-
1
-
-
0025773554
-
Mutator phenotype may be required for multistage carcinogenesis
-
Loeb LA. Mutator phenotype may be required for multistage carcinogenesis. Cancer Res. 51:1991;3075-3079.
-
(1991)
Cancer Res
, vol.51
, pp. 3075-3079
-
-
Loeb, L.A.1
-
2
-
-
0013579690
-
Repair tracts in mismatched DNA heteroduplexes
-
Wagner R, Meselson M. Repair tracts in mismatched DNA heteroduplexes. Proc Natl Acad Sci USA. 73:1976;4135-4139.
-
(1976)
Proc Natl Acad Sci USA
, vol.73
, pp. 4135-4139
-
-
Wagner, R.1
Meselson, M.2
-
3
-
-
0016609698
-
Pleiotropic effects of a DNA adenine methylation mutation (dam-3) in Escherichia coli K12
-
Marinus MG, Morris NR. Pleiotropic effects of a DNA adenine methylation mutation (dam-3) in Escherichia coli K12. Mutat Res. 28:1975;15-26.
-
(1975)
Mutat Res
, vol.28
, pp. 15-26
-
-
Marinus, M.G.1
Morris, N.R.2
-
4
-
-
0026536644
-
Repair of DNA heteroduplexes containing small heterologous sequences in Escherichia coli
-
Parker BO, Marinus MG. Repair of DNA heteroduplexes containing small heterologous sequences in Escherichia coli. Proc Natl Acad Sci USA. 89:1992;1730-1734.
-
(1992)
Proc Natl Acad Sci USA
, vol.89
, pp. 1730-1734
-
-
Parker, B.O.1
Marinus, M.G.2
-
5
-
-
0000083876
-
Escherichia coli mutS-encoded protein binds to mismatched DNA base pairs
-
Su SS, Modrich P. Escherichia coli mutS-encoded protein binds to mismatched DNA base pairs. Proc Natl Acad Sci USA. 83:1986;5057-5061.
-
(1986)
Proc Natl Acad Sci USA
, vol.83
, pp. 5057-5061
-
-
Su, S.S.1
Modrich, P.2
-
8
-
-
0024494766
-
Isolation and characterization of the Escherichia coli mutL gene product
-
Grilley M, Welsh KM, Su SS, Modrich P. Isolation and characterization of the Escherichia coli mutL gene product. J Biol Chem. 264:1989;1000-1004.
-
(1989)
J Biol Chem
, vol.264
, pp. 1000-1004
-
-
Grilley, M.1
Welsh, K.M.2
Su, S.S.3
Modrich, P.4
-
9
-
-
0027522357
-
Molecular matchmakers
-
Sancar A, Hearst JE. Molecular matchmakers. Science. 259:1993;1415-1420.
-
(1993)
Science
, vol.259
, pp. 1415-1420
-
-
Sancar, A.1
Hearst, J.E.2
-
10
-
-
0024430850
-
Cloning and nucleotide sequence of DNA mismatch repair gene PMS1 from Saccharomyces cerevisiae: Homology of PMS1 to procaryotic MutL and HexB
-
Kramer W, Kramer B, Williamson MS, Fogel S. Cloning and nucleotide sequence of DNA mismatch repair gene PMS1 from Saccharomyces cerevisiae: homology of PMS1 to procaryotic MutL and HexB. J Bacteriol. 171:1989;5339-5346.
-
(1989)
J Bacteriol
, vol.171
, pp. 5339-5346
-
-
Kramer, W.1
Kramer, B.2
Williamson, M.S.3
Fogel, S.4
-
11
-
-
0028157956
-
Dual requirement in yeast DNA mismatch repair for MLH1 and PMS1, two homologs of the bacterial mutL gene
-
Prolla TA, Christie DM, Liskay RM. Dual requirement in yeast DNA mismatch repair for MLH1 and PMS1, two homologs of the bacterial mutL gene. Mol Cell Biol. 14:1994;407-415.
-
(1994)
Mol Cell Biol
, vol.14
, pp. 407-415
-
-
Prolla, T.A.1
Christie, D.M.2
Liskay, R.M.3
-
12
-
-
0026446241
-
Isolation and characterization of two Saccharomyces cerevisiae genes encoding homologs of the bacterial HexA and MutS mismatch repair proteins
-
Reenan RA, Kolodner RD. Isolation and characterization of two Saccharomyces cerevisiae genes encoding homologs of the bacterial HexA and MutS mismatch repair proteins. Genetics. 132:1992;963-973.
-
(1992)
Genetics
, vol.132
, pp. 963-973
-
-
Reenan, R.A.1
Kolodner, R.D.2
-
13
-
-
0026445628
-
Characterization of insertion mutations in the Saccharomyces cerevisiae MSH1 and MSH2 genes: Evidence for separate mitochondrial and nuclear functions
-
Reenan RA, Kolodner RD. Characterization of insertion mutations in the Saccharomyces cerevisiae MSH1 and MSH2 genes: evidence for separate mitochondrial and nuclear functions. Genetics. 132:1992;975-985.
-
(1992)
Genetics
, vol.132
, pp. 975-985
-
-
Reenan, R.A.1
Kolodner, R.D.2
-
14
-
-
0028128601
-
MLH1, PMS1, and MSH2 interactions during the initiation of DNA mismatch repair in yeast
-
Prolla TA, Pang Q, Alani E, Kolodner RD, Liskay RM. MLH1, PMS1, and MSH2 interactions during the initiation of DNA mismatch repair in yeast. Science. 265:1994;1091-1093.
-
(1994)
Science
, vol.265
, pp. 1091-1093
-
-
Prolla, T.A.1
Pang, Q.2
Alani, E.3
Kolodner, R.D.4
Liskay, R.M.5
-
15
-
-
0030755372
-
Functional domains of the Saccharomyces cerevisiae Mlh1p and Pms1p DNA mismatch repair proteins and their relevance to human hereditary nonpolyposis colorectal cancer-associated mutations
-
Pang Q, Prolla TA, Liskay RM. Functional domains of the Saccharomyces cerevisiae Mlh1p and Pms1p DNA mismatch repair proteins and their relevance to human hereditary nonpolyposis colorectal cancer-associated mutations. Mol Cell Biol. 17:1997;4465-4473.
-
(1997)
Mol Cell Biol
, vol.17
, pp. 4465-4473
-
-
Pang, Q.1
Prolla, T.A.2
Liskay, R.M.3
-
16
-
-
0029868110
-
Redundancy of Saccharomyces cerevisiae MSH3 and MSH6 in MSH2-dependent mismatch repair
-
of outstanding interest. S. cerevisiae has two pathways of MSH2-dependent mismatch repair: one that recognizes single-base mispairs and requires MSH2 and MSH6, and a second that recognizes insertion/deletion mispairs and requires a combination of either MSH2 and MSH6, or MSH2 and MSH3. The redundancy of MSH3 and MSH6 function may explain the rarity of mismatch mutations in hMSH6 and hMSH3 in human cancer.
-
Marsischky GT, Filosi N, Kane MF, Kolodner R. Redundancy of Saccharomyces cerevisiae MSH3 and MSH6 in MSH2-dependent mismatch repair. of outstanding interest Genes Dev. 10:1996;407-420 S. cerevisiae has two pathways of MSH2-dependent mismatch repair: one that recognizes single-base mispairs and requires MSH2 and MSH6, and a second that recognizes insertion/deletion mispairs and requires a combination of either MSH2 and MSH6, or MSH2 and MSH3. The redundancy of MSH3 and MSH6 function may explain the rarity of mismatch mutations in hMSH6 and hMSH3 in human cancer.
-
(1996)
Genes Dev
, vol.10
, pp. 407-420
-
-
Marsischky, G.T.1
Filosi, N.2
Kane, M.F.3
Kolodner, R.4
-
17
-
-
0029813614
-
The Saccharomyces cerevisiae Msh2 and Msh6 proteins form a complex that specifically binds to duplex oligonucleotides containing mismatched DNA base pairs
-
Alani E. The Saccharomyces cerevisiae Msh2 and Msh6 proteins form a complex that specifically binds to duplex oligonucleotides containing mismatched DNA base pairs. Mol Cell Biol. 16:1996;5604-5615.
-
(1996)
Mol Cell Biol
, vol.16
, pp. 5604-5615
-
-
Alani, E.1
-
18
-
-
0030962031
-
Genetic and biochemical analysis of Msh2p-Msh6p: Role of ATP hydrolysis and Msh2p-Msh6p subunit interactions in mismatch base pair recognition
-
of special interest. Genetic and biochemical analysis of the Msh2p - Msh6p complex was performed through the introduction of mutations in the ATP binding and putative helix-turn-helix domains of MSH2. The study suggests that the ability of the Msh2p - Msh6p complex to induce ATP hydrolysis following DNA mismatch binding is a good indicator of biological activity. This study implies that monitoring ATP hydrolysis by the Msh2p - Msh6p complex should be performed to help determine if recognition of a given DNA lesion in vitro is relevant to biological repair activity in vivo.
-
Alani E, Sokolsky T, Studamire B, Miret JJ, Lahue RS. Genetic and biochemical analysis of Msh2p-Msh6p: role of ATP hydrolysis and Msh2p-Msh6p subunit interactions in mismatch base pair recognition. of special interest Mol Cell Biol. 17:1997;2436-2447 Genetic and biochemical analysis of the Msh2p - Msh6p complex was performed through the introduction of mutations in the ATP binding and putative helix-turn-helix domains of MSH2. The study suggests that the ability of the Msh2p - Msh6p complex to induce ATP hydrolysis following DNA mismatch binding is a good indicator of biological activity. This study implies that monitoring ATP hydrolysis by the Msh2p - Msh6p complex should be performed to help determine if recognition of a given DNA lesion in vitro is relevant to biological repair activity in vivo.
-
(1997)
Mol Cell Biol
, vol.17
, pp. 2436-2447
-
-
Alani, E.1
Sokolsky, T.2
Studamire, B.3
Miret, J.J.4
Lahue, R.S.5
-
19
-
-
0028862897
-
Mutations in the MSH3 gene preferentially lead to deletions within tracts of simple repetitive DNA in Saccharomyces cerevisiae
-
Strand M, Earley MC, Crouse GF, Petes TD. Mutations in the MSH3 gene preferentially lead to deletions within tracts of simple repetitive DNA in Saccharomyces cerevisiae. Proc Natl Acad Sci USA. 92:1995;10418-10421.
-
(1995)
Proc Natl Acad Sci USA
, vol.92
, pp. 10418-10421
-
-
Strand, M.1
Earley, M.C.2
Crouse, G.F.3
Petes, T.D.4
-
20
-
-
0027306173
-
Destabilization of tracts of simple repetitive DNA in yeast by mutations affecting DNA mismatch repair
-
Strand M, Prolla TA, Liskay RM, Petes TD. Destabilization of tracts of simple repetitive DNA in yeast by mutations affecting DNA mismatch repair. Nature. 365:1993;274-276.
-
(1993)
Nature
, vol.365
, pp. 274-276
-
-
Strand, M.1
Prolla, T.A.2
Liskay, R.M.3
Petes, T.D.4
-
21
-
-
0023649836
-
High frequencies of short frameshifts in poly-CA/TG tandem repeats borne by bacteriophage M13 in Escherichia coli K-12
-
Levinson G, Gutman GA. High frequencies of short frameshifts in poly-CA/TG tandem repeats borne by bacteriophage M13 in Escherichia coli K-12. Nucleic Acids Res. 15:1987;5323-5338.
-
(1987)
Nucleic Acids Res
, vol.15
, pp. 5323-5338
-
-
Levinson, G.1
Gutman, G.A.2
-
22
-
-
0028981276
-
The Saccharomyces cerevisiae Msh2 protein specifically binds to duplex oligonucleotides containing mismatched DNA base pairs and insertions
-
Alani E, Chi NW, Kolodner R. The Saccharomyces cerevisiae Msh2 protein specifically binds to duplex oligonucleotides containing mismatched DNA base pairs and insertions. Genes Dev. 9:1995;234-247.
-
(1995)
Genes Dev
, vol.9
, pp. 234-247
-
-
Alani, E.1
Chi, N.W.2
Kolodner, R.3
-
23
-
-
0028277915
-
Error-prone replication of repeated DNA sequences by T7 DNA polymerase in the absence of its processivity subunit
-
Kunkel TA, Patel SS, Johnson KA. Error-prone replication of repeated DNA sequences by T7 DNA polymerase in the absence of its processivity subunit. Proc Natl Acad Sci USA. 91:1994;6830-6834.
-
(1994)
Proc Natl Acad Sci USA
, vol.91
, pp. 6830-6834
-
-
Kunkel, T.A.1
Patel, S.S.2
Johnson, K.A.3
-
24
-
-
0027285475
-
Ubiquitous somatic mutations in simple repeated sequences reveal a new mechanism for colonic carcinogenesis
-
Ionov Y, Peinado MA, Malkhosyan S, Shibata D, Perucho M. Ubiquitous somatic mutations in simple repeated sequences reveal a new mechanism for colonic carcinogenesis. Nature. 363:1993;558-561.
-
(1993)
Nature
, vol.363
, pp. 558-561
-
-
Ionov, Y.1
Peinado, M.A.2
Malkhosyan, S.3
Shibata, D.4
Perucho, M.5
-
25
-
-
0027158031
-
Clues to the pathogenesis of familial colorectal cancer
-
Aaltonen LA, Peltomaki P, Leach FS, Sistonen P, Pylkkanen L, Mecklin JP, Jarvinen H, Powell SM, Jen J, Hamilton SR, et al. Clues to the pathogenesis of familial colorectal cancer. Science. 260:1993;812-826.
-
(1993)
Science
, vol.260
, pp. 812-826
-
-
Aaltonen, L.A.1
Peltomaki, P.2
Leach, F.S.3
Sistonen, P.4
Pylkkanen, L.5
Mecklin, J.P.6
Jarvinen, H.7
Powell, S.M.8
Jen, J.9
Hamilton, S.R.10
-
26
-
-
0029833872
-
Hereditary nonpolyposis colorectal cancer (Lynch syndrome). An updated review
-
Lynch HT, Smyrk T. Hereditary nonpolyposis colorectal cancer (Lynch syndrome). An updated review. Cancer. 78:1996;1149-1167.
-
(1996)
Cancer
, vol.78
, pp. 1149-1167
-
-
Lynch, H.T.1
Smyrk, T.2
-
27
-
-
0028221943
-
Mutation in the DNA mismatch repair gene homologue hMLH1 is associated with hereditary nonpolyposis colon cancer
-
Bronner CE, Baker SM, Morrison PT, Warren G, Smith LG, Lescoe MK, Kane M, Earabino C, Lipford J, Lindblom A, et al. Mutation in the DNA mismatch repair gene homologue hMLH1 is associated with hereditary nonpolyposis colon cancer. Nature. 368:1994;258-261.
-
(1994)
Nature
, vol.368
, pp. 258-261
-
-
Bronner, C.E.1
Baker, S.M.2
Morrison, P.T.3
Warren, G.4
Smith, L.G.5
Lescoe, M.K.6
Kane, M.7
Earabino, C.8
Lipford, J.9
Lindblom, A.10
-
28
-
-
0027933070
-
Mutations of two PMS homologues in hereditary nonpolyposis colon cancer
-
Nicolaides NC, Papadopoulos N, Liu B, Wei YF, Carter KC, Ruben SM, Rosen CA, Haseltine WA, Fleischmann RD, Fraser CM, et al. Mutations of two PMS homologues in hereditary nonpolyposis colon cancer. Nature. 371:1994;75-80.
-
(1994)
Nature
, vol.371
, pp. 75-80
-
-
Nicolaides, N.C.1
Papadopoulos, N.2
Liu, B.3
Wei, Y.F.4
Carter, K.C.5
Ruben, S.M.6
Rosen, C.A.7
Haseltine, W.A.8
Fleischmann, R.D.9
Fraser, C.M.10
-
29
-
-
0027145633
-
Mutations of a mutS homolog in hereditary nonpolyposis colorectal cancer
-
Leach FS, Nicolaides NC, Papadopoulos N, Liu B, Jen J, Parsons R, Peltomaki P, Sistonen P, Aaltonen LA, Nystrom-Lahti M, et al. Mutations of a mutS homolog in hereditary nonpolyposis colorectal cancer. Cell. 75:1993;1215-1225.
-
(1993)
Cell
, vol.75
, pp. 1215-1225
-
-
Leach, F.S.1
Nicolaides, N.C.2
Papadopoulos, N.3
Liu, B.4
Jen, J.5
Parsons, R.6
Peltomaki, P.7
Sistonen, P.8
Aaltonen, L.A.9
Nystrom-Lahti, M.10
-
30
-
-
0027742295
-
The human mutator gene homolog MSH2 and its association with hereditary nonpolyposis colon cancer
-
Fishel R, Lescoe MK, Rao MR, Copeland NG, Jenkins NA, Garber J, Kane M, Kolodner R. The human mutator gene homolog MSH2 and its association with hereditary nonpolyposis colon cancer. Cell. 75:1993;1027-1038.
-
(1993)
Cell
, vol.75
, pp. 1027-1038
-
-
Fishel, R.1
Lescoe, M.K.2
Rao, M.R.3
Copeland, N.G.4
Jenkins, N.A.5
Garber, J.6
Kane, M.7
Kolodner, R.8
-
31
-
-
2942569549
-
Analysis of mismatch repair genes in hereditary nonpolyposis colorectal cancer patients
-
Liu B, Parsons R, Papadopoulos N, Nicolaides NC, Lynch HT, Watson P, Jass JR, Dunlop M, Wyllie A, Peltomaki P, et al. Analysis of mismatch repair genes in hereditary nonpolyposis colorectal cancer patients. Nat Med. 2:1996;169-174.
-
(1996)
Nat Med
, vol.2
, pp. 169-174
-
-
Liu, B.1
Parsons, R.2
Papadopoulos, N.3
Nicolaides, N.C.4
Lynch, H.T.5
Watson, P.6
Jass, J.R.7
Dunlop, M.8
Wyllie, A.9
Peltomaki, P.10
-
32
-
-
0028941627
-
Restoration of mismatch repair to nuclear extracts of H6 colorectal tumor cells by a heterodimer of human MutL homologs
-
Li GM, Modrich P. Restoration of mismatch repair to nuclear extracts of H6 colorectal tumor cells by a heterodimer of human MutL homologs. Proc Natl Acad Sci USA. 92:1995;1950-1954.
-
(1995)
Proc Natl Acad Sci USA
, vol.92
, pp. 1950-1954
-
-
Li, G.M.1
Modrich, P.2
-
33
-
-
0029069972
-
Mutations of GTBP in genetically unstable cells
-
Papadopoulos N, Nicolaides NC, Liu B, Parsons R, Lengauer C, Palombo F, D'Arrigo A, Markowitz S, Willson JK, Kinzler KW, et al. Mutations of GTBP in genetically unstable cells. Science. 268:1995;1915-1917.
-
(1995)
Science
, vol.268
, pp. 1915-1917
-
-
Papadopoulos, N.1
Nicolaides, N.C.2
Liu, B.3
Parsons, R.4
Lengauer, C.5
Palombo, F.6
D'Arrigo, A.7
Markowitz, S.8
Willson, J.K.9
Kinzler, K.W.10
-
34
-
-
0030870631
-
Germ-line mutation of the hMSH6/GTBP gene in an atypical hereditary nonpolyposis colorectal cancer kindred
-
of special interest. This is the first report of an hMSH6 mutation in hereditary cancer. The patient had rectal cancer and two colon adenomas at 62 years of age, and a weak family history of gastrointestinal tumors. He does not meet HNPCC classification criteria because of the weak family history. This study suggests that hereditary cancer associated with hMSH6 mutation is not likely to be detected by genetic testing of patients that meet standard HNPCC classification criteria (Amsterdam criteria).
-
Akiyama Y, Sato H, Yamada T, Nagasaki H, Tsuchiya A, Abe R, Yuasa Y. Germ-line mutation of the hMSH6/GTBP gene in an atypical hereditary nonpolyposis colorectal cancer kindred. of special interest Cancer Res. 57:1997;3920-3923 This is the first report of an hMSH6 mutation in hereditary cancer. The patient had rectal cancer and two colon adenomas at 62 years of age, and a weak family history of gastrointestinal tumors. He does not meet HNPCC classification criteria because of the weak family history. This study suggests that hereditary cancer associated with hMSH6 mutation is not likely to be detected by genetic testing of patients that meet standard HNPCC classification criteria (Amsterdam criteria).
-
(1997)
Cancer Res
, vol.57
, pp. 3920-3923
-
-
Akiyama, Y.1
Sato, H.2
Yamada, T.3
Nagasaki, H.4
Tsuchiya, A.5
Abe, R.6
Yuasa, Y.7
-
35
-
-
0029783835
-
Mutation of MSH3 in endometrial cancer and evidence for its functional role in heteroduplex repair
-
of special interest. A frameshift mutation in the human MSH3 gene was detected in an endometrial carcinoma cell line. This cell line displays deficiency in the repair of DNA substrates containing mismatches and extra nucleotides. This phenotype is attenuated by introduction of chromosome 5, encoding MSH3. Further study demonstrated that this cell line contains additional mutations in G·T mismatch binding protein, the human homolog of yeast MSH6. This observation confirms that the partial redundancy of MSH3 and MSH6 in yeast mismatch repair is also likely to exist in mammals.
-
Risinger JI, Umar A, Boyd J, Berchuck A, Kunkel TA, Barrett JC. Mutation of MSH3 in endometrial cancer and evidence for its functional role in heteroduplex repair. of special interest Nat Genet. 14:1996;102-105 A frameshift mutation in the human MSH3 gene was detected in an endometrial carcinoma cell line. This cell line displays deficiency in the repair of DNA substrates containing mismatches and extra nucleotides. This phenotype is attenuated by introduction of chromosome 5, encoding MSH3. Further study demonstrated that this cell line contains additional mutations in G·T mismatch binding protein, the human homolog of yeast MSH6. This observation confirms that the partial redundancy of MSH3 and MSH6 in yeast mismatch repair is also likely to exist in mammals.
-
(1996)
Nat Genet
, vol.14
, pp. 102-105
-
-
Risinger, J.I.1
Umar, A.2
Boyd, J.3
Berchuck, A.4
Kunkel, T.A.5
Barrett, J.C.6
-
36
-
-
0027137935
-
+ tumor cells
-
+ tumor cells. Cell. 75:1993;1227-1236.
-
(1993)
Cell
, vol.75
, pp. 1227-1236
-
-
Parsons, R.1
Li, G.M.2
Longley, M.J.3
Fang, W.H.4
Papadopoulos, N.5
Jen, J.6
De La Chapelle, A.7
Kinzler, K.W.8
Vogelstein, B.9
Modrich, P.10
-
37
-
-
0028847412
-
Molecular analysis of mutations in mutator colorectal carcinoma cell lines
-
Bhattacharyya NP, Ganesh A, Phear G, Richards B, Skandalis A, Meuth M. Molecular analysis of mutations in mutator colorectal carcinoma cell lines. Hum Mol Genet. 4:1995;2057-2064.
-
(1995)
Hum Mol Genet
, vol.4
, pp. 2057-2064
-
-
Bhattacharyya, N.P.1
Ganesh, A.2
Phear, G.3
Richards, B.4
Skandalis, A.5
Meuth, M.6
-
38
-
-
0030001787
-
Microsatellite instability and DNA mismatch repair in human cancer
-
Karran P. Microsatellite instability and DNA mismatch repair in human cancer. Semin Cancer Biol. 7:1996;15-24.
-
(1996)
Semin Cancer Biol
, vol.7
, pp. 15-24
-
-
Karran, P.1
-
39
-
-
0029066689
-
Inactivation of the type II TGF-beta receptor in colon cancer cells with microsatellite instability
-
Markowitz S, Wang J, Myeroff L, Parsons R, Sun L, Lutterbaugh J, Fan RS, Zborowska E, Kinzler KW, Vogelstein B, et al. Inactivation of the type II TGF-beta receptor in colon cancer cells with microsatellite instability. Science. 268:1995;1336-1338.
-
(1995)
Science
, vol.268
, pp. 1336-1338
-
-
Markowitz, S.1
Wang, J.2
Myeroff, L.3
Parsons, R.4
Sun, L.5
Lutterbaugh, J.6
Fan, R.S.7
Zborowska, E.8
Kinzler, K.W.9
Vogelstein, B.10
-
40
-
-
0031018674
-
Somatic frameshift mutations in the BAX gene in colon cancers of the microsatellite mutator phenotype
-
8 tracts in the genome, and found that mutation in BAX was significantly higher. This observation provides strong support for a role of BAX deficiency in intestinal tumorigenesis.
-
8 tracts in the genome, and found that mutation in BAX was significantly higher. This observation provides strong support for a role of BAX deficiency in intestinal tumorigenesis.
-
(1997)
Science
, vol.275
, pp. 967-969
-
-
Rampino, N.1
Yamamoto, H.2
Ionov, Y.3
Li, Y.4
Sawai, H.5
Reed, J.C.6
Perucho, M.7
-
41
-
-
0010945939
-
APC mutations in colorectal tumors with mismatch repair deficiency
-
+ large bowel tumors.
-
+ large bowel tumors.
-
(1996)
Proc Natl Acad Sci USA
, vol.93
, pp. 9049-9054
-
-
Huang, J.1
Papadopoulos, N.2
McKinley, A.J.3
Farrington, S.M.4
Curtis, L.J.5
Wyllie, A.H.6
Zheng, S.7
Willson, J.K.8
Markowitz, S.D.9
Morin, P.10
-
42
-
-
8944232867
-
Involvement of mouse Mlh1 in DNA mismatch repair and meiotic crossing over
-
of special interest. Mice deficient for Mlh1 display microsatellite instability in somatic tissues and spermatocytes, and are sterile. Sterility is associated with high levels of prematurely separated chromosomes and arrest in first division meiosis. Chiasma formation in Mlh1-deficient nuclei is reduced 10- to 100-fold. Immunostaining experiments show that Mlh1 localizes to sites of chiasmata. Since chromosome synapsis does occur in Mlh1-deficient spermatocytes as opposed to Pms2-deficient spermatocytes, Mlh1 appears to function at a later step in meiosis than Pms2.
-
Baker SM, Plug AW, Prolla TA, Bronner CE, Harris AC, Yao X, Christie DM, Monell C, Arnheim N, Bradley A, et al. Involvement of mouse Mlh1 in DNA mismatch repair and meiotic crossing over. of special interest Nat Genet. 13:1996;336-342 Mice deficient for Mlh1 display microsatellite instability in somatic tissues and spermatocytes, and are sterile. Sterility is associated with high levels of prematurely separated chromosomes and arrest in first division meiosis. Chiasma formation in Mlh1-deficient nuclei is reduced 10- to 100-fold. Immunostaining experiments show that Mlh1 localizes to sites of chiasmata. Since chromosome synapsis does occur in Mlh1-deficient spermatocytes as opposed to Pms2-deficient spermatocytes, Mlh1 appears to function at a later step in meiosis than Pms2.
-
(1996)
Nat Genet
, vol.13
, pp. 336-342
-
-
Baker, S.M.1
Plug, A.W.2
Prolla, T.A.3
Bronner, C.E.4
Harris, A.C.5
Yao, X.6
Christie, D.M.7
Monell, C.8
Arnheim, N.9
Bradley, A.10
-
43
-
-
0029099989
-
Male mice defective in the DNA mismatch repair gene PMS2 exhibit abnormal chromosome synapsis in meiosis
-
Baker SM, Bronner CE, Zhang L, Plug AW, Robatzek M, Warren G, Elliott EA, Yu J, Ashley T, Arnheim N, Liskay RM. Male mice defective in the DNA mismatch repair gene PMS2 exhibit abnormal chromosome synapsis in meiosis. Cell. 82:1995;309-319.
-
(1995)
Cell
, vol.82
, pp. 309-319
-
-
Baker, S.M.1
Bronner, C.E.2
Zhang, L.3
Plug, A.W.4
Robatzek, M.5
Warren, G.6
Elliott, E.A.7
Yu, J.8
Ashley, T.9
Arnheim, N.10
Liskay, R.M.11
-
44
-
-
15844367099
-
Meiotic pachytene arrest in MLH1-deficient mice
-
Edelmann W, Cohen PE, Kane M, Lau K, Morrow B, Bennett S, Umar A, Kunkel T, Cattoretti G, Chaganti R, et al. Meiotic pachytene arrest in MLH1-deficient mice. Cell. 85:1996;1125-1134.
-
(1996)
Cell
, vol.85
, pp. 1125-1134
-
-
Edelmann, W.1
Cohen, P.E.2
Kane, M.3
Lau, K.4
Morrow, B.5
Bennett, S.6
Umar, A.7
Kunkel, T.8
Cattoretti, G.9
Chaganti, R.10
-
45
-
-
0029101616
-
Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer
-
de Wind N, Dekker M, Berns A, Radman M, te Riele H. Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer. Cell. 82:1995;321-330.
-
(1995)
Cell
, vol.82
, pp. 321-330
-
-
De Wind, N.1
Dekker, M.2
Berns, A.3
Radman, M.4
Te Riele, H.5
-
46
-
-
0031882250
-
Tumor susceptibility and spontaneous mutation in mice deficient for Mlh1, Pms1 and Pms2 DNA mismatch repair
-
of outstanding interest. The study provides the first side by side comparison of tumor susceptibility and mutation frequencies in DNA mismatch repair deficient mice. Mlh1-, Pms2- and Pms1-deficient mice develop different tumor profiles, and DNA replication errors within simple-repeat tracts in the intestinal epithelium are unlikely to be sufficient to initiate intestinal tumor development: Pms2-deficient mice display high levels of mutation at microsatellites, and yet do not develop intestinal tumors. The lack of intestinal tumorigenesis in Pms2- and Pms1-deficient mice also suggests that there is partial redundancy in Pms2 and Pms1 function. These observations may explain the rarity of mutations in hPMS2 and hPMS1 in human HNPCC.
-
Prolla TA, Baker S, Harris A, Tsao J-L, Yao X, Bronner EC, Zheng B, Gordon M, Reneker J, Arnheim N, et al. Tumor susceptibility and spontaneous mutation in mice deficient for Mlh1, Pms1 and Pms2 DNA mismatch repair. of outstanding interest Nat Genet. 18:1998;276-279 The study provides the first side by side comparison of tumor susceptibility and mutation frequencies in DNA mismatch repair deficient mice. Mlh1-, Pms2- and Pms1-deficient mice develop different tumor profiles, and DNA replication errors within simple-repeat tracts in the intestinal epithelium are unlikely to be sufficient to initiate intestinal tumor development: Pms2-deficient mice display high levels of mutation at microsatellites, and yet do not develop intestinal tumors. The lack of intestinal tumorigenesis in Pms2- and Pms1-deficient mice also suggests that there is partial redundancy in Pms2 and Pms1 function. These observations may explain the rarity of mutations in hPMS2 and hPMS1 in human HNPCC.
-
(1998)
Nat Genet
, vol.18
, pp. 276-279
-
-
Prolla, T.A.1
Baker, S.2
Harris, A.3
Tsao J-L4
Yao, X.5
Bronner, E.C.6
Zheng, B.7
Gordon, M.8
Reneker, J.9
Arnheim, N.10
-
47
-
-
9444271133
-
Spontaneous intestinal carcinomas and skin neoplasms in Msh2-deficient mice
-
Reitmair AH, Redston M, Cai JC, Chuang TC, Bjerknes M, Cheng H, Hay K, Gallinger S, Bapat B, Mak TW. Spontaneous intestinal carcinomas and skin neoplasms in Msh2-deficient mice. Cancer Res. 56:1996;3842-3849.
-
(1996)
Cancer Res
, vol.56
, pp. 3842-3849
-
-
Reitmair, A.H.1
Redston, M.2
Cai, J.C.3
Chuang, T.C.4
Bjerknes, M.5
Cheng, H.6
Hay, K.7
Gallinger, S.8
Bapat, B.9
Mak, T.W.10
-
48
-
-
0030709433
-
Mutation in the mismatch repair gene Msh6 causes cancer susceptibility
-
of outstanding interest. Mice deficient for Msh6 develop a variety of tumors, including intestinal carcinomas, lymphoma and hepatoma. Cell lines derived from Msh6-deficient mice displayed a defect in the repair of single nucleotide mismatches, but repair of nucleotide insertion loops was unaffected. The authors predict that mutations in human hMSH6 may be associated with tumor formation in the absence of high levels of microsatellite instability.
-
Edelmann W, Yang K, Umar A, Heyer J, Lau K, Fan K, Liedtke W, Cohen PE, Kane MF, Lipford JR, et al. Mutation in the mismatch repair gene Msh6 causes cancer susceptibility. of outstanding interest Cell. 91:1997;467-477 Mice deficient for Msh6 develop a variety of tumors, including intestinal carcinomas, lymphoma and hepatoma. Cell lines derived from Msh6-deficient mice displayed a defect in the repair of single nucleotide mismatches, but repair of nucleotide insertion loops was unaffected. The authors predict that mutations in human hMSH6 may be associated with tumor formation in the absence of high levels of microsatellite instability.
-
(1997)
Cell
, vol.91
, pp. 467-477
-
-
Edelmann, W.1
Yang, K.2
Umar, A.3
Heyer, J.4
Lau, K.5
Fan, K.6
Liedtke, W.7
Cohen, P.E.8
Kane, M.F.9
Lipford, J.R.10
-
49
-
-
0029007870
-
DNA mismatch binding defects, DNA damage tolerance, and mutator phenotypes in human colorectal carcinoma cell lines
-
Branch P, Hampson R, Karran P. DNA mismatch binding defects, DNA damage tolerance, and mutator phenotypes in human colorectal carcinoma cell lines. Cancer Res. 55:1995;2304-2309.
-
(1995)
Cancer Res
, vol.55
, pp. 2304-2309
-
-
Branch, P.1
Hampson, R.2
Karran, P.3
-
50
-
-
0027936057
-
Human chromosome 3 corrects mismatch repair deficiency and microsatellite instability and reduces N-methyl-N'-nitro-N-nitrosoguanidine tolerance in colon tumor cells with homozygous hMLH1 mutation
-
Koi M, Umar A, Chauhan DP, Cherian SP, Carethers JM, Kunkel TA, Boland CR. Human chromosome 3 corrects mismatch repair deficiency and microsatellite instability and reduces N-methyl-N'-nitro-N-nitrosoguanidine tolerance in colon tumor cells with homozygous hMLH1 mutation. Cancer Res. 54:1994;4308-4312.
-
(1994)
Cancer Res
, vol.54
, pp. 4308-4312
-
-
Koi, M.1
Umar, A.2
Chauhan, D.P.3
Cherian, S.P.4
Carethers, J.M.5
Kunkel, T.A.6
Boland, C.R.7
-
51
-
-
0020332947
-
Mismatch correction at O6-methylguanine residues in E. coli DNA
-
Karran P, Marinus MG. Mismatch correction at O6-methylguanine residues in E. coli DNA. Nature. 296:1982;868-869.
-
(1982)
Nature
, vol.296
, pp. 868-869
-
-
Karran, P.1
Marinus, M.G.2
-
52
-
-
0019832687
-
N-Methyl-N'-nitro-N-nitrosoguanidine sensitivity of E. coli mutants deficient in DNA methylation and mismatch repair
-
Jones M, Wagner R. N-Methyl-N'-nitro-N-nitrosoguanidine sensitivity of E. coli mutants deficient in DNA methylation and mismatch repair. Mol Gen Genet. 184:1981;562-563.
-
(1981)
Mol Gen Genet
, vol.184
, pp. 562-563
-
-
Jones, M.1
Wagner, R.2
-
53
-
-
0020171139
-
An adaptive response to the cytotoxic effects of N-methyl-N-nitrosourea is apparently absent in normal human fibroblasts
-
Karran P, Arlett CF, Broughton BC. An adaptive response to the cytotoxic effects of N-methyl-N-nitrosourea is apparently absent in normal human fibroblasts. Biochimie. 64:1982;717-721.
-
(1982)
Biochimie
, vol.64
, pp. 717-721
-
-
Karran, P.1
Arlett, C.F.2
Broughton, B.C.3
-
54
-
-
0029822592
-
Role of postreplicative DNA mismatch repair in the cytotoxic action of thioguanine
-
6-methylthioguanine-T base pairs using a gel shift assay. These observations provide support for the concept that the cytotoxic action of thioguanine, and related compounds, is due to DNA mismatch repair activity.
-
6-methylthioguanine-T base pairs using a gel shift assay. These observations provide support for the concept that the cytotoxic action of thioguanine, and related compounds, is due to DNA mismatch repair activity.
-
(1996)
Science
, vol.273
, pp. 1109-1111
-
-
Swann, P.F.1
Waters, T.R.2
Moulton, D.C.3
Xu, Y.Z.4
Zheng, Q.5
Edwards, M.6
MacE, R.7
-
55
-
-
0030811508
-
Selective recognition of a cisplatin-DNA adduct by human mismatch repair proteins
-
of special interest. Binding assays were used to demonstrate that human cell lines contain proteins that recognize 1,2-diguanyl cisplatin intrastrand cross-links. Binding activity is sequence-context-specific, and is absent in colorectal carcinoma cell lines deficient for hMSH2 (LoVo) or hMSH6 (GTBP) DNA mismatch repair activity.
-
Yamada M, O'Regan E, Brown R, Karran P. Selective recognition of a cisplatin-DNA adduct by human mismatch repair proteins. of special interest Nucleic Acids Res. 25:1997;491-496 Binding assays were used to demonstrate that human cell lines contain proteins that recognize 1,2-diguanyl cisplatin intrastrand cross-links. Binding activity is sequence-context-specific, and is absent in colorectal carcinoma cell lines deficient for hMSH2 (LoVo) or hMSH6 (GTBP) DNA mismatch repair activity.
-
(1997)
Nucleic Acids Res
, vol.25
, pp. 491-496
-
-
Yamada, M.1
O'Regan, E.2
Brown, R.3
Karran, P.4
-
56
-
-
0030741503
-
HMLH1 expression and cellular responses of ovarian tumour cells to treatment with cytotoxic anticancer agents
-
Brown R, Hirst GL, Gallagher WM, McIlwrath AJ, Margison GP, van der Zee AG, Anthoney DA. hMLH1 expression and cellular responses of ovarian tumour cells to treatment with cytotoxic anticancer agents. Oncogene. 15:1997;45-52.
-
(1997)
Oncogene
, vol.15
, pp. 45-52
-
-
Brown, R.1
Hirst, G.L.2
Gallagher, W.M.3
McIlwrath, A.J.4
Margison, G.P.5
Van Der Zee, A.G.6
Anthoney, D.A.7
-
57
-
-
8944230189
-
Loss of DNA mismatch repair in acquired resistance to cisplatin
-
Aebi S, Kurdi-Haidar B, Gordon R, Cenni B, Zheng H, Fink D, Christen RD, Boland CR, Koi M, Fishel R, Howell SB. Loss of DNA mismatch repair in acquired resistance to cisplatin. Cancer Res. 56:1996;3087-3090.
-
(1996)
Cancer Res
, vol.56
, pp. 3087-3090
-
-
Aebi, S.1
Kurdi-Haidar, B.2
Gordon, R.3
Cenni, B.4
Zheng, H.5
Fink, D.6
Christen, R.D.7
Boland, C.R.8
Koi, M.9
Fishel, R.10
Howell, S.B.11
-
58
-
-
15444350120
-
In vitro and in vivo resistance to cisplatin in cells that have lost DNA mismatch repair
-
+/+ tumors. Clinical resistance to cisplatin treatment may be associated with MMR deficiency.
-
+/+ tumors. Clinical resistance to cisplatin treatment may be associated with MMR deficiency.
-
(1997)
Cancer Res
, vol.57
, pp. 1841-1845
-
-
Fink, D.1
Zheng, H.2
Nebel, S.3
Norris, P.S.4
Aebi, S.5
Lin, T.P.6
Nehme, A.7
Christen, R.D.8
Haas, M.9
MacLeod, C.L.10
Howell, S.B.11
-
59
-
-
15444348851
-
Role of DNA mismatch repair in the cytotoxicity of ionizing radiation
-
-/- cell lines were found to exhibit higher levels of clonogenic survival following radiation treatment. The authors propose that introduction of modified bases, such as 8-oxo-G, in replicating DNA of wild-type cells may lead to MMR-mediated cell death. Presumably, the presence of modified bases in the parental DNA strands leads to futile repair attempts that eventually lead to DNA strand breaks and cell death.
-
-/- cell lines were found to exhibit higher levels of clonogenic survival following radiation treatment. The authors propose that introduction of modified bases, such as 8-oxo-G, in replicating DNA of wild-type cells may lead to MMR-mediated cell death. Presumably, the presence of modified bases in the parental DNA strands leads to futile repair attempts that eventually lead to DNA strand breaks and cell death.
-
(1997)
Cancer Res
, vol.57
, pp. 5143-5147
-
-
Fritzell, J.A.1
Narayanan, L.2
Baker, S.M.3
Bronner, C.E.4
Andrew, S.E.5
Prolla, T.A.6
Bradley, A.7
Jirik, F.R.8
Liskay, R.M.9
Glazer, P.M.10
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