eflornithine and Colorectal Cancer studies

Eflornithine: An inhibitor of ORNITHINE DECARBOXYLASE, the rate limiting enzyme of the polyamine biosynthetic pathway.
eflornithine : A fluoroamino acid that is ornithine substituted by a difluoromethyl group at position 2.

Research Excerpts

Excerpt	Relevance	Reference
"Chemoprevention with the polyamine-inhibitory regimen difluoromethylornithine (DFMO) + sulindac markedly reduces risk of recurrent adenoma in colorectal adenoma patients."	9.16	Role of obesity in a randomized placebo-controlled trial of difluoromethylornithine (DFMO) + sulindac for the prevention of sporadic colorectal adenomas. ( Gerner, EW; Lin, BS; Madson, N; McLaren, CE; Meyskens, FL; Zell, JA, 2012)
" We evaluated the effect of baseline CV risk on adverse CV events in a phase III trial of difluoromethylornithine (DFMO) plus the NSAID sulindac versus placebo in preventing colorectal adenomas."	9.14	Risk of cardiovascular events in a randomized placebo-controlled, double-blind trial of difluoromethylornithine plus sulindac for the prevention of sporadic colorectal adenomas. ( Chen, WP; Gerner, EW; McLaren, CE; Meyskens, FL; Pelot, D; Zell, JA, 2009)
"The polyamine-inhibitory regimen difluoromethylornithine (DFMO)+sulindac has marked efficacy in preventing metachronous colorectal adenomas."	7.79	Role of dietary polyamines in a phase III clinical trial of difluoromethylornithine (DFMO) and sulindac for prevention of sporadic colorectal adenomas. ( Gerner, EW; McLaren, CE; Meyskens, FL; Raj, KP; Rock, CL; Zell, JA; Zoumas-Morse, C, 2013)
"Chemoprevention with the polyamine-inhibitory regimen difluoromethylornithine (DFMO) + sulindac markedly reduces risk of recurrent adenoma in colorectal adenoma patients."	5.16	Role of obesity in a randomized placebo-controlled trial of difluoromethylornithine (DFMO) + sulindac for the prevention of sporadic colorectal adenomas. ( Gerner, EW; Lin, BS; Madson, N; McLaren, CE; Meyskens, FL; Zell, JA, 2012)
" We evaluated the effect of baseline CV risk on adverse CV events in a phase III trial of difluoromethylornithine (DFMO) plus the NSAID sulindac versus placebo in preventing colorectal adenomas."	5.14	Risk of cardiovascular events in a randomized placebo-controlled, double-blind trial of difluoromethylornithine plus sulindac for the prevention of sporadic colorectal adenomas. ( Chen, WP; Gerner, EW; McLaren, CE; Meyskens, FL; Pelot, D; Zell, JA, 2009)
"The polyamine-inhibitory regimen difluoromethylornithine (DFMO)+sulindac has marked efficacy in preventing metachronous colorectal adenomas."	3.79	Role of dietary polyamines in a phase III clinical trial of difluoromethylornithine (DFMO) and sulindac for prevention of sporadic colorectal adenomas. ( Gerner, EW; McLaren, CE; Meyskens, FL; Raj, KP; Rock, CL; Zell, JA; Zoumas-Morse, C, 2013)
" Aspirin and celecoxib are the promising preventive agents to effectively reduce the risk of colorectal cancer, but such agents are associated with severe gastrointestinal and cardiovascular side effects in long-term administration at high doses."	2.48	Combination chemoprevention: future direction of colorectal cancer prevention. ( Cheng, SW; Liu, J; Wang, B; Yang, R; Zhou, P, 2012)
"Colorectal cancer is a disease with a high mortality at present, due to the late stage at which many cases present."	2.42	Review article: chemoprevention of colorectal cancer. ( Courtney, ED; Leicester, RJ; Melville, DM, 2004)
" Epidemiological studies have consistently shown that chronic intake of nonsteroidal anti-inflammatory drugs (NSAIDs), principally aspirin, can reduce the incidence of colorectal adenomas and carcinomas."	2.41	Chemoprevention of colorectal cancer. ( Gwyn, K; Sinicrope, FA, 2002)
"Chemoprevention of colorectal cancer has been extensively investigated in animal models and in high-risk human populations with inherited or acquired genetic changes, using anticarcinogenic agents from natural and synthetic sources."	2.40	[An overview on chemoprevention of colorectal cancer]. ( Narisawa, T, 1998)
"Polyamine transport occurred in all colorectal cancer cell lines tested but to varying extents."	1.56	Upregulation of Polyamine Transport in Human Colorectal Cancer Cells. ( Corral, M; Wallace, HM, 2020)
"Celecoxib has shown benefit in regressing colorectal adenomas and appears to have some duodenal activity as well."	1.35	Chemoprevention with special reference to inherited colorectal cancer. ( Lynch, PM, 2008)

Research

Studies (31)

Authors

Clinical Trials (1)

Trial Overview

Trial Outcomes

Adverse Events With a Grade of 3 and Above

Timeframe	Studies, this research(%)	All Research%
pre-1990	0 (0.00)	18.7374
1990's	6 (19.35)	18.2507
2000's	13 (41.94)	29.6817
2010's	11 (35.48)	24.3611
2020's	1 (3.23)	2.80

Authors	Studies
Corral, M	1
Wallace, HM	1
Half, E	1
Arber, N	1
Witherspoon, M	1
Chen, Q	1
Kopelovich, L	1
Gross, SS	1
Lipkin, SM	1
Casero, RA	1
Meyskens, FL	9
McLaren, CE	7
Pelot, D	3
Fujikawa-Brooks, S	1
Carpenter, PM	1
Hawk, E	1
Kelloff, G	1
Lawson, MJ	1
Kidao, J	1
McCracken, J	1
Albers, CG	1
Ahnen, DJ	1
Turgeon, DK	1
Goldschmid, S	1
Lance, P	1
Hagedorn, CH	1
Gillen, DL	1
Gerner, EW	10
Sporn, MB	1
Hong, WK	1
Zell, JA	6
Chen, WP	3
Thompson, PA	2
Wertheim, BC	1
LaFleur, BJ	1
Laukaitis, CM	1
Derech-Haim, S	1
Teiblum, G	1
Kadosh, R	1
Rahav, G	1
Bonda, E	1
Sredni, B	1
Bakhanashvili, M	1
Zhou, P	1
Cheng, SW	1
Yang, R	1
Wang, B	1
Liu, J	1
Lin, BS	1
Madson, N	1
Rial, NS	1
Cohen, AM	1
Raj, KP	1
Rock, CL	1
Zoumas-Morse, C	1
Courtney, ED	1
Melville, DM	1
Leicester, RJ	1
Gill, S	1
Sinicrope, FA	2
Lynch, PM	1
Siemer, S	1
Kriener, S	1
König, J	1
Remberger, K	1
Issinger, OG	1
Emerson, SS	1
Meshkinpour, H	1
Shassetz, LR	1
Einspahr, J	1
Alberts, DS	1
Krishnan, K	2
Brenner, DE	2
Narisawa, T	1
Love, RR	1
Jacoby, R	1
Newton, MA	1
Tutsch, KD	1
Simon, K	1
Pomplun, M	1
Verma, AK	1
Ruffin, MT	1
Scheppach, W	1
Melcher, R	1
Lührs, H	1
Menzel, T	1
Doyle, KJ	1
Shanks, JE	1
Galus, CM	1
Umar, A	1
Viner, JL	1
Hawk, ET	1
Gwyn, K	1
Benamouzig, R	1
Chaussade, S	1
Ajani, JA	1
Ota, DM	1
Grossie, VB	1
Abbruzzese, JL	1
Faintuch, JS	1
Patt, YZ	1
Jackson, DE	1
Levin, B	1
Nishioka, K	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

Baseline Putrescine by ODC Genotype

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

Baseline Spermidine by ODC Genotype

Intervention	nmol/mg protein (Median)
ODC1 AA/GA	0.47
ODC1 GG	0.56

Baseline Spermine by ODC Genotype

Intervention	nmol/mg protein (Median)
ODC1 AA/GA	1.99
ODC1 GG	2.17

Biomarker in Adenoma - Ki-67

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

Biomarker in Adenoma - p53

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

Number of Participants Have Adenoma Recurrence in Each ODC1 Genotytpe by Treatment Group

Intervention	percentage of cells that are positive (Mean)
Arm I (Eflornithine and Sulindac)	75.6
Arm II (Placebo)	70.3

At the End of the Study - Putrescine Response by ODC Genotype

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

At the End of the Study - Spermidine Response by ODC Genotype

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

At the End of the Study - Spermine Response by ODC Genotype

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

Biomarker in Adenoma: Apoptosis

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

Biomarker in Adenoma: Bcl-2

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

Biomarker in Adenoma: CEA

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

Biomarker in Adenoma: Sialyl-TN (B72.3)

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

Detection of Any Adenoma 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

Detection of Any Adenoma at the End of the Study Stratified by Baseline Prostaglandin E2 (PGE2) and Treatment

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

Detection of Any Adenoma at the End of the Study Stratified by Baseline Putrescine and Treatment

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

Detection of Any Adenoma at the End of the Study Stratified by Baseline Spermidine-to-spermine Ratio and Treatment

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

Detection of Any Adenoma at the End of the Study Stratified by Prostaglandin E2 (PGE2) Response and Treatment

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

Detection of Any Adenoma at the End of the Study Stratified by Putrescine Response and Treatment

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

Detection of Any Adenoma at the End of the Study Stratified by Spermidine-to-spermine Ratio Response and Treatment

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

Article	Year
Chemoprevention of gastrointestinal neoplasia. Current gastroenterology reports, 2013, Volume: 15, Issue:5 Topics: Adenocarcinoma; Anti-Inflammatory Agents, Non-Steroidal; Antineoplastic Agents; Chemoprevention; Col	2013
DFMO: targeted risk reduction therapy for colorectal neoplasia. Best practice & research. Clinical gastroenterology, 2011, Volume: 25, Issue:4-5 Topics: Adenoma; Animals; Anticarcinogenic Agents; Chemoprevention; Colorectal Neoplasms; Eflornithine; Enzy	2011
Combination chemoprevention: future direction of colorectal cancer prevention. European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP), 2012, Volume: 21, Issue:3 Topics: Anti-Inflammatory Agents, Non-Steroidal; Anticarcinogenic Agents; Antineoplastic Combined Chemothera	2012
Clinical end points for developing pharmaceuticals to manage patients with a sporadic or genetic risk of colorectal cancer. Expert review of gastroenterology & hepatology, 2012, Volume: 6, Issue:4 Topics: Adenomatous Polyposis Coli; Antineoplastic Agents; Chemoprevention; Clinical Trials as Topic; Colono	2012
Review article: chemoprevention of colorectal cancer. Alimentary pharmacology & therapeutics, 2004, Jan-01, Volume: 19, Issue:1 Topics: Anti-Inflammatory Agents, Non-Steroidal; Calcium; Chemoprevention; Colorectal Neoplasms; Cyclooxygen	2004
Polyamines and cancer: old molecules, new understanding. Nature reviews. Cancer, 2004, Volume: 4, Issue:10 Topics: Anti-Inflammatory Agents, Non-Steroidal; Antineoplastic Agents; Chemoprevention; Colorectal Neoplasm	2004
Colorectal cancer prevention: is an ounce of prevention worth a pound of cure? Seminars in oncology, 2005, Volume: 32, Issue:1 Topics: Adenoma; Animals; Anti-Inflammatory Agents, Non-Steroidal; Anticarcinogenic Agents; Aspirin; Calcium	2005
Chemoprevention of colorectal cancer. Gastroenterology clinics of North America, 1996, Volume: 25, Issue:4 Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Anticarcinogenic Agents; Antioxidants; Calcium; Co	1996
[An overview on chemoprevention of colorectal cancer]. Nihon Geka Gakkai zasshi, 1998, Volume: 99, Issue:6 Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Antineoplastic Agents; Carotenoids; Colorectal Neo	1998
Chemoprevention for colorectal cancer. Critical reviews in oncology/hematology, 2000, Volume: 33, Issue:3 Topics: Adenoma; Animals; Anti-Inflammatory Agents, Non-Steroidal; Anticarcinogenic Agents; Antioxidants; Ap	2000
[Primary prevention of sporadic colorectal carcinoma by diet modification and drugs?]. Der Internist, 2000, Volume: 41, Issue:9 Topics: Anti-Inflammatory Agents, Non-Steroidal; Anticarcinogenic Agents; Carcinoma; Colorectal Neoplasms; D	2000
The future of colon cancer prevention. Annals of the New York Academy of Sciences, 2001, Volume: 952 Topics: Adenocarcinoma; Adenoma; Animals; Anti-Inflammatory Agents, Non-Steroidal; Anticarcinogenic Agents;	2001
Chemoprevention of colorectal cancer. The American journal of gastroenterology, 2002, Volume: 97, Issue:1 Topics: Anti-Inflammatory Agents, Non-Steroidal; Ascorbic Acid; beta Carotene; Calcium Compounds; Colorectal	2002
[Chemoprevention of colorectal cancer]. Presse medicale (Paris, France : 1983), 2002, Jan-26, Volume: 31, Issue:3 Topics: Adenomatous Polyposis Coli; Animals; Anti-Inflammatory Agents, Non-Steroidal; Antineoplastic Agents;	2002

Article	Year
Difluoromethylornithine plus sulindac for the prevention of sporadic colorectal adenomas: a randomized placebo-controlled, double-blind trial. Cancer prevention research (Philadelphia, Pa.), 2008, Volume: 1, Issue:1 Topics: Adenoma; Adult; Aged; Algorithms; Antineoplastic Combined Chemotherapy Protocols; Colonoscopy; Color	2008
Risk of cardiovascular events in a randomized placebo-controlled, double-blind trial of difluoromethylornithine plus sulindac for the prevention of sporadic colorectal adenomas. Cancer prevention research (Philadelphia, Pa.), 2009, Volume: 2, Issue:3 Topics: Adenoma; Adult; Aged; Anti-Inflammatory Agents, Non-Steroidal; Anticarcinogenic Agents; Antineoplast	2009
Levels of rectal mucosal polyamines and prostaglandin E2 predict ability of DFMO and sulindac to prevent colorectal adenoma. Gastroenterology, 2010, Volume: 139, Issue:3 Topics: Adenoma; Aged; Anticarcinogenic Agents; Biomarkers, Pharmacological; Biopsy; Colonoscopy; Colorectal	2010
Ornithine decarboxylase-1 polymorphism, chemoprevention with eflornithine and sulindac, and outcomes among colorectal adenoma patients. Journal of the National Cancer Institute, 2010, Oct-06, Volume: 102, Issue:19 Topics: Adenoma; Aged; Antineoplastic Combined Chemotherapy Protocols; Colorectal Neoplasms; Confounding Fac	2010
Role of obesity in a randomized placebo-controlled trial of difluoromethylornithine (DFMO) + sulindac for the prevention of sporadic colorectal adenomas. Cancer causes & control : CCC, 2012, Volume: 23, Issue:10 Topics: Adenoma; Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Colorectal	2012
Dose de-escalation chemoprevention trial of alpha-difluoromethylornithine in patients with colon polyps. Journal of the National Cancer Institute, 1994, Aug-03, Volume: 86, Issue:15 Topics: Administration, Oral; Adult; Aged; Biogenic Polyamines; Colonic Polyps; Colorectal Neoplasms; Drug A	1994
A randomized, placebo-controlled trial of low-dose alpha-difluoromethylornithine in individuals at risk for colorectal cancer. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 1998, Volume: 7, Issue:11 Topics: Adult; Aged; Aged, 80 and over; Colorectal Neoplasms; Eflornithine; Enzyme Inhibitors; Female; Human	1998
Effects of difluoromethylornithine chemoprevention on audiometry thresholds and otoacoustic emissions. Archives of otolaryngology--head & neck surgery, 2001, Volume: 127, Issue:5 Topics: Antineoplastic Agents; Audiometry, Pure-Tone; Auditory Threshold; Colonic Polyps; Colorectal Neoplas	2001

Article	Year
Upregulation of Polyamine Transport in Human Colorectal Cancer Cells. Biomolecules, 2020, 03-25, Volume: 10, Issue:4 Topics: Biological Transport; Cell Line, Tumor; Colorectal Neoplasms; Eflornithine; Humans; Polyamines; Up-R	2020
Unbiased metabolite profiling indicates that a diminished thymidine pool is the underlying mechanism of colon cancer chemoprevention by alpha-difluoromethylornithine. Cancer discovery, 2013, Volume: 3, Issue:9 Topics: Animals; Cell Line, Tumor; Chemoprevention; Colorectal Neoplasms; Eflornithine; Enzyme Inhibitors; H	2013
Say what? The activity of the polyamine biosynthesis inhibitor difluoromethylornithine in chemoprevention is a result of reduced thymidine pools? Cancer discovery, 2013, Volume: 3, Issue:9 Topics: Animals; Colorectal Neoplasms; Eflornithine; Enzyme Inhibitors; Humans; Thymidine	2013
Clinical prevention of recurrence of colorectal adenomas by the combination of difluoromethylornithine and sulindac: an important milestone. Cancer prevention research (Philadelphia, Pa.), 2008, Volume: 1, Issue:1 Topics: Adenoma; Antineoplastic Combined Chemotherapy Protocols; Clinical Trials as Topic; Colorectal Neopla	2008
Ribonuclease activity of p53 in cytoplasm in response to various stress signals. Cell cycle (Georgetown, Tex.), 2012, Apr-01, Volume: 11, Issue:7 Topics: Cell Line, Tumor; Colorectal Neoplasms; Cytoplasm; Doxorubicin; Eflornithine; ELAV Proteins; Ethylen	2012
Role of dietary polyamines in a phase III clinical trial of difluoromethylornithine (DFMO) and sulindac for prevention of sporadic colorectal adenomas. British journal of cancer, 2013, Feb-19, Volume: 108, Issue:3 Topics: Adenoma; Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Clinical Tr	2013
Chemoprevention with special reference to inherited colorectal cancer. Familial cancer, 2008, Volume: 7, Issue:1 Topics: Adenomatous Polyposis Coli; Anti-Inflammatory Agents, Non-Steroidal; Antineoplastic Agents; Ascorbic	2008
Influence of indomethacin and difluoromethylornithine on human tumour growth in nude mice. European journal of cancer (Oxford, England : 1990), 1995, Volume: 31A, Issue:6 Topics: Animals; Cell Division; Colorectal Neoplasms; Drug Screening Assays, Antitumor; Eflornithine; Humans	1995
Evaluation of continuous-infusion alpha-difluoromethylornithine therapy for colorectal carcinoma. Cancer chemotherapy and pharmacology, 1990, Volume: 26, Issue:3 Topics: Carcinoma; Colorectal Neoplasms; Drug Evaluation; Drug Tolerance; Eflornithine; Humans; Infusions, I	1990

eflornithine and Colorectal Cancer