Death; Cell Line, Tumo | 2018 |
Epidermal growth factor receptor promotes glioma progression by regulating xCT and GluN2B-containing N-methyl-d-aspartate-sensitive glutamate receptor signaling.
Topics: Amino Acid Transport System y+; Animals; Brain Neoplasms; Cell Line, Tumor; Cell Movement; Cell Prol | 2018 |
Erastin sensitizes glioblastoma cells to temozolomide by restraining xCT and cystathionine-γ-lyase function.
Topics: Amino Acid Transport System y+; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocol | 2015 |
Drug repurposing: sulfasalazine sensitizes gliomas to gamma knife radiosurgery by blocking cystine uptake through system Xc-, leading to glutathione depletion.
Topics: Amino Acid Transport System y+; Animals; Brain Neoplasms; Cell Line, Tumor; Cystine; DNA; Drug Repos | 2015 |
High-Throughput Assay Development for Cystine-Glutamate Antiporter (xc-) Highlights Faster Cystine Uptake than Glutamate Release in Glioma Cells.
Topics: Amino Acid Transport System y+; Benzoates; Brain Neoplasms; Cell Line, Tumor; Cystine; Databases, Ch | 2015 |
Neurodegeneration and the Brain Tumor Microenvironment. [corrected].
Topics: Amino Acid Transport Systems; Animals; Anti-Inflammatory Agents, Non-Steroidal; Brain Neoplasms; Glu | 2015 |
Celecoxib and LLW-3-6 Reduce Survival of Human Glioma Cells Independently and Synergistically with Sulfasalazine.
Topics: Antineoplastic Combined Chemotherapy Protocols; Benzimidazoles; Brain Neoplasms; Celecoxib; Cell Lin | 2015 |
The EGF Receptor Promotes the Malignant Potential of Glioma by Regulating Amino Acid Transport System xc(-).
Topics: Amino Acid Transport System y+; Animals; Antioxidants; Apoptosis; Brain Neoplasms; Cell Membrane; Ce | 2016 |
Sulfasalazine impacts on ferroptotic cell death and alleviates the tumor microenvironment and glioma-induced brain edema.
Topics: Amino Acid Transport System X-AG; Animals; Animals, Newborn; Anti-Inflammatory Agents, Non-Steroidal | 2016 |
Increased Expression of System xc- in Glioblastoma Confers an Altered Metabolic State and Temozolomide Resistance.
Topics: Amino Acid Transport System y+; Animals; Brain Neoplasms; Cell Line, Tumor; Cell Proliferation; Cell | 2016 |
Idiopathic intracranial hypertension associated with sulphasalazine treatment.
Topics: Amino Acid Transport System y+; Anti-Inflammatory Agents, Non-Steroidal; Brain Neoplasms; Glioma; Hu | 2008 |
Sulfasalazine inhibits the growth of primary brain tumors independent of nuclear factor-kappaB.
Topics: Amino Acid Transport System y+; Animals; Antineoplastic Agents; Brain Neoplasms; Cell Death; Cell Li | 2009 |
Glutamate release by primary brain tumors induces epileptic activity.
Topics: Amino Acid Transport System y+; Analysis of Variance; Animals; Brain Neoplasms; Cell Transplantation | 2011 |
Sulfasalazine for brain cancer fits.
Topics: Amino Acid Transport System y+; Animals; Anticonvulsants; Antineoplastic Agents; Brain Neoplasms; Ep | 2012 |
Human glioma cells induce hyperexcitability in cortical networks.
Topics: Action Potentials; Animals; Brain; Brain Neoplasms; Disease Models, Animal; Electrophysiology; Femal | 2012 |
In vitro and in vivo activity of the nuclear factor-kappaB inhibitor sulfasalazine in human glioblastomas.
Topics: Anti-Inflammatory Agents, Non-Steroidal; Antineoplastic Agents; Brain Neoplasms; Cell Line, Tumor; G | 2004 |
Inhibition of cystine uptake disrupts the growth of primary brain tumors.
Topics: Amino Acid Transport Systems; Animals; Apoptosis; Benzoates; Brain Neoplasms; Caspases; Cell Divisio | 2005 |
Inhibition of cystine uptake disrupts the growth of primary brain tumors.
Topics: Amino Acid Transport Systems; Animals; Apoptosis; Benzoates; Brain Neoplasms; Caspases; Cell Divisio | 2005 |
Inhibition of cystine uptake disrupts the growth of primary brain tumors.
Topics: Amino Acid Transport Systems; Animals; Apoptosis; Benzoates; Brain Neoplasms; Caspases; Cell Divisio | 2005 |
Inhibition of cystine uptake disrupts the growth of primary brain tumors.
Topics: Amino Acid Transport Systems; Animals; Apoptosis; Benzoates; Brain Neoplasms; Caspases; Cell Divisio | 2005 |
Autocrine glutamate signaling promotes glioma cell invasion.
Topics: Amino Acid Transport System y+; Animals; Brain Neoplasms; Calcium; Cell Line, Tumor; Cell Movement; | 2007 |