benzyl isothiocyanate has been researched along with Neoplasms in 8 studies
benzyl isothiocyanate: inhibits carcinogen-induced neoplasia; structure in Negwer, 5th ed, #715; also promotes urinary bladder carcinoma
Neoplasms: New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
| Excerpt | Relevance | Reference |
|---|---|---|
| " Benzyl isothiocyanate (BITC) showed the inhibitory effect of tumor and AGPS activity, therefore, we screened a group of small molecular compound based on BITC by computer-aid design targeting AGPS and the results showed that the derivants could suppress the proliferation, the expression of tumor related genes such as survivin and Bcl-2, and the level of ether lipids such as lysophosphatidic acid ether (LPAe) and platelet activating factor ether (PAFe); however, the activity of caspase-3/8 was improved in glioma U87MG and hepatic carcinoma HepG2 cells in vitro." | 3.81 | Inhibitory effect of isothiocyanate derivant targeting AGPS by computer-aid drug design on proliferation of glioma and hepatic carcinoma cells. ( Li, WM; Xue, J; Yang, P; Zhang, L; Zhao, M; Zhu, Y, 2015) |
| "This review highlights the anticancer efficacy of BITC through modulation of various signaling pathways involved in apoptosis, cell proliferation, cell cycle arrest, metastasis, angiogenesis, autophagy and the effects of BITC in combination with other drugs." | 2.72 | Anticancer activities of dietary benzyl isothiocyanate: A comprehensive review. ( Dinh, TN; Khaw, KY; Ong, YS; Parat, MO, 2021) |
| "The anti-cancer activities of BITC have been studied for decades." | 1.56 | Suppression of multiple processes relevant to cancer progression by benzyl isothiocyanate may result from the inhibition of Aurora A kinase activity. ( Chang, CJ; Chang, MY; Hsieh, YJ; Yu, TT, 2020) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 1 (12.50) | 18.2507 |
| 2000's | 2 (25.00) | 29.6817 |
| 2010's | 3 (37.50) | 24.3611 |
| 2020's | 2 (25.00) | 2.80 |
| Authors | Studies |
|---|---|
| Lin, R | 1 |
| Elf, S | 1 |
| Shan, C | 1 |
| Kang, HB | 1 |
| Ji, Q | 1 |
| Zhou, L | 1 |
| Hitosugi, T | 1 |
| Zhang, L | 2 |
| Zhang, S | 1 |
| Seo, JH | 1 |
| Xie, J | 1 |
| Tucker, M | 1 |
| Gu, TL | 1 |
| Sudderth, J | 1 |
| Jiang, L | 1 |
| Mitsche, M | 1 |
| DeBerardinis, RJ | 1 |
| Wu, S | 1 |
| Li, Y | 1 |
| Mao, H | 1 |
| Chen, PR | 1 |
| Wang, D | 1 |
| Chen, GZ | 1 |
| Hurwitz, SJ | 1 |
| Lonial, S | 1 |
| Arellano, ML | 1 |
| Khoury, HJ | 1 |
| Khuri, FR | 1 |
| Lee, BH | 1 |
| Lei, Q | 1 |
| Brat, DJ | 1 |
| Ye, K | 1 |
| Boggon, TJ | 1 |
| He, C | 1 |
| Kang, S | 1 |
| Fan, J | 1 |
| Chen, J | 1 |
| Yu, TT | 1 |
| Chang, MY | 1 |
| Hsieh, YJ | 1 |
| Chang, CJ | 1 |
| Dinh, TN | 1 |
| Parat, MO | 1 |
| Ong, YS | 1 |
| Khaw, KY | 1 |
| Janczewski, Ł | 1 |
| Psurski, M | 1 |
| Świtalska, M | 1 |
| Gajda, A | 1 |
| Goszczyński, TM | 1 |
| Oleksyszyn, J | 1 |
| Wietrzyk, J | 1 |
| Gajda, T | 1 |
| Zhu, Y | 1 |
| Li, WM | 1 |
| Xue, J | 1 |
| Zhao, M | 1 |
| Yang, P | 1 |
| Basu, A | 1 |
| Haldar, S | 1 |
| Miyoshi, N | 1 |
| Takabayashi, S | 1 |
| Osawa, T | 1 |
| Nakamura, Y | 1 |
| Wattenberg, LW | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Randomized Trial of PEITC as a Modifier of NNK Metabolism in Smokers[NCT00691132] | Phase 2 | 107 participants (Actual) | Interventional | 2009-02-28 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
% Difference in ratio of urinary [pyridine-D4]hydroxy acid : total [pyridine-D4]NNAL while on PEITC compared to while on Placebo ((PEITC - Placebo) / PEITC) x 100% (NCT00691132)
Timeframe: After 5 days of treatment
| Intervention | percentage of change in ratio (Geometric Mean) |
|---|---|
| GSTM1 and GSTT1 Both Genes Null | -15.6 |
| GSTM1 and GSTT1 Only One Gene Present | -3.1 |
| GSTM1 and GSTT1 Both Genes Present | -9.4 |
(NCT00691132)
Timeframe: After 5 days of treatment
| Intervention | nmol/mg creatinine (Geometric Mean) | |
|---|---|---|
| PEITC-NAC | Total ITC | |
| GSTM1 and GSTT1 Both Genes Null | 85.4 | 59.6 |
| GSTM1 and GSTT1 Both Genes Present | 56.9 | 41.5 |
| GSTM1 and GSTT1 Only One Gene Present | 60.5 | 47.1 |
Measured by high-performance liquid chromatography (HPLC). The aim is to determine the possible differential effects of GSTM1 genotype on PEITC excretion, using the method of Chung et al. The method will result in quantitative recovery of the PEITC-NAC. (NCT00691132)
Timeframe: After 5 days of PEITC treatment
| Intervention | nmol/mg creatinine (Geometric Mean) | |
|---|---|---|
| PEITC-NAC | Total ITC | |
| GSTM1 Null | 71.7 | 53.7 |
| GSTM1 Present | 54.8 | 40.5 |
Measured by high-performance liquid chromatography (HPLC). The aim is to determine the possible differential effects of GSTT1 genotype on PEITC excretion, using the method of Chung et al. The method will result in quantitative recovery of the PEITC-NAC. (NCT00691132)
Timeframe: After 5 days of treatment
| Intervention | nmol/mg creatinine (Geometric Mean) | |
|---|---|---|
| PEITC-NAC | Total ITC | |
| GSTT1 Null | 67.1 | 49.2 |
| GSTT1 Present | 60.4 | 45.1 |
The ratio of urinary [pyridine-D4]hydroxy acid : total [pyridine-D4]NNAL will be measured. This ratio is not expected to be influenced by the number of cigarettes smoked per day, or smoking topography. (NCT00691132)
Timeframe: After 5 days of treatment
| Intervention | pmol/mg creatinine (Geometric Mean) | ||
|---|---|---|---|
| Total [pyridine-D4]NNAL | [pyridine-D4]Hydroxy acid | [pyridine-D4]Hydroxy acid :[pyridine-D4]total NNAL | |
| PEITC | 0.366 | 0.140 | 0.420 |
| Placebo | 0.366 | 0.150 | 0.455 |
Urinary levels of Total ITC and PEITC-NAC by treatment sequence groups and treatment period. (NCT00691132)
Timeframe: 2 periods, 5 days each on PEITC or Placebo, with washout week between
| Intervention | pmol/mg creatinine (Geometric Mean) | |||
|---|---|---|---|---|
| Period 1 - Total ITC | Period 2 - Total ITC | Period 1 - PEITC-NAC | Period 2 - PEITC-NAC | |
| PEITC-Placebo | 42.8 | 0.28 | 56.7 | 0.36 |
| Placebo - PEITC | 0.36 | 49.7 | 0.27 | 68.1 |
3 reviews available for benzyl isothiocyanate and Neoplasms
| Article | Year |
|---|---|
6-Phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumour growth by inhibiting LKB1-AMPK signalling.
Topics: AMP-Activated Protein Kinase Kinases; AMP-Activated Protein Kinases; Humans; Lipogenesis; Neoplasms; | 2015 |
Anticancer activities of dietary benzyl isothiocyanate: A comprehensive review.
Topics: Animals; Antineoplastic Agents; Apoptosis; Autophagy; Cell Cycle; Cell Proliferation; Diet; Humans; | 2021 |
Inhibition of carcinogenesis by minor anutrient constituents of the diet.
Topics: Allium; Animals; Citrus; Diet; Disulfiram; Humans; Isothiocyanates; Neoplasms; Terpenes; Thiocyanate | 1990 |
5 other studies available for benzyl isothiocyanate and Neoplasms
| Article | Year |
|---|---|
Suppression of multiple processes relevant to cancer progression by benzyl isothiocyanate may result from the inhibition of Aurora A kinase activity.
Topics: Antineoplastic Agents; Apoptosis; Aurora Kinase A; Cell Line, Tumor; Disease Progression; G2 Phase C | 2020 |
Design, Synthesis, and Evaluation of ω-(Isothiocyanato)alkylphosphinates and Phosphine Oxides as Antiproliferative Agents.
Topics: Animals; Antineoplastic Agents; Apoptosis; Cell Cycle Checkpoints; Cell Line, Tumor; Cell Proliferat | 2018 |
Inhibitory effect of isothiocyanate derivant targeting AGPS by computer-aid drug design on proliferation of glioma and hepatic carcinoma cells.
Topics: Alkyl and Aryl Transferases; Antineoplastic Agents; Blotting, Western; Carcinoma, Hepatocellular; Ce | 2015 |
Dietary isothiocyanate mediated apoptosis of human cancer cells is associated with Bcl-xL phosphorylation.
Topics: Apoptosis; bcl-X Protein; Caspase 8; Caspase 9; Cell Line, Tumor; Cell Nucleus; Cell Separation; Enz | 2008 |
Benzyl isothiocyanate inhibits excessive superoxide generation in inflammatory leukocytes: implication for prevention against inflammation-related carcinogenesis.
Topics: Anticarcinogenic Agents; Cell Differentiation; Glutathione; HL-60 Cells; Humans; Inflammation; Isoth | 2004 |