spermine has been researched along with Colorectal Cancer in 24 studies
| Excerpt | Relevance | Reference |
|---|---|---|
| "N (1),N (12)-Diacetylspermine (DiAcSpm) is a tumor marker featured by increase in the urine of patients with cancers, including early colorectal cancer, but where and how DiAcSpm is made remains unclear." | 7.79 | Increase of N1, N12-diacetylspermine in tissues from colorectal cancer and its liver metastasis. ( Hiramatsu, K; Horiguchi, S; Iwasaki, K; Kawakita, M; Kobayashi, M; Koizumi, K; Kuwata, G; Moriya, SS; Samejima, K; Takahashi, K, 2013) |
| "N(1),N(12)-diacetylspermine (DiAcSpm) in the urine of colorectal and breast cancer patients was examined to establish its usefulness as a novel diagnostic tool for detecting these cancers at clinically early stages." | 7.73 | N(1),N(12)-Diacetylspermine as a sensitive and specific novel marker for early- and late-stage colorectal and breast cancers. ( Hiramatsu, K; Imajo, M; Kawaguchi, M; Kawakita, M; Matsumoto, H; Miyamoto, H; Mori, T; Takahashi, K; Tamamori, Y; Tanaka, C; Tanaka, S; Toi, M; Yamaguchi, T, 2005) |
| "We analyzed the significance of the measurement of urine di-acetyl spermine (DiAcSpm) as a cancer marker for colorectal cancer treatment." | 7.72 | [The significance of urine di-acetyl spermine level as a cancer marker for colorectal cancer]. ( Hiramatsu, K; Kawakita, M; Matsumoto, H; Miyamoto, H; Mori, T; Takahashi, K; Tamamori, Y; Yamaguchi, T, 2004) |
| "In patients with colorectal cancer, the sensitivity of DiAcSpm and DiAcSpd was 69." | 5.36 | Evaluating the utility of N1,N12-diacetylspermine and N1,N8-diacetylspermidine in urine as tumor markers for breast and colorectal cancers. ( Hirata, K; Kameshima, H; Kuribayashi, K; Nishidate, T; Ohe, Y; Tsuji, N; Umemori, Y; Watanabe, N, 2010) |
| "N (1),N (12)-Diacetylspermine (DiAcSpm) is a tumor marker featured by increase in the urine of patients with cancers, including early colorectal cancer, but where and how DiAcSpm is made remains unclear." | 3.79 | Increase of N1, N12-diacetylspermine in tissues from colorectal cancer and its liver metastasis. ( Hiramatsu, K; Horiguchi, S; Iwasaki, K; Kawakita, M; Kobayashi, M; Koizumi, K; Kuwata, G; Moriya, SS; Samejima, K; Takahashi, K, 2013) |
| "To construct a recombinant adenovirus that can express human spermidine/ spermine N1-acetyltransferase (SSAT) and detect its inhibitory effect on colorectal cancer cell growth in vitro." | 3.74 | Adenovirus-mediated expression of SSAT inhibits colorectal cancer cell growth in vitro. ( Liu, B; Liu, XX; Sun, H; Wang, W; Xu, CX; Yan, YF; Yang, YP, 2008) |
| "N(1),N(12)-diacetylspermine (DiAcSpm) in the urine of colorectal and breast cancer patients was examined to establish its usefulness as a novel diagnostic tool for detecting these cancers at clinically early stages." | 3.73 | N(1),N(12)-Diacetylspermine as a sensitive and specific novel marker for early- and late-stage colorectal and breast cancers. ( Hiramatsu, K; Imajo, M; Kawaguchi, M; Kawakita, M; Matsumoto, H; Miyamoto, H; Mori, T; Takahashi, K; Tamamori, Y; Tanaka, C; Tanaka, S; Toi, M; Yamaguchi, T, 2005) |
| "Naproxen, sulindac and salicylate, three NSAIDs (non-steroidal anti-inflammatory drugs), were cytotoxic to human colorectal cancer cells in culture." | 3.72 | Polyamines reverse non-steroidal anti-inflammatory drug-induced toxicity in human colorectal cancer cells. ( Hughes, A; Smith, NI; Wallace, HM, 2003) |
| "We analyzed the significance of the measurement of urine di-acetyl spermine (DiAcSpm) as a cancer marker for colorectal cancer treatment." | 3.72 | [The significance of urine di-acetyl spermine level as a cancer marker for colorectal cancer]. ( Hiramatsu, K; Kawakita, M; Matsumoto, H; Miyamoto, H; Mori, T; Takahashi, K; Tamamori, Y; Yamaguchi, T, 2004) |
| "We assayed the estrogen receptors and polyamine levels (putrescine, spermidine and spermine) in the neoplastic and "normal" surrounding tissue of patients with colorectal cancer." | 3.68 | Polyamines and estrogen-receptor concentrations in human colorectal carcinomas. ( Cavallini, A; Di Leo, A; Guerra, V; Lacatena, M; Lantone, G; Linsalata, M; Messa, C; Notarnicola, M; Russo, F, 1992) |
| "We assayed the estrogen and progesterone cytosolic receptors by using the enzyme immunoassay method, the epidermal growth factor (EGF) cell surface receptors by using 125I-labeled hormone, and the levels of polyamines (putrescine, spermine, and spermidine) by using a high-pressure liquid chromatography (HPLC) procedure in neoplastic and surrounding normal tissues of patients with colorectal cancer." | 3.68 | Sex steroid hormone receptors, epidermal growth factor receptor, and polyamines in human colorectal cancer. ( Cavallini, A; Di Leo, A; Linsalata, M; Messa, C; Russo, F, 1992) |
| "Chemoprevention is the long-term use of different chemical agents, both synthetic and natural, to prevent or delay the onset of disease." | 2.50 | Pharmacological and dietary agents for colorectal cancer chemoprevention: effects on polyamine metabolism (review). ( Linsalata, M; Orlando, A; Russo, F, 2014) |
| "Spermine was conjugated to oxidized dextran by reductive amination process to obtain cationized dextran, so-called dextran-spermine, in order to prepare CXCR4-siRNAs/dextran-spermine nanoparticles." | 1.38 | Cationized dextran nanoparticle-encapsulated CXCR4-siRNA enhanced correlation between CXCR4 expression and serum alkaline phosphatase in a mouse model of colorectal cancer. ( Abedini, F; Chong, PP; Domb, AJ; Farber, IY; Hong, PD; Hosseinkhani, H; Ismail, M; Omar, AR; Yu, DS, 2012) |
| "As many cancer cell types including pancreatic cancer cells express high levels of polyamines, the possibility to develop anti-tumor strategies to deplete polyamine pools has drawn considerable attention in recent years." | 1.37 | Role of polyamines in determining the cellular response to chemotherapeutic agents: modulation of protein kinase CK2 expression and activity. ( Guerra, B; Issinger, OG; Kreutzer, JN; Lech, K; Olsen, BB, 2011) |
| "In patients with colorectal cancer, the sensitivity of DiAcSpm and DiAcSpd was 69." | 1.36 | Evaluating the utility of N1,N12-diacetylspermine and N1,N8-diacetylspermidine in urine as tumor markers for breast and colorectal cancers. ( Hirata, K; Kameshima, H; Kuribayashi, K; Nishidate, T; Ohe, Y; Tsuji, N; Umemori, Y; Watanabe, N, 2010) |
| "Mean putrescine content was 1." | 1.28 | Colonic polyamine content and ornithine decarboxylase activity as markers for adenomas. ( Bartholomew, MJ; McGarrity, TJ; Pegg, AE; Peiffer, LP, 1990) |
| "Spermidine content was also significantly increased in the distal colon of EtOH-treated animals compared to baseline values." | 1.27 | The effects of chronic ethanol administration on polyamine content during dimethylhydrazine-induced colorectal carcinogenesis in the rat. ( Colony, PC; McGarrity, TJ; Pegg, AE; Peiffer, LP, 1988) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 1 (4.17) | 18.7374 |
| 1990's | 7 (29.17) | 18.2507 |
| 2000's | 6 (25.00) | 29.6817 |
| 2010's | 9 (37.50) | 24.3611 |
| 2020's | 1 (4.17) | 2.80 |
| Authors | Studies |
|---|---|
| Coradduzza, D | 1 |
| Arru, C | 1 |
| Culeddu, N | 1 |
| Congiargiu, A | 1 |
| Azara, EG | 1 |
| Scanu, AM | 1 |
| Zinellu, A | 1 |
| Muroni, MR | 1 |
| Rallo, V | 1 |
| Medici, S | 1 |
| Carru, C | 1 |
| Angius, A | 1 |
| De Miglio, MR | 1 |
| Venäläinen, MK | 1 |
| Roine, AN | 1 |
| Häkkinen, MR | 1 |
| Vepsäläinen, JJ | 1 |
| Kumpulainen, PS | 1 |
| Kiviniemi, MS | 1 |
| Lehtimäki, T | 1 |
| Oksala, NK | 1 |
| Rantanen, TK | 1 |
| Kuwata, G | 1 |
| Hiramatsu, K | 3 |
| Samejima, K | 1 |
| Iwasaki, K | 1 |
| Takahashi, K | 3 |
| Koizumi, K | 1 |
| Horiguchi, S | 1 |
| Moriya, SS | 1 |
| Kobayashi, M | 1 |
| Kawakita, M | 3 |
| Linsalata, M | 3 |
| Orlando, A | 1 |
| Russo, F | 3 |
| Rossi, G | 1 |
| Cerquetella, M | 1 |
| Pengo, G | 1 |
| Mari, S | 1 |
| Balint, E | 1 |
| Bassotti, G | 1 |
| Manolescu, N | 1 |
| Xie, Y | 1 |
| Murray-Stewart, T | 1 |
| Wang, Y | 1 |
| Yu, F | 1 |
| Li, J | 1 |
| Marton, LJ | 1 |
| Casero, RA | 3 |
| Oupický, D | 1 |
| Thompson, PA | 1 |
| Wertheim, BC | 1 |
| Zell, JA | 1 |
| Chen, WP | 1 |
| McLaren, CE | 1 |
| LaFleur, BJ | 1 |
| Meyskens, FL | 2 |
| Gerner, EW | 2 |
| Umemori, Y | 1 |
| Ohe, Y | 1 |
| Kuribayashi, K | 1 |
| Tsuji, N | 1 |
| Nishidate, T | 1 |
| Kameshima, H | 1 |
| Hirata, K | 1 |
| Watanabe, N | 1 |
| Kreutzer, JN | 1 |
| Olsen, BB | 1 |
| Lech, K | 1 |
| Issinger, OG | 1 |
| Guerra, B | 1 |
| Abedini, F | 1 |
| Hosseinkhani, H | 1 |
| Ismail, M | 1 |
| Domb, AJ | 1 |
| Omar, AR | 1 |
| Chong, PP | 1 |
| Hong, PD | 1 |
| Yu, DS | 1 |
| Farber, IY | 1 |
| Hughes, A | 1 |
| Smith, NI | 1 |
| Wallace, HM | 2 |
| Mori, T | 2 |
| Yamaguchi, T | 2 |
| Matsumoto, H | 2 |
| Miyamoto, H | 2 |
| Tamamori, Y | 2 |
| Qutob, SS | 1 |
| Proulx, D | 1 |
| Mesak, FM | 1 |
| Ng, CE | 1 |
| Tanaka, S | 1 |
| Tanaka, C | 1 |
| Imajo, M | 1 |
| Kawaguchi, M | 1 |
| Toi, M | 1 |
| Allen, WL | 1 |
| McLean, EG | 1 |
| Boyer, J | 1 |
| McCulla, A | 1 |
| Wilson, PM | 1 |
| Coyle, V | 1 |
| Longley, DB | 1 |
| Johnston, PG | 1 |
| Sun, H | 1 |
| Liu, B | 1 |
| Yang, YP | 1 |
| Xu, CX | 1 |
| Yan, YF | 1 |
| Wang, W | 2 |
| Liu, XX | 1 |
| Mackarel, AJ | 1 |
| Emerson, SS | 1 |
| Pelot, D | 1 |
| Meshkinpour, H | 1 |
| Shassetz, LR | 1 |
| Einspahr, J | 1 |
| Alberts, DS | 1 |
| Liu, LQ | 1 |
| Higuchi, CM | 1 |
| Giardiello, FM | 1 |
| Hamilton, SR | 1 |
| Hylind, LM | 1 |
| Yang, VW | 1 |
| Tamez, P | 1 |
| Messa, C | 2 |
| Cavallini, A | 2 |
| Notarnicola, M | 1 |
| Guerra, V | 1 |
| Lantone, G | 1 |
| Lacatena, M | 1 |
| Di Leo, A | 2 |
| McGarrity, TJ | 2 |
| Peiffer, LP | 2 |
| Bartholomew, MJ | 1 |
| Pegg, AE | 2 |
| Colony, PC | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Phase III Randomized, Double-Blind, Placebo-Controlled Clinical Trial of the Combination of DFMO and Sulindac to Decrease the Rate of Recurrence of Adenomatous Polyps in the Colon[NCT00118365] | Phase 3 | 375 participants (Actual) | Interventional | 1998-07-31 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
"Participants reported at least 1 adverse event with a grade of 3 and above, regardless if the event is defined as serious per protocol or other.~Per protocol, not all grade 3 events are considered as serious events." (NCT00118365)
Timeframe: Up to 36 months
| Intervention | participants (Number) |
|---|---|
| Arm I (Eflornithine and Sulindac) | 46 |
| Arm II (Placebo) | 37 |
ODC genotype is the genotype of single nucleotide polymorphisms (SNP) in the ornithine decarboxylase (ODC) promoter The analysis cohort is based on the participants whose data are available and complete. (NCT00118365)
Timeframe: Baseline
| Intervention | nmol/mg protein (Median) |
|---|---|
| ODC1 AA/GA | 0.47 |
| ODC1 GG | 0.56 |
ODC genotype is the genotype of single nucleotide polymorphisms (SNP) in the ornithine decarboxylase (ODC) promoter The analysis cohort is based on the participants whose data are available and complete. (NCT00118365)
Timeframe: Baseline
| Intervention | nmol/mg protein (Median) |
|---|---|
| ODC1 AA/GA | 1.99 |
| ODC1 GG | 2.17 |
ODC genotype is the genotype of single nucleotide polymorphisms (SNP) in the ornithine decarboxylase (ODC) promoter The analysis cohort is based on the participants whose data are available and complete. (NCT00118365)
Timeframe: Baseline
| Intervention | nmol/mg protein (Median) |
|---|---|
| ODC1 AA/GA | 6.82 |
| ODC1 GG | 7.29 |
Estimated mean percent of cells staining postivie for the Ki-67 based on the GEE approach with adjustment for covariates (NCT00118365)
Timeframe: At the end of the study
| Intervention | percentage of cells that are positive (Mean) |
|---|---|
| Arm I (Eflornithine and Sulindac) | 59.5 |
| Arm II (Placebo) | 63.9 |
"Estimated mean percent of cells staining postivie for p53 based on GEE approach with adjument for covariates.~Tumor protein p53, also known as p53, cellular tumor antigen p53, phosphoprotein p53, or tumor suppressor p53, is a protein that in humans is encoded by the TP53 gene." (NCT00118365)
Timeframe: At the end of the study
| Intervention | percentage of cells that are positive (Mean) |
|---|---|
| Arm I (Eflornithine and Sulindac) | 75.6 |
| Arm II (Placebo) | 70.3 |
ODC genotype is the genotype of single nucleotide polymorphisms (SNP) in the ornithine decarboxylase (ODC) promoter The analysis cohort is based on the participants whose data are available and complete. (NCT00118365)
Timeframe: Up to 36 months
| Intervention | participants (Number) |
|---|---|
| DFMO + Sulindac - GG | 7 |
| DFMO + Sulindac - AA/GA | 9 |
| Placebo - GG | 22 |
| Placebo - AA/GA | 18 |
"Putrescine responder was defined as (tissue putrescine value at baseline - tissue putrescine value at the end of the study)/(tissue putrescine value at baseline) ≥ the threshold. Putrescine non-responder was defined as (tissue putrescine value at baseline - tissue putrescine value at the end of the study)/(tissue putrescine value at baseline) < the threshold. The thresholds range from 0.25 to 0.45 with an increment of 0.5. The below data are shown for the threshold of 0.30.~ODC genotype is the genotype of single nucleotide polymorphisms (SNP) in the ornithine decarboxylase (ODC) promoter The analysis cohort is based on the participants whose data are available and complete." (NCT00118365)
Timeframe: At the end of the study
| Intervention | participants (Number) | |
|---|---|---|
| Responder | Non-Responder | |
| DFMO + Sulindac - AA/GA | 21 | 19 |
| DFMO + Sulindac - GG | 26 | 32 |
| Placebo - AA/GA | 12 | 37 |
| Placebo - GG | 12 | 31 |
"Spermidine responder was defined as (tissue spermidine value at baseline - tissue spermidine value at the end of the study)/(tissue spermidine value at baseline) ≥ the threshold. Spermidine non-responder was defined as (tissue spermidine value at baseline - tissue spermidine value at the end of the study)/(tissue spermidine value at baseline) < the threshold. The thresholds range from 0.25 to 0.45 with an increment of 0.5. The below data are shown for the threshold of 0.30.~ODC genotype is the genotype of single nucleotide polymorphisms (SNP) in the ornithine decarboxylase (ODC) promoter The analysis cohort is based on the participants whose data are available and complete." (NCT00118365)
Timeframe: At the end of the study
| Intervention | participants (Number) | |
|---|---|---|
| Responder | Non-Responder | |
| DFMO + Sulindac - AA/GA | 12 | 28 |
| DFMO + Sulindac - GG | 25 | 32 |
| Placebo - AA/GA | 11 | 38 |
| Placebo - GG | 15 | 28 |
"Spermine responder was defined as (tissue spermine value at baseline - tissue spermine value at the end of the study)/(tissue spermine value at baseline) ≥ the threshold. Spermine non-responder was defined as (tissue spermine value at baseline - tissue spermine value at the end of the study)/(tissue spermine value at baseline) < the threshold. The thresholds range from 0.25 to 0.45 with an increment of 0.5. The below data are shown for the threshold of 0.30.~ODC genotype is the genotype of single nucleotide polymorphisms (SNP) in the ornithine decarboxylase (ODC) promoter The analysis cohort is based on the participants whose data are available and complete." (NCT00118365)
Timeframe: At the end of the study
| Intervention | participants (Number) | |
|---|---|---|
| Responder | Non-Responder | |
| DFMO + Sulindac - AA/GA | 7 | 33 |
| DFMO + Sulindac - GG | 7 | 51 |
| Placebo - AA/GA | 10 | 39 |
| Placebo - GG | 18 | 25 |
Apoptosis expression was assessed using cytoplasmic staining. The definitions for the category level for the Apoptosis are: 1. focal (less than 10% cells that are positively stained); 2. less than 50% cells are positively stained; 3. more than 50% cells are positively stained. (NCT00118365)
Timeframe: At the end of the study
| Intervention | adenoma (Number) | |||
|---|---|---|---|---|
| A pattern equal to normal mucosa | 1.focal (<10%) | 2.cyto less than 50% | 3.cyto more than 50% | |
| Arm I (Eflornithine and Sulindac) | 2 | 7 | 1 | 2 |
| Arm II (Placebo) | 4 | 20 | 23 | 13 |
bcl-2 is the anti-apoptotic protein BCL2 (NCT00118365)
Timeframe: At the end of the study, up to 3 years
| Intervention | Adenoma (Number) | ||||
|---|---|---|---|---|---|
| A pattern equal to normal mucosa | 1.<10% of the cells in the adenoma showed staining | 2.10-50% cells showed staining | 3.>50% cells showed staining | Insufficient tissue | |
| Arm I (Eflornithine and Sulindac) | 4 | 4 | 3 | 1 | 0 |
| Arm II (Placebo) | 17 | 25 | 14 | 8 | 2 |
carcino-embryonic antigen (CEA) is adenocarcinoma tissue marker that is expressed during adenoma formation. (NCT00118365)
Timeframe: At the end of the study
| Intervention | Adenoma (Number) | ||||
|---|---|---|---|---|---|
| A pattern equal to normal mucosa | 1.<50% of cells showed staining | 2.50-90% of cells showed staining | 3.>90% of cells showed staining | Insufficient tissue | |
| Arm I (Eflornithine and Sulindac) | 1 | 5 | 6 | 0 | 0 |
| Arm II (Placebo) | 5 | 15 | 35 | 9 | 2 |
sialyl-Tn (B72.3) is adenocarcinoma tissue marker that is expressed during adenoma formation. (NCT00118365)
Timeframe: At the end of the study
| Intervention | Adenoma (Number) | ||||
|---|---|---|---|---|---|
| a pattern equal to normal mucosa | 1.<10% of the cells in the adenoma showed staining | 2.10-50% cells showed staining | 3.>50% cells showed staining | Insufficient tissue | |
| Arm I (Eflornithine and Sulindac) | 3 | 7 | 2 | 0 | 0 |
| Arm II (Placebo) | 11 | 32 | 17 | 5 | 1 |
Detection of any adenoma at the end of the study. This analysis is based on the participants who had the end-of-study colonscopy procedure done. (NCT00118365)
Timeframe: Up to 36 months
| Intervention | participants (Number) | |
|---|---|---|
| Yes | No | |
| Arm I (Eflornithine and Sulindac) | 17 | 121 |
| Arm II (Placebo) | 53 | 76 |
This analysis is based on the participants who had the end-of-study colonscopy procedure done and their baseline PGE2 values are available. The low PGE2 is defined as the values that are below the median PGE2 value in the analysis cohort. The high PGE2 is defined as the values that are above the median PGE2 value in the analysis cohort. (NCT00118365)
Timeframe: Up to 36 months
| Intervention | participants (Number) | |
|---|---|---|
| Yes | No | |
| Eflornithine and Sulindac + High PGE2 at Baseline | 3 | 41 |
| Eflornithine and Sulindac + Low PGE2 at Baseline | 12 | 41 |
| Placebo + High PGE2 at Baseline | 21 | 32 |
| Placebo + Low PGE2 at Baseline | 19 | 23 |
The low is defined as the values that are below the median putrescine level in the analysis cohort. The high is defined as the values that are above the median putrescine level in the analysis cohort. (NCT00118365)
Timeframe: Up 36 months
| Intervention | participants (Number) | |
|---|---|---|
| Yes | No | |
| Eflornithine and Sulindac + High Putrescine at Baseline | 10 | 56 |
| Eflornithine and Sulindac + Low Putrescine at Baseline | 7 | 63 |
| Placebo + High Putrescine at Baseline | 31 | 36 |
| Placebo + Low Putrescine at Baseline | 24 | 38 |
"The low is defined as the ratios that are below the median spermidine-to-spermine ratio in the analysis cohort. The high is defined as the ratios that are above the median spermidine-to-spermine ratio in the analysis cohort.~In the finalized datasaet, the total number of adnoma detected in the placebo group is 55. The descrepancy in the total number of adnoma detected in placebo group between Outcome Measure 1 and this oucome is due to the revolution of the datatset.~The analysis cohort is based on the participants whose data are available and complete." (NCT00118365)
Timeframe: Up 36 months
| Intervention | participants (Number) | |
|---|---|---|
| Yes | No | |
| Eflornithine and Sulindac + High Spd:Spm at Baseline | 12 | 60 |
| Eflornithine and Sulindac + Low Spd:Spm at Baseline | 5 | 59 |
| Placebo + High Spd:Spm at Baseline | 24 | 37 |
| Placebo + Low Spd:Spm at Baseline | 31 | 37 |
PGE2 Responder = PGE2 values at 36-month are decreased by >=30% in PGE2 values from baseline PGE2 nonresponder = PGE2 values at 36-month are increased, or decreased by < 30% from baseline The analysis cohort is based on the participants whose data are available and complete. (NCT00118365)
Timeframe: Up to 36 months
| Intervention | participants (Number) | |
|---|---|---|
| Yes | No | |
| Eflornithine and Sulindac + PGE2 Nonresponders | 8 | 27 |
| Eflornithine and Sulindac + PGE2 Responders | 1 | 10 |
| Placebo + PGE2 Nonresponders | 15 | 17 |
| Placebo + PGE2 Responders | 4 | 13 |
Putrescine responder = Putrescine values at 36-month are decreased by >=30% from baseline Putrescine nonresponder = Putrescine values at 36-month are increased, or decreased by < 30% from baseline The analysis cohort is based on the participants whose data are available and complete. (NCT00118365)
Timeframe: Up to 36 months
| Intervention | participants (Number) | |
|---|---|---|
| Yes | No | |
| Eflornithine and Sulindac + Putrescine Nonresponders | 7 | 53 |
| Eflornithine and Sulindac + Putrescine Responders | 9 | 52 |
| Placebo + Putrescine Nonresponders | 28 | 44 |
| Placebo + Putrescine Responders | 22 | 24 |
Spermidine-to-spermine ratio responder = ratios at 36-month are decreased by >=30% from baseline Spermidine-to-spermine ratio nonresponder = ratios at 36-month are increased, or decreased by < 30% from baseline The analysis cohort is based on the participants whose data are available and complete. (NCT00118365)
Timeframe: Up to 36 months
| Intervention | participants (Number) | |
|---|---|---|
| Yes | No | |
| Eflornithine and Sulindac + Spd:Spm Nonresponders | 8 | 30 |
| Eflornithine and Sulindac + Spd:Spm Responders | 8 | 75 |
| Placebo + Spd:Spm Nonresponders | 33 | 44 |
| Placebo + Spd:Spm Responders | 17 | 24 |
1 review available for spermine and Colorectal Cancer
| Article | Year |
|---|---|
Pharmacological and dietary agents for colorectal cancer chemoprevention: effects on polyamine metabolism (review).
Topics: Anticarcinogenic Agents; Cell Transformation, Neoplastic; Chemoprevention; Colorectal Neoplasms; Hum | 2014 |
2 trials available for spermine and Colorectal Cancer
| Article | Year |
|---|---|
Levels of rectal mucosal polyamines and prostaglandin E2 predict ability of DFMO and sulindac to prevent colorectal adenoma.
Topics: Adenoma; Aged; Anticarcinogenic Agents; Biomarkers, Pharmacological; Biopsy; Colonoscopy; Colorectal | 2010 |
Dose de-escalation chemoprevention trial of alpha-difluoromethylornithine in patients with colon polyps.
Topics: Administration, Oral; Adult; Aged; Biogenic Polyamines; Colonic Polyps; Colorectal Neoplasms; Drug A | 1994 |
21 other studies available for spermine and Colorectal Cancer
| Article | Year |
|---|---|
Quantitative Metabolomics to Explore the Role of Plasma Polyamines in Colorectal Cancer.
Topics: Chromatography, Liquid; Colorectal Neoplasms; Humans; Polyamines; Spermidine; Spermine | 2022 |
Altered Polyamine Profiles in Colorectal Cancer.
Topics: Adult; Aged; Biomarkers, Tumor; Chromatography, Liquid; Colorectal Neoplasms; Early Diagnosis; Femal | 2018 |
Increase of N1, N12-diacetylspermine in tissues from colorectal cancer and its liver metastasis.
Topics: Adult; Aged; Aged, 80 and over; Biomarkers, Tumor; Chromatography, High Pressure Liquid; Colorectal | 2013 |
Immunohistochemical expression of ornithine decarboxylase, diamine oxidase, putrescine, and spermine in normal canine enterocolic mucosa, in chronic colitis, and in colorectal cancer.
Topics: Amine Oxidase (Copper-Containing); Animals; Chronic Disease; Colitis; Colorectal Neoplasms; Dogs; In | 2015 |
Self-immolative nanoparticles for simultaneous delivery of microRNA and targeting of polyamine metabolism in combination cancer therapy.
Topics: Animals; Antineoplastic Agents; Colon; Colorectal Neoplasms; Drug Carriers; Female; HCT116 Cells; Hu | 2017 |
Evaluating the utility of N1,N12-diacetylspermine and N1,N8-diacetylspermidine in urine as tumor markers for breast and colorectal cancers.
Topics: Aged; Aged, 80 and over; Biomarkers, Tumor; Breast Neoplasms; Carcinoembryonic Antigen; Colorectal N | 2010 |
Role of polyamines in determining the cellular response to chemotherapeutic agents: modulation of protein kinase CK2 expression and activity.
Topics: Acetyltransferases; Antineoplastic Agents; Casein Kinase II; Cell Death; Cell Line, Tumor; Cell Prol | 2011 |
Cationized dextran nanoparticle-encapsulated CXCR4-siRNA enhanced correlation between CXCR4 expression and serum alkaline phosphatase in a mouse model of colorectal cancer.
Topics: Alkaline Phosphatase; Animals; Cations; Colorectal Neoplasms; Dextrans; Down-Regulation; Female; Imm | 2012 |
Polyamines reverse non-steroidal anti-inflammatory drug-induced toxicity in human colorectal cancer cells.
Topics: Anti-Inflammatory Agents, Non-Steroidal; Apoptosis; Cell Division; Cell Membrane; Cell Survival; Col | 2003 |
[The significance of urine di-acetyl spermine level as a cancer marker for colorectal cancer].
Topics: Biomarkers, Tumor; Carcinoembryonic Antigen; Colorectal Neoplasms; Humans; Neoplasm Staging; Predict | 2004 |
Effects of N1, N13-diethylnorspermine (DENSPM) and X-radiation treatment on human colorectal tumor clones with varying X-radiation and drug responses.
Topics: Antineoplastic Agents; Cell Line, Tumor; Cell Survival; Cloning, Molecular; Colorectal Neoplasms; Co | 2005 |
N(1),N(12)-Diacetylspermine as a sensitive and specific novel marker for early- and late-stage colorectal and breast cancers.
Topics: Adult; Biomarkers, Tumor; Breast Neoplasms; CA-19-9 Antigen; Carcinoembryonic Antigen; Colorectal Ne | 2005 |
The role of spermidine/spermine N1-acetyltransferase in determining response to chemotherapeutic agents in colorectal cancer cells.
Topics: Acetyltransferases; Antineoplastic Agents; Cell Death; Cell Survival; Colorectal Neoplasms; Drug Res | 2007 |
Adenovirus-mediated expression of SSAT inhibits colorectal cancer cell growth in vitro.
Topics: Acetyltransferases; Adenoviridae; Base Sequence; Cell Line; Colorectal Neoplasms; DNA, Complementary | 2008 |
An investigation of the mechanism of polyamine efflux from human colorectal carcinoma cells.
Topics: Cell Line; Colorectal Neoplasms; Humans; Kinetics; Polyamines; Putrescine; Spermidine; Spermine; Tum | 1994 |
Mucosal polyamine measurements and colorectal cancer risk.
Topics: Aged; Colorectal Neoplasms; Female; Humans; Intestinal Mucosa; Male; Middle Aged; Polyamines; Risk F | 1996 |
Ornithine decarboxylase and polyamines in familial adenomatous polyposis.
Topics: Adenomatous Polyposis Coli; Adolescent; Adult; Biomarkers, Tumor; Child; Colorectal Neoplasms; Femal | 1997 |
Polyamines and estrogen-receptor concentrations in human colorectal carcinomas.
Topics: Adenocarcinoma; Adult; Aged; Carcinoembryonic Antigen; Colorectal Neoplasms; Female; Humans; Intesti | 1992 |
Sex steroid hormone receptors, epidermal growth factor receptor, and polyamines in human colorectal cancer.
Topics: Adult; Aged; Colon; Colorectal Neoplasms; ErbB Receptors; Female; Humans; Intestinal Mucosa; Male; M | 1992 |
Colonic polyamine content and ornithine decarboxylase activity as markers for adenomas.
Topics: Aged; Biogenic Polyamines; Biomarkers, Tumor; Colonic Polyps; Colorectal Neoplasms; Female; Humans; | 1990 |
The effects of chronic ethanol administration on polyamine content during dimethylhydrazine-induced colorectal carcinogenesis in the rat.
Topics: Animals; Colon; Colorectal Neoplasms; Dimethylhydrazines; Ethanol; Polyamines; Putrescine; Rats; Rat | 1988 |