niacinamide has been researched along with Neuroendocrine Tumors in 14 studies
nicotinamide : A pyridinecarboxamide that is pyridine in which the hydrogen at position 3 is replaced by a carboxamide group.
Neuroendocrine Tumors: Tumors whose cells possess secretory granules and originate from the neuroectoderm, i.e., the cells of the ectoblast or epiblast that program the neuroendocrine system. Common properties across most neuroendocrine tumors include ectopic hormone production (often via APUD CELLS), the presence of tumor-associated antigens, and isozyme composition.
| Excerpt | Relevance | Reference |
|---|---|---|
| "Sorafenib and everolimus are both active against neuroendocrine tumors (NET)." | 9.17 | Phase I study of sorafenib in combination with everolimus (RAD001) in patients with advanced neuroendocrine tumors. ( Chan, JA; Jackson, N; Kulke, MH; Malinowski, P; Mayer, RJ; Regan, E, 2013) |
| "Preclinical trials of a mouse model of pancreatic neuroendocrine tumors (PNET) were conducted to determine whether dual FGF/VEGF pathway inhibition with brivanib can improve first-line efficacy in comparison with VEGF inhibitors lacking fibroblast growth factor (FGF)-inhibitory activity and to characterize second-line brivanib activity before and after the onset of evasive resistance to VEGF-selective therapy." | 7.77 | Brivanib, a dual FGF/VEGF inhibitor, is active both first and second line against mouse pancreatic neuroendocrine tumors developing adaptive/evasive resistance to VEGF inhibition. ( Allen, E; Hanahan, D; Walters, IB, 2011) |
| "Sorafenib and everolimus are both active against neuroendocrine tumors (NET)." | 5.17 | Phase I study of sorafenib in combination with everolimus (RAD001) in patients with advanced neuroendocrine tumors. ( Chan, JA; Jackson, N; Kulke, MH; Malinowski, P; Mayer, RJ; Regan, E, 2013) |
| " In endocrine tumors, several molecules have demonstrated efficacy in terms of progression free survival during phase III trials such as vandetanib and cabozantinib in medullary thyroid carcinoma, sorafenib in differentiated thyroid carcinoma and everolimus or sunitinib for pancreatic neuroendocrine tumors." | 4.89 | [Targeted therapies, prognostic and predictive factors in endocrine oncology]. ( Baudin, E; Borson-Chazot, F; Hescot, S; Lombès, M, 2013) |
| "Preclinical trials of a mouse model of pancreatic neuroendocrine tumors (PNET) were conducted to determine whether dual FGF/VEGF pathway inhibition with brivanib can improve first-line efficacy in comparison with VEGF inhibitors lacking fibroblast growth factor (FGF)-inhibitory activity and to characterize second-line brivanib activity before and after the onset of evasive resistance to VEGF-selective therapy." | 3.77 | Brivanib, a dual FGF/VEGF inhibitor, is active both first and second line against mouse pancreatic neuroendocrine tumors developing adaptive/evasive resistance to VEGF inhibition. ( Allen, E; Hanahan, D; Walters, IB, 2011) |
| "Both the soft tissue sarcomas and the neuroendocrine tumors are rare diseases." | 2.52 | [Molecular targeted drugs for soft tissue sarcoma and neuroendocrine tumor]. ( Kato, S, 2015) |
| "The paucity of effective treatment in neuroendocrine tumors (NETs) encouraged us to investigate the therapeutic value of artesunate (ART) promised by its inhibitory effect against various tumors and broad safety profile." | 1.56 | Multiple modes of cell death in neuroendocrine tumors induced by artesunate. ( Böckers, M; Dawood, M; Efferth, T; Fottner, C; Klauck, SM; Weber, MM; Yan, G, 2020) |
| "Sorafenib is considered to be a potent inhibitor of tumor angiogenesis and neovascularization in various solid tumors." | 1.38 | Sorafenib inhibits tumor growth and improves survival in a transgenic mouse model of pancreatic islet cell tumors. ( Bartsch, DK; Buchholz, M; Fendrich, V; Holler, JP; Maschuw, K; Rehm, J; Slater, EP; Waldmann, J, 2012) |
| "Sorafenib was continued despite two episodes of grade 3 skin toxicity; it delayed tumor progression compared to the previous immunotherapy and chemotherapy." | 1.37 | Pancreatic endocrine tumors: a report on a patient treated with sorafenib. ( Hong, SH; Jeon, EK; Jeong, HK; Ko, YH; Lee, SL; Roh, SY; Shin, OR; Won, HS, 2011) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 1 (7.14) | 29.6817 |
| 2010's | 12 (85.71) | 24.3611 |
| 2020's | 1 (7.14) | 2.80 |
| Authors | Studies |
|---|---|
| Yan, G | 1 |
| Dawood, M | 1 |
| Böckers, M | 1 |
| Klauck, SM | 1 |
| Fottner, C | 1 |
| Weber, MM | 1 |
| Efferth, T | 1 |
| Kato, Y | 1 |
| Masuno, K | 1 |
| Fujisawa, K | 1 |
| Tsuchiya, N | 1 |
| Torii, M | 1 |
| Hishikawa, A | 1 |
| Izawa, T | 1 |
| Kuwamura, M | 1 |
| Yamate, J | 1 |
| Lubner, S | 1 |
| Feng, Y | 1 |
| Mulcahy, M | 1 |
| O'Dwyer, P | 1 |
| Giang, GY | 1 |
| Hinshaw, JL | 1 |
| Deming, D | 1 |
| Klein, L | 1 |
| Teitelbaum, U | 1 |
| Payne, J | 1 |
| Engstrom, P | 1 |
| Stella, P | 1 |
| Meropol, N | 1 |
| Benson, A | 1 |
| Quintela-Fandino, M | 1 |
| Krzyzanowska, M | 1 |
| Duncan, G | 1 |
| Young, A | 1 |
| Moore, MJ | 1 |
| Chen, EX | 1 |
| Stathis, A | 1 |
| Colomer, R | 1 |
| Petronis, J | 1 |
| Grewal, M | 1 |
| Webster, S | 1 |
| Wang, L | 1 |
| Siu, LL | 1 |
| Chan, JA | 1 |
| Mayer, RJ | 1 |
| Jackson, N | 1 |
| Malinowski, P | 1 |
| Regan, E | 1 |
| Kulke, MH | 1 |
| Castellano, D | 1 |
| Capdevila, J | 1 |
| Sastre, J | 1 |
| Alonso, V | 1 |
| Llanos, M | 1 |
| García-Carbonero, R | 1 |
| Manzano Mozo, JL | 1 |
| Sevilla, I | 1 |
| Durán, I | 1 |
| Salazar, R | 1 |
| Hescot, S | 1 |
| Baudin, E | 1 |
| Borson-Chazot, F | 1 |
| Lombès, M | 1 |
| Kato, S | 1 |
| Bouma, G | 1 |
| van Faassen, M | 1 |
| Kats-Ugurlu, G | 1 |
| de Vries, EG | 1 |
| Kema, IP | 1 |
| Walenkamp, AM | 1 |
| Allen, E | 1 |
| Walters, IB | 1 |
| Hanahan, D | 1 |
| Jeong, HK | 1 |
| Roh, SY | 1 |
| Hong, SH | 1 |
| Won, HS | 1 |
| Jeon, EK | 1 |
| Shin, OR | 1 |
| Lee, SL | 1 |
| Ko, YH | 1 |
| Naraev, BG | 1 |
| Strosberg, JR | 1 |
| Halfdanarson, TR | 1 |
| Fendrich, V | 2 |
| Maschuw, K | 1 |
| Rehm, J | 1 |
| Buchholz, M | 1 |
| Holler, JP | 1 |
| Slater, EP | 1 |
| Bartsch, DK | 2 |
| Waldmann, J | 1 |
| Karhoff, D | 1 |
| Sauer, S | 1 |
| Schrader, J | 1 |
| Arnold, R | 1 |
| Hörsch, D | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Phase II Clinical and Biologic Study of AMG 706 and Octreotide in Patients With Low-Grade Neuroendocrine Tumors[NCT00427349] | Phase 2 | 46 participants (Actual) | Interventional | 2008-11-07 | Completed | ||
| Phase I Study of Sorafenib in Combination With RAD001 in Patients With Advanced Neuroendocrine Tumors[NCT00942682] | Phase 1 | 21 participants (Actual) | Interventional | 2009-07-31 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Four-month progression-free survival (PFS) rate is defined as number of patients who are still progression free at 4 months after study entry divided by number of eligible and treated patients enrolled to the study. Progression is evaluated using the Response Evaluation Criteria in Solid Tumors (RECIST) version 1.0, and defined as at least a 20% increase in the sum of the longest diameters of target lesions, taking as reference the smallest sum longest diameter recorded since the baseline measurements, or the appearance of one or more new lesion(s), or unequivocal progression of existing non-target lesions. (NCT00427349)
Timeframe: assessed every 4 weeks while on treatment and at three months post-treatment for participants treated for one cycle, up to month four
| Intervention | percentage of participants (Number) |
|---|---|
| AMG 706+Octreotide | 78.5 |
Tumor response was evaluated using the Response Evaluation Criteria in Solid Tumors (RECIST) version 1.0. Objective response rate is defined as number of patients with complete response (CR) or partial response (PR) divided by the total number of analyzable patients. CR is defined as complete disappearance of all tumor lesions, and partial response is defined as at least a 30% decrease in the sum of the longest diameters of target lesions, taking as reference the baseline sum longest diameter. (NCT00427349)
Timeframe: assessed every 8 weeks while on treatment, and frequency of tumor measurements during follow-up were determined by the treating physician, assessed up to 5 years
| Intervention | percentage of participants (Number) |
|---|---|
| AMG 706+Octreotide | 13.6 |
Overall survival (OS) is defined as the time from registration until death (event), or censored at last date known alive. OS was estimated using the Kaplan-Meier method , with 95% confidence intervals calculated using Greenwood's formula (NCT00427349)
Timeframe: assessed every 3 months if patient is < 2 years from study entry, then every 6 months up to 5 years
| Intervention | months (Median) |
|---|---|
| AMG 706+Octreotide | 27.5 |
3 reviews available for niacinamide and Neuroendocrine Tumors
| Article | Year |
|---|---|
[Targeted therapies, prognostic and predictive factors in endocrine oncology].
Topics: Antineoplastic Agents; Carcinoma, Neuroendocrine; Clinical Trials, Phase III as Topic; Disease-Free | 2013 |
[Molecular targeted drugs for soft tissue sarcoma and neuroendocrine tumor].
Topics: Antibodies, Monoclonal, Humanized; Benzamides; Denosumab; Drug Discovery; Everolimus; Gastrointestin | 2015 |
Current status and perspectives of targeted therapy in well-differentiated neuroendocrine tumors.
Topics: Antineoplastic Agents; Benzenesulfonates; Cell Differentiation; ErbB Receptors; Everolimus; Histone | 2012 |
3 trials available for niacinamide and Neuroendocrine Tumors
| Article | Year |
|---|---|
In vivo RAF signal transduction as a potential biomarker for sorafenib efficacy in patients with neuroendocrine tumours.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Biomarkers, Tumor; C | 2013 |
Phase I study of sorafenib in combination with everolimus (RAD001) in patients with advanced neuroendocrine tumors.
Topics: Antineoplastic Combined Chemotherapy Protocols; Disease Progression; Everolimus; Feasibility Studies | 2013 |
Sorafenib and bevacizumab combination targeted therapy in advanced neuroendocrine tumour: a phase II study of Spanish Neuroendocrine Tumour Group (GETNE0801).
Topics: Adult; Aged; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Protocols; Asth | 2013 |
8 other studies available for niacinamide and Neuroendocrine Tumors
| Article | Year |
|---|---|
Multiple modes of cell death in neuroendocrine tumors induced by artesunate.
Topics: Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Artesunate; Autoph | 2020 |
Characterization of pancreatic islet cell tumors and renal tumors induced by a combined treatment of streptozotocin and nicotinamide in male SD rats.
Topics: Adenoma, Islet Cell; Animals; Antibiotics, Antineoplastic; Disease Models, Animal; Kidney Neoplasms; | 2017 |
E4206: AMG 706 and Octreotide in Patients with Low-Grade Neuroendocrine Tumors.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Agents, Hormonal; Humans; Indoles; Middle Aged; Neuro | 2018 |
Niacin (Vitamin B3) Supplementation in Patients with Serotonin-Producing Neuroendocrine Tumor.
Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Female; Humans; Male; Middle Aged; Neuroendocr | 2016 |
Brivanib, a dual FGF/VEGF inhibitor, is active both first and second line against mouse pancreatic neuroendocrine tumors developing adaptive/evasive resistance to VEGF inhibition.
Topics: Alanine; Animals; Antibodies, Monoclonal; Antineoplastic Combined Chemotherapy Protocols; Benzenesul | 2011 |
Pancreatic endocrine tumors: a report on a patient treated with sorafenib.
Topics: Adult; Antineoplastic Agents; Benzenesulfonates; Humans; Liver Neoplasms; Male; Neuroendocrine Tumor | 2011 |
Sorafenib inhibits tumor growth and improves survival in a transgenic mouse model of pancreatic islet cell tumors.
Topics: Adenoma, Islet Cell; Animals; Antigens, Polyomavirus Transforming; Apoptosis; Disease Progression; F | 2012 |
Rap1/B-Raf signaling is activated in neuroendocrine tumors of the digestive tract and Raf kinase inhibition constitutes a putative therapeutic target.
Topics: Benzenesulfonates; Digestive System Neoplasms; Dose-Response Relationship, Drug; Enzyme Activation; | 2007 |