adenine has been researched along with Colorectal Neoplasms in 33 studies
Colorectal Neoplasms: Tumors or cancer of the COLON or the RECTUM or both. Risk factors for colorectal cancer include chronic ULCERATIVE COLITIS; FAMILIAL POLYPOSIS COLI; exposure to ASBESTOS; and irradiation of the CERVIX UTERI.
| Excerpt | Relevance | Reference |
|---|---|---|
| "Amonafide, a benzisoquinoline-1,3-dione with anti-tumor activity in preclinical screens, was administered to patients with recurrent or metastatic bidimensionally measurable colorectal cancer." | 9.07 | Phase II study of amonafide (nafidamide, NSC 308847) in advanced colorectal cancer. ( Comis, RL; Hudes, GR; O'Dwyer, PJ; Ozols, RF; Paul, AR; Walczak, J, 1991) |
| "Our previous reports showed that justicidin A (JA), a novel and pure arylnaphthalide lignan isolated from Justicia procumbens, induces apoptosis of human colorectal cancer cells and hepatocellular carcinoma cells, leading to the suppression of both tumor cell growth in NOD-SCID mice." | 7.81 | Justicidin A-induced autophagy flux enhances apoptosis of human colorectal cancer cells via class III PI3K and Atg5 pathway. ( Jiang-Shieh, YF; Lan, SH; Lin, CN; Liu, HS; Su, CL; Won, SJ; Wu, SY; Yen, CH, 2015) |
| "We observed that bortezomib-induced protective autophagy in cultured PANC-1 pancreatic cancer cells and HT-29 colorectal cancer cells." | 7.80 | Bortezomib induces protective autophagy through AMP-activated protein kinase activation in cultured pancreatic and colorectal cancer cells. ( Chen, ZR; Huang, M; Min, H; Xu, M; Zheng, K; Zhou, JD; Zou, XP, 2014) |
| " In the present study, we found that, in human colorectal cancer cells, low-dose camptothecin (CPT) simultaneously induced autophagy and premature senescence through AMPK-TSC2-mTOR pathway and ATM-Chk2-p53-p21 pathway respectively." | 7.80 | Autophagy inhibition switches low-dose camptothecin-induced premature senescence to apoptosis in human colorectal cancer cells. ( Li, R; Liu, WT; Song, JR; Sun, K; Wei, LX; Wu, MC; Zhang, JW; Zhang, SS; Zhao, QD; Zong, C, 2014) |
| "Amonafide is a substituted benzisoquinolinedione that exerts its cytotoxicity through effects on macromolecular synthesis and intercalation of DNA." | 6.67 | Phase II trial of amonafide in advanced colorectal cancer: a SouthWest Oncology Group study. ( Brown, TD; Craig, JB; Einstein, AB; Fleming, T; Goodman, PJ; Macdonald, JS, 1993) |
| "Amonafide, a benzisoquinoline-1,3-dione with anti-tumor activity in preclinical screens, was administered to patients with recurrent or metastatic bidimensionally measurable colorectal cancer." | 5.07 | Phase II study of amonafide (nafidamide, NSC 308847) in advanced colorectal cancer. ( Comis, RL; Hudes, GR; O'Dwyer, PJ; Ozols, RF; Paul, AR; Walczak, J, 1991) |
| " To identify functional phosphorylation sites involved in 5-fluorouracil (5-FU) resistance during its treatment of colorectal cancer cells, CRISPR-mediated cytosine base editor (CBE) and adenine base editor (ABE) are utilized for functional screens by mutating phosphorylated amino acids with two libraries specifically targeting 7779 and 10 149 phosphorylation sites." | 4.12 | Functional Phosphoproteomics in Cancer Chemoresistance Using CRISPR-Mediated Base Editors. ( Guo, J; Huang, S; Huang, X; Li, J; Li, M; Lin, J; Qiao, Y; Yu, W; Zhang, P; Zhao, Y, 2022) |
| " Therefore, the aim of our study was to use human colorectal cancer HCT116 cells to explore whether inhibition of autophagy by 3-Methyladenine (3-MA, an autophagy inhibitor) is able to enhance hypoxia-induced apoptosis in vitro." | 3.91 | Inhibition of autophagy by 3-MA promotes hypoxia-induced apoptosis in human colorectal cancer cells. ( Dong, Y; Wu, Y; Xing, CG; Yang, XD; Ye, ZY; Zhao, GL, 2019) |
| "Our previous reports showed that justicidin A (JA), a novel and pure arylnaphthalide lignan isolated from Justicia procumbens, induces apoptosis of human colorectal cancer cells and hepatocellular carcinoma cells, leading to the suppression of both tumor cell growth in NOD-SCID mice." | 3.81 | Justicidin A-induced autophagy flux enhances apoptosis of human colorectal cancer cells via class III PI3K and Atg5 pathway. ( Jiang-Shieh, YF; Lan, SH; Lin, CN; Liu, HS; Su, CL; Won, SJ; Wu, SY; Yen, CH, 2015) |
| "We observed that bortezomib-induced protective autophagy in cultured PANC-1 pancreatic cancer cells and HT-29 colorectal cancer cells." | 3.80 | Bortezomib induces protective autophagy through AMP-activated protein kinase activation in cultured pancreatic and colorectal cancer cells. ( Chen, ZR; Huang, M; Min, H; Xu, M; Zheng, K; Zhou, JD; Zou, XP, 2014) |
| " In the present study, we found that, in human colorectal cancer cells, low-dose camptothecin (CPT) simultaneously induced autophagy and premature senescence through AMPK-TSC2-mTOR pathway and ATM-Chk2-p53-p21 pathway respectively." | 3.80 | Autophagy inhibition switches low-dose camptothecin-induced premature senescence to apoptosis in human colorectal cancer cells. ( Li, R; Liu, WT; Song, JR; Sun, K; Wei, LX; Wu, MC; Zhang, JW; Zhang, SS; Zhao, QD; Zong, C, 2014) |
| " The highest tested dose of ibrutinib, 560 mg once daily, was combined with a fixed dose of pembrolizumab 200 mg every 3 weeks for the phase 2 portion." | 3.01 | A phase 1/2 trial of ibrutinib in combination with pembrolizumab in patients with mismatch repair proficient metastatic colorectal cancer. ( Carballido, E; Imanirad, I; Kim, DW; Kim, RD; Martinez, M; Mehta, R; Schell, MJ; Strosberg, J; Tan, E; Yu, J; Zhou, JM, 2021) |
| "Amonafide is a substituted benzisoquinolinedione that exerts its cytotoxicity through effects on macromolecular synthesis and intercalation of DNA." | 2.67 | Phase II trial of amonafide in advanced colorectal cancer: a SouthWest Oncology Group study. ( Brown, TD; Craig, JB; Einstein, AB; Fleming, T; Goodman, PJ; Macdonald, JS, 1993) |
| " Toxic effects of the combination of ibrutinib and cetuximab have been reported in a patient with metastatic CRC." | 1.72 | Ibrutinib and panitumumab used in combination safely in a patient with metachronous colorectal cancer and chronic lymphocytic leukemia. ( Araz, M; Artaç, M; Çeneli, Ö; Karaağaç, M; Karakurt Eryilmaz, M; Korkmaz, M, 2022) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 5 (15.15) | 18.2507 |
| 2000's | 9 (27.27) | 29.6817 |
| 2010's | 16 (48.48) | 24.3611 |
| 2020's | 3 (9.09) | 2.80 |
| Authors | Studies |
|---|---|
| Korkmaz, M | 1 |
| Karakurt Eryilmaz, M | 1 |
| Karaağaç, M | 1 |
| Araz, M | 1 |
| Çeneli, Ö | 1 |
| Artaç, M | 1 |
| Li, J | 1 |
| Lin, J | 1 |
| Huang, S | 1 |
| Li, M | 1 |
| Yu, W | 1 |
| Zhao, Y | 1 |
| Guo, J | 1 |
| Zhang, P | 1 |
| Huang, X | 1 |
| Qiao, Y | 1 |
| Kim, DW | 1 |
| Tan, E | 1 |
| Zhou, JM | 1 |
| Schell, MJ | 1 |
| Martinez, M | 1 |
| Yu, J | 1 |
| Carballido, E | 1 |
| Mehta, R | 1 |
| Strosberg, J | 1 |
| Imanirad, I | 1 |
| Kim, RD | 1 |
| Liu, M | 1 |
| Zhao, G | 1 |
| Zhang, D | 1 |
| An, W | 1 |
| Lai, H | 1 |
| Li, X | 1 |
| Cao, S | 1 |
| Lin, X | 1 |
| Yang, JW | 1 |
| Zhang, QH | 1 |
| Liu, T | 1 |
| Nelson, SR | 1 |
| Kathe, SD | 1 |
| Hilzinger, TS | 1 |
| Averill, AM | 1 |
| Warshaw, DM | 1 |
| Wallace, SS | 1 |
| Lee, AJ | 1 |
| Dong, Y | 1 |
| Wu, Y | 1 |
| Zhao, GL | 1 |
| Ye, ZY | 1 |
| Xing, CG | 1 |
| Yang, XD | 1 |
| Chao, XL | 1 |
| Wang, LL | 1 |
| Liu, R | 1 |
| Li, Y | 1 |
| Zhou, XJ | 1 |
| Raina, K | 1 |
| Agarwal, C | 1 |
| Wadhwa, R | 1 |
| Serkova, NJ | 1 |
| Agarwal, R | 1 |
| Lee, Y | 1 |
| Sung, B | 1 |
| Kang, YJ | 1 |
| Kim, DH | 1 |
| Jang, JY | 1 |
| Hwang, SY | 1 |
| Kim, M | 1 |
| Lim, HS | 1 |
| Yoon, JH | 1 |
| Chung, HY | 1 |
| Kim, ND | 1 |
| Min, H | 1 |
| Xu, M | 1 |
| Chen, ZR | 1 |
| Zhou, JD | 1 |
| Huang, M | 1 |
| Zheng, K | 1 |
| Zou, XP | 1 |
| Zhang, JW | 1 |
| Zhang, SS | 1 |
| Song, JR | 1 |
| Sun, K | 1 |
| Zong, C | 1 |
| Zhao, QD | 1 |
| Liu, WT | 1 |
| Li, R | 1 |
| Wu, MC | 1 |
| Wei, LX | 1 |
| Won, SJ | 1 |
| Yen, CH | 1 |
| Liu, HS | 1 |
| Wu, SY | 1 |
| Lan, SH | 1 |
| Jiang-Shieh, YF | 1 |
| Lin, CN | 1 |
| Su, CL | 1 |
| Shi, Y | 2 |
| Han, Y | 1 |
| Xie, F | 1 |
| Wang, A | 1 |
| Feng, X | 1 |
| Li, N | 1 |
| Guo, H | 2 |
| Chen, D | 2 |
| Yan, X | 1 |
| Kou, B | 1 |
| Zhu, Z | 1 |
| Chai, J | 1 |
| Jing, Z | 1 |
| Fei, W | 1 |
| Zhou, J | 1 |
| Zhang, L | 1 |
| Chen, L | 1 |
| Zhang, X | 1 |
| Liang, X | 1 |
| Xie, J | 1 |
| Fang, Y | 1 |
| Sui, X | 1 |
| Han, W | 1 |
| Pan, H | 1 |
| Zhou, W | 1 |
| Xu, G | 1 |
| Wang, Y | 1 |
| Xu, Z | 1 |
| Liu, X | 1 |
| Xu, X | 1 |
| Ren, G | 1 |
| Tian, K | 1 |
| Ali, M | 1 |
| Kim, H | 1 |
| Cleary, S | 1 |
| Cupples, C | 1 |
| Gallinger, S | 1 |
| Bristow, R | 1 |
| Ko, H | 1 |
| Kim, YJ | 1 |
| Amor, EC | 1 |
| Lee, JW | 1 |
| Kim, HC | 1 |
| Kim, HJ | 1 |
| Yang, HO | 1 |
| Zulhabri, O | 1 |
| Rahman, J | 1 |
| Ismail, S | 1 |
| Isa, MR | 1 |
| Wan Zurinah, WN | 1 |
| Chmiel, NH | 1 |
| Livingston, AL | 1 |
| David, SS | 1 |
| Parker, AR | 1 |
| O'Meally, RN | 1 |
| Sahin, F | 1 |
| Su, GH | 1 |
| Racke, FK | 1 |
| Nelson, WG | 1 |
| DeWeese, TL | 1 |
| Eshleman, JR | 1 |
| Le Marchand, L | 1 |
| Seifried, A | 1 |
| Lum-Jones, A | 1 |
| Donlon, T | 1 |
| Wilkens, LR | 1 |
| Gismondi, V | 1 |
| Meta, M | 1 |
| Bonelli, L | 1 |
| Radice, P | 1 |
| Sala, P | 1 |
| Bertario, L | 1 |
| Viel, A | 1 |
| Fornasarig, M | 1 |
| Arrigoni, A | 1 |
| Gentile, M | 1 |
| Ponz de Leon, M | 1 |
| Anselmi, L | 1 |
| Mareni, C | 1 |
| Bruzzi, P | 1 |
| Varesco, L | 1 |
| Shin, Y | 1 |
| Kim, IJ | 1 |
| Kang, HC | 1 |
| Park, JH | 1 |
| Park, HW | 1 |
| Jang, SG | 1 |
| Lee, MR | 1 |
| Jeong, SY | 1 |
| Chang, HJ | 1 |
| Ku, JL | 1 |
| Park, JG | 1 |
| Morel, A | 1 |
| Boisdron-Celle, M | 1 |
| Fey, L | 1 |
| Lainé-Cessac, P | 1 |
| Gamelin, E | 1 |
| Takahashi, T | 1 |
| Nosho, K | 1 |
| Yamamoto, H | 1 |
| Mikami, M | 1 |
| Taniguchi, H | 1 |
| Miyamoto, N | 1 |
| Adachi, Y | 1 |
| Itoh, F | 1 |
| Imai, K | 1 |
| Shinomura, Y | 1 |
| Marschke, RF | 1 |
| Wieand, HS | 1 |
| O'Connell, MJ | 1 |
| Rubin, J | 1 |
| Schutt, AJ | 1 |
| Burch, PA | 1 |
| Kovach, JS | 1 |
| Brown, TD | 1 |
| Goodman, PJ | 1 |
| Fleming, T | 1 |
| Macdonald, JS | 1 |
| Craig, JB | 1 |
| Einstein, AB | 1 |
| Harwood, J | 1 |
| Tachibana, A | 1 |
| Davis, R | 1 |
| Bhattacharyya, NP | 1 |
| Meuth, M | 1 |
| Esteller, M | 1 |
| Toyota, M | 1 |
| Sanchez-Cespedes, M | 1 |
| Capella, G | 1 |
| Peinado, MA | 1 |
| Watkins, DN | 1 |
| Issa, JP | 1 |
| Sidransky, D | 1 |
| Baylin, SB | 1 |
| Herman, JG | 1 |
| O'Dwyer, PJ | 1 |
| Paul, AR | 1 |
| Hudes, GR | 1 |
| Walczak, J | 1 |
| Ozols, RF | 1 |
| Comis, RL | 1 |
| Scheithauer, W | 1 |
| Kornek, G | 1 |
| Haider, K | 1 |
| Depisch, D | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Phase I/II Study of Pembrolizumab in Combination With Ibrutinib for Advanced, Refractory Colorectal Cancers[NCT03332498] | Phase 1/Phase 2 | 40 participants (Actual) | Interventional | 2018-01-24 | Completed | ||
| NIVOLUMAB Plus IPILIMUMAB and TEMOZOLOMIDE in Combination in Microsatellite Stable (MSS), MGMT Silenced Metastatic Colorectal Cancer (mCRC): the MAYA Study[NCT03832621] | Phase 2 | 135 participants (Actual) | Interventional | 2019-03-25 | Completed | ||
| Multicenter Phase II Study of Preoperative Chemoradiotherapy With CApecitabine Plus Temozolomide in Patients With MGMT Silenced and Microsatellite Stable Locally Advanced RecTal Cancer: the CATARTIC Trial[NCT05136326] | Phase 2 | 21 participants (Anticipated) | Interventional | 2021-12-01 | Recruiting | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Standard 3+3 Design: The first cohort will enroll a minimum of 3 participants, according to a standard 3+3 design. If 0 out of the first 3 participants in the first cohort experience a dose-limiting toxicity (DLT), then dose escalation will continue as planned. If 1 out of the first 3 participants experience a DLT, then the cohort will be expanded to a total of 6 participants, and if no more than 1 out of 6 participants experiences a DLT in a given dose cohort, dose escalation will continue as planned. If ≥ 2 DLTs are observed in the first dose cohort, the principle investigator will discuss with Janssen on how to proceed. The DLT evaluation period will be defined as the time from the first dose of pembrolizumab and ibrutinib to 42 days after the first dose or if a participant experiences a DLT within this time period. (NCT03332498)
Timeframe: 42 days post first dose
| Intervention | mg (Number) |
|---|---|
| Pembrolizumab and Ibrutinib | 560 |
Percentage of participants who achieved disease control at 4 months. Disease control rate = Complete Response (CR) + Partial Response (PR) + Stable Disease (SD). Tumor response by Response Evaluation Criteria in Solid Tumors (RECIST) 1.1 and RECIST based immune-related response criteria (irRC). (NCT03332498)
Timeframe: 4 months
| Intervention | percentage of participants (Number) |
|---|---|
| Phase 2: Treatment at RP2D | 13 |
4 trials available for adenine and Colorectal Neoplasms
| Article | Year |
|---|---|
A phase 1/2 trial of ibrutinib in combination with pembrolizumab in patients with mismatch repair proficient metastatic colorectal cancer.
Topics: Adenine; Adenocarcinoma; Adult; Aged; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Che | 2021 |
Advanced colorectal adenocarcinoma: treatment with amonafide.
Topics: Adenine; Antineoplastic Agents; Carcinoma; Colorectal Neoplasms; Humans; Imides; Intercalating Agent | 1994 |
Phase II trial of amonafide in advanced colorectal cancer: a SouthWest Oncology Group study.
Topics: Adenine; Adenocarcinoma; Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Colorectal Neoplasms | 1993 |
Phase II study of amonafide (nafidamide, NSC 308847) in advanced colorectal cancer.
Topics: Adenine; Adenocarcinoma; Antineoplastic Agents; Colorectal Neoplasms; Drug Evaluation; Humans; Imide | 1991 |
29 other studies available for adenine and Colorectal Neoplasms
| Article | Year |
|---|---|
Ibrutinib and panitumumab used in combination safely in a patient with metachronous colorectal cancer and chronic lymphocytic leukemia.
Topics: Adenine; Colorectal Neoplasms; Humans; Leukemia, Lymphocytic, Chronic, B-Cell; Male; Middle Aged; Pa | 2022 |
Functional Phosphoproteomics in Cancer Chemoresistance Using CRISPR-Mediated Base Editors.
Topics: Adenine; Amino Acids; Clustered Regularly Interspaced Short Palindromic Repeats; Colorectal Neoplasm | 2022 |
Active fraction of clove induces apoptosis via PI3K/Akt/mTOR-mediated autophagy in human colorectal cancer HCT-116 cells.
Topics: Adenine; Antineoplastic Agents, Phytogenic; Apoptosis; Autophagy; Cell Proliferation; Cell Survival; | 2018 |
Autophagy facilitates anticancer effect of 5-fluorouracil in HCT-116 cells.
Topics: Adenine; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Autophagy; Beclin-1; Cell Prolif | 2018 |
Single molecule glycosylase studies with engineered 8-oxoguanine DNA damage sites show functional defects of a MUTYH polyposis variant.
Topics: Adenine; Adenomatous Polyposis Coli; Animals; Colorectal Neoplasms; DNA Damage; DNA Glycosylases; Es | 2019 |
Inhibition of autophagy by 3-MA promotes hypoxia-induced apoptosis in human colorectal cancer cells.
Topics: Adenine; Annexin A5; Apoptosis; Autophagy; Cell Line, Tumor; Cell Proliferation; Colorectal Neoplasm | 2019 |
Association between CA repeat polymorphism in IGF1 gene promoter and colorectal cancer risk in a native Chinese population.
Topics: Adenine; Case-Control Studies; China; Colorectal Neoplasms; Cytosine; Female; Genetic Predisposition | 2019 |
Energy deprivation by silibinin in colorectal cancer cells: a double-edged sword targeting both apoptotic and autophagic machineries.
Topics: Adenine; AMP-Activated Protein Kinases; Animals; Apoptosis; Autophagy; Cell Line, Tumor; Cell Shape; | 2013 |
Apigenin-induced apoptosis is enhanced by inhibition of autophagy formation in HCT116 human colon cancer cells.
Topics: Adenine; Antineoplastic Agents; Apigenin; Apoptosis; Autophagy; Cell Cycle; Cell Line, Tumor; Colore | 2014 |
Bortezomib induces protective autophagy through AMP-activated protein kinase activation in cultured pancreatic and colorectal cancer cells.
Topics: Adenine; AMP-Activated Protein Kinases; Antineoplastic Agents; Autophagy; Boronic Acids; Bortezomib; | 2014 |
Autophagy inhibition switches low-dose camptothecin-induced premature senescence to apoptosis in human colorectal cancer cells.
Topics: Adenine; AMP-Activated Protein Kinases; Antineoplastic Agents; Apoptosis; Ataxia Telangiectasia Muta | 2014 |
Justicidin A-induced autophagy flux enhances apoptosis of human colorectal cancer cells via class III PI3K and Atg5 pathway.
Topics: Adenine; Animals; Apoptosis; Autophagy; Autophagy-Related Protein 5; Colorectal Neoplasms; Dioxolane | 2015 |
ASPP2 enhances oxaliplatin (L-OHP)-induced colorectal cancer cell apoptosis in a p53-independent manner by inhibiting cell autophagy.
Topics: Adenine; Animals; Antineoplastic Agents; Apoptosis; Apoptosis Regulatory Proteins; Autophagy; Cell L | 2015 |
[Keratin 18 phosphorylation increases autophagy of colorectal cancer HCT116 cells and enhanced its sensitivity to oxaliplatin].
Topics: Adenine; Antineoplastic Agents; Apoptosis; Autophagy; Blotting, Western; Colorectal Neoplasms; Flow | 2016 |
Salvianolic acid B, a novel autophagy inducer, exerts antitumor activity as a single agent in colorectal cancer cells.
Topics: Adenine; Animals; Antineoplastic Agents; Autophagosomes; Autophagy; Autophagy-Related Protein 5; Ben | 2016 |
Oxidative stress induced autophagy in cancer associated fibroblast enhances proliferation and metabolism of colorectal cancer cells.
Topics: Acetylcysteine; Adenine; Autophagy; Blotting, Western; Cancer-Associated Fibroblasts; Cell Line, Tum | 2017 |
Characterization of mutant MUTYH proteins associated with familial colorectal cancer.
Topics: Adenine; Adenomatous Polyposis Coli; Amino Acid Sequence; Cloning, Molecular; Colorectal Neoplasms; | 2008 |
Induction of autophagy by dimethyl cardamonin is associated with proliferative arrest in human colorectal carcinoma HCT116 and LOVO cells.
Topics: Adenine; Antineoplastic Agents; Apoptosis; Apoptosis Regulatory Proteins; Autophagy; Autophagy-Relat | 2011 |
Predominance of G to A codon 12 mutation K-ras gene in Dukes' B colorectal cancer.
Topics: Adenine; Adenoma; Adult; Aged; Aged, 80 and over; Aspartic Acid; Carcinoma; Codon; Colorectal Neopla | 2012 |
Insight into the functional consequences of inherited variants of the hMYH adenine glycosylase associated with colorectal cancer: complementation assays with hMYH variants and pre-steady-state kinetics of the corresponding mutated E.coli enzymes.
Topics: 8-Hydroxy-2'-Deoxyguanosine; Adenine; Adenomatous Polyposis Coli; Base Pair Mismatch; Binding Sites; | 2003 |
Defective human MutY phosphorylation exists in colorectal cancer cell lines with wild-type MutY alleles.
Topics: Adenine; Adjuvants, Immunologic; Alleles; Amino Acid Sequence; Base Pair Mismatch; Carcinogens; Case | 2003 |
Association of the cyclin D1 A870G polymorphism with advanced colorectal cancer.
Topics: Adenine; Aged; Asian People; Case-Control Studies; Colorectal Neoplasms; Female; Gene Dosage; Genes, | 2003 |
Prevalence of the Y165C, G382D and 1395delGGA germline mutations of the MYH gene in Italian patients with adenomatous polyposis coli and colorectal adenomas.
Topics: Adenine; Adenoma; Adenomatous Polyposis Coli; Adult; Aged; Aspartic Acid; Case-Control Studies; Colo | 2004 |
A functional polymorphism (-347 G-->GA) in the E-cadherin gene is associated with colorectal cancer.
Topics: Adenine; Adolescent; Adult; Aged; Aged, 80 and over; Cadherins; Colorectal Neoplasms; Female; Guanin | 2004 |
Identification of a novel mutation in the dihydropyrimidine dehydrogenase gene in a patient with a lethal outcome following 5-fluorouracil administration and the determination of its frequency in a population of 500 patients with colorectal carcinoma.
Topics: Adenine; Aged; Alleles; Colorectal Neoplasms; Dihydrouracil Dehydrogenase (NADP); DNA Mutational Ana | 2007 |
Flat-type colorectal advanced adenomas (laterally spreading tumors) have different genetic and epigenetic alterations from protruded-type advanced adenomas.
Topics: Adaptor Proteins, Signal Transducing; Adenine; Adenoma; Aged; beta Catenin; Carrier Proteins; Colore | 2007 |
High rate of multilocus deletion in a human tumor cell line.
Topics: Adenine; Adenine Phosphoribosyltransferase; Adenocarcinoma; Alleles; Base Sequence; Cell Transformat | 1993 |
Inactivation of the DNA repair gene O6-methylguanine-DNA methyltransferase by promoter hypermethylation is associated with G to A mutations in K-ras in colorectal tumorigenesis.
Topics: Adenine; Adenoma; Carcinoma; Colorectal Neoplasms; DNA Methylation; Gene Silencing; Genes, p53; Gene | 2000 |
Inactivation of the DNA repair gene O6-methylguanine-DNA methyltransferase by promoter hypermethylation is associated with G to A mutations in K-ras in colorectal tumorigenesis.
Topics: Adenine; Adenoma; Carcinoma; Colorectal Neoplasms; DNA Methylation; Gene Silencing; Genes, p53; Gene | 2000 |
Inactivation of the DNA repair gene O6-methylguanine-DNA methyltransferase by promoter hypermethylation is associated with G to A mutations in K-ras in colorectal tumorigenesis.
Topics: Adenine; Adenoma; Carcinoma; Colorectal Neoplasms; DNA Methylation; Gene Silencing; Genes, p53; Gene | 2000 |
Inactivation of the DNA repair gene O6-methylguanine-DNA methyltransferase by promoter hypermethylation is associated with G to A mutations in K-ras in colorectal tumorigenesis.
Topics: Adenine; Adenoma; Carcinoma; Colorectal Neoplasms; DNA Methylation; Gene Silencing; Genes, p53; Gene | 2000 |
Amonafide in metastatic colorectal carcinoma.
Topics: Adenine; Aged; Antineoplastic Agents; Colorectal Neoplasms; Female; Humans; Imides; Isoquinolines; M | 1990 |