-
1
-
-
0027318112
-
Somatic mutation, monoclonality and stochastic models of stem cell organization in the intestinal crypt
-
Loeffler M, Birke A, Winton D, Potten C. Somatic mutation, monoclonality and stochastic models of stem cell organization in the intestinal crypt. J Theor Biol. 160:1993;471-491.
-
(1993)
J Theor Biol
, vol.160
, pp. 471-491
-
-
Loeffler, M.1
Birke, A.2
Winton, D.3
Potten, C.4
-
2
-
-
0025308617
-
Migration of fetal intestinal intervillous cells in neonatal mice
-
Calvert R, Pothier P. Migration of fetal intestinal intervillous cells in neonatal mice. Anat Rec. 227:1990;199-206.
-
(1990)
Anat Rec
, vol.227
, pp. 199-206
-
-
Calvert, R.1
Pothier, P.2
-
3
-
-
0023780022
-
Development of the pattern of cell renewal in the crypt-villus unit of chimaeric mouse small intestine
-
Schmidt GH, Winton DJ, Ponder BAJ. Development of the pattern of cell renewal in the crypt-villus unit of chimaeric mouse small intestine. Development. 103:1988;785-790.
-
(1988)
Development
, vol.103
, pp. 785-790
-
-
Schmidt, G.H.1
Winton, D.J.2
Ponder, B.A.J.3
-
4
-
-
0023390121
-
The crypt cycle. Crypt and villus production in the adult intestinal epithelium
-
Totafurno J, Bjerknes M, Cheng H. The crypt cycle. Crypt and villus production in the adult intestinal epithelium. Biophys J. 52:1987;279-294.
-
(1987)
Biophys J
, vol.52
, pp. 279-294
-
-
Totafurno, J.1
Bjerknes, M.2
Cheng, H.3
-
5
-
-
0030592517
-
Lessons from hereditary colorectal cancer
-
Kinzler KW, Vogelstein B. Lessons from hereditary colorectal cancer. Cell. 87:1996;159-170.
-
(1996)
Cell
, vol.87
, pp. 159-170
-
-
Kinzler, K.W.1
Vogelstein, B.2
-
6
-
-
0032524104
-
Landscaping the cancer terrain
-
of outstanding interest. An expansion of their 1996 Cell paper [5]. An elegant conceptualization of how gatekeepers (genes that control levels of proliferation in self-renewing systems), caretakers (genes that ensure the integrity of the genome), and landscapers (genes that participate in mesenchymal-epithelial crosstalk) affect tumorigenesis in the gut.
-
Kinzler KW, Vogelstein B. Landscaping the cancer terrain. of outstanding interest Science. 280:1998;1036-1037 An expansion of their 1996 Cell paper [5]. An elegant conceptualization of how gatekeepers (genes that control levels of proliferation in self-renewing systems), caretakers (genes that ensure the integrity of the genome), and landscapers (genes that participate in mesenchymal-epithelial crosstalk) affect tumorigenesis in the gut.
-
(1998)
Science
, vol.280
, pp. 1036-1037
-
-
Kinzler, K.W.1
Vogelstein, B.2
-
7
-
-
0026562404
-
Multiple intestinal neoplasia caused by a mutation in the murine homolog of the APC gene
-
Su L-K, Kinzler KW, Vogelstein B, Preisinger AC, Moser AR, Luongo C, Gould KA, Dove WF. Multiple intestinal neoplasia caused by a mutation in the murine homolog of the APC gene. Science. 256:1992;668-670.
-
(1992)
Science
, vol.256
, pp. 668-670
-
-
Su L-K1
Kinzler, K.W.2
Vogelstein, B.3
Preisinger, A.C.4
Moser, A.R.5
Luongo, C.6
Gould, K.A.7
Dove, W.F.8
-
8
-
-
0030843461
-
Rapid colorectal adenoma formation initiated by conditional targeting of the Apc gene
-
of outstanding interest. This paper reports disruption of the Apc gene in the colonic epithelium in mice by administration of an enema containing an adenoviral vector that directs expression of Cre recombinase. Multiple tumors form within four weeks, thus proving that loss of Apc alone is sufficient for initiation of tumori-genesis. The need for developing strategies for inducing gene disruption at various points in time is great in the case of the gut, which continues to evolve as animals age. Targeting the stem cell is also critical. Adenoviral enemas appear to be a workable solution, at least for the distal gut, and you do not have to worry about altering the genetic background.
-
Shibata H, Toyama K, Shioya H, Ito M, Hirota M, Hasegawa S, Matsumoto H, Takano H, Akiyama T, Toyoshima K, et al. Rapid colorectal adenoma formation initiated by conditional targeting of the Apc gene. of outstanding interest Science. 278:1997;120-123 This paper reports disruption of the Apc gene in the colonic epithelium in mice by administration of an enema containing an adenoviral vector that directs expression of Cre recombinase. Multiple tumors form within four weeks, thus proving that loss of Apc alone is sufficient for initiation of tumori-genesis. The need for developing strategies for inducing gene disruption at various points in time is great in the case of the gut, which continues to evolve as animals age. Targeting the stem cell is also critical. Adenoviral enemas appear to be a workable solution, at least for the distal gut, and you do not have to worry about altering the genetic background.
-
(1997)
Science
, vol.278
, pp. 120-123
-
-
Shibata, H.1
Toyama, K.2
Shioya, H.3
Ito, M.4
Hirota, M.5
Hasegawa, S.6
Matsumoto, H.7
Takano, H.8
Akiyama, T.9
Toyoshima, K.10
-
9
-
-
0029047954
-
Loss of Apc heterozygosity and abnormal tissue building in nascent intestinal polyps in mice carrying a truncated Apc gene
-
Oshima M, Oshima H, Kitagawa K, Kobayashi M, Itakura C, Taketo M. Loss of Apc heterozygosity and abnormal tissue building in nascent intestinal polyps in mice carrying a truncated Apc gene. Proc Natl Acad Sci USA. 92:1995;4482-4486.
-
(1995)
Proc Natl Acad Sci USA
, vol.92
, pp. 4482-4486
-
-
Oshima, M.1
Oshima, H.2
Kitagawa, K.3
Kobayashi, M.4
Itakura, C.5
Taketo, M.6
-
11
-
-
0029938751
-
Polyclonal origin of colonic adenomas in an XO↔XY patient with FAP
-
Novelli MR, Williamson JA, Tomlinson IP, Elia G, Hodgson SV, Talbot IC, Bodmer W, Wright NA. Polyclonal origin of colonic adenomas in an XO↔XY patient with FAP. Science. 272:1996;1187-1190.
-
(1996)
Science
, vol.272
, pp. 1187-1190
-
-
Novelli, M.R.1
Williamson, J.A.2
Tomlinson, I.P.3
Elia, G.4
Hodgson, S.V.5
Talbot, I.C.6
Bodmer, W.7
Wright, N.A.8
-
12
-
-
0031059392
-
Clonality of dysplastic epithelium in colorectal adenomas from familial adenomatous polyposis patients
-
Bjerknes M, Cheng H, Kim H, Schnitzler M, Gallinger S. Clonality of dysplastic epithelium in colorectal adenomas from familial adenomatous polyposis patients. Cancer Res. 57:1997;355-361.
-
(1997)
Cancer Res
, vol.57
, pp. 355-361
-
-
Bjerknes, M.1
Cheng, H.2
Kim, H.3
Schnitzler, M.4
Gallinger, S.5
-
13
-
-
0031458850
-
+ from all tumor lineages
-
Min. Bottom line: polyclonal adenomas are observed. Polyclonality in microadenomas argues against simple collision of two independently initiated clones. The authors provide several possible scenarios to explain how multiply initiated clones could interact to promote tumorigenesis. The issue of polyclonality may have relevance to the initiation of other epithelial cancers: the mouse gut provides a good system for documenting and studying this interesting question.
-
Min. Bottom line: polyclonal adenomas are observed. Polyclonality in microadenomas argues against simple collision of two independently initiated clones. The authors provide several possible scenarios to explain how multiply initiated clones could interact to promote tumorigenesis. The issue of polyclonality may have relevance to the initiation of other epithelial cancers: the mouse gut provides a good system for documenting and studying this interesting question.
-
(1997)
Proc Natl Acad Sci USA
, vol.94
, pp. 13927-13931
-
-
Merritt, A.J.1
Gould, K.A.2
Dove, W.F.3
-
14
-
-
0031059349
-
APC mutation and the crypt cycle in murine and human intestine
-
Bjerknes M, Cheng H, Hay K, Gallinger S. APC mutation and the crypt cycle in murine and human intestine. Am J Pathol. 150:1997;833-839.
-
(1997)
Am J Pathol
, vol.150
, pp. 833-839
-
-
Bjerknes, M.1
Cheng, H.2
Hay, K.3
Gallinger, S.4
-
15
-
-
0032562603
-
Functional interaction of an axin homolog, conductin, with β-catenin, APC and GSK3β
-
Behrens J, Jerchow B-A, Würtele M, Grimm J, Asbrand C, Wirtz R, Kühl M, Wedlich D, Birchmeier W. Functional interaction of an axin homolog, conductin, with β-catenin, APC and GSK3β Science. 280:1998;596-599.
-
(1998)
Science
, vol.280
, pp. 596-599
-
-
Behrens, J.1
Jerchow B-A2
Würtele, M.3
Grimm, J.4
Asbrand, C.5
Wirtz, R.6
Kühl, M.7
Wedlich, D.8
Birchmeier, W.9
-
16
-
-
0032054828
-
Wnt signaling: Why is everything so negative?
-
Brown JD, Moon RT. Wnt signaling: why is everything so negative? Curr Opin Cell Biol. 10:1998;182-187.
-
(1998)
Curr Opin Cell Biol
, vol.10
, pp. 182-187
-
-
Brown, J.D.1
Moon, R.T.2
-
17
-
-
0029781509
-
Functional interaction of β-catenin with the transcription factor LEF-1
-
Behrens J, von Kries JP, Kühl M, Bruhn L, Wedlich D, Grosschedl R, Birchmeier W. Functional interaction of β-catenin with the transcription factor LEF-1. Nature. 382:1996;638-642.
-
(1996)
Nature
, vol.382
, pp. 638-642
-
-
Behrens, J.1
Von Kries, J.P.2
Kühl, M.3
Bruhn, L.4
Wedlich, D.5
Grosschedl, R.6
Birchmeier, W.7
-
18
-
-
0345343608
-
Nuclear localization of β-catenin by interaction with transcription factor LEF-1
-
Huber O, Korn R, McLaughlin J, Ohsugi M, Herrmann BG, Kemler R. Nuclear localization of β-catenin by interaction with transcription factor LEF-1. Mech Dev. 59:1996;3-10.
-
(1996)
Mech Dev
, vol.59
, pp. 3-10
-
-
Huber, O.1
Korn, R.2
McLaughlin, J.3
Ohsugi, M.4
Herrmann, B.G.5
Kemler, R.6
-
19
-
-
0030975671
-
-/- colon carcinoma
-
of outstanding interest. See annotation to [20].
-
-/- colon carcinoma. of outstanding interest Science. 275:1997;1784-1787 See annotation to [20].
-
(1997)
Science
, vol.275
, pp. 1784-1787
-
-
Korinek, V.1
Barker, N.2
Morin, P.J.3
Van Wichen, D.4
De Weger, R.5
Kinzler, K.W.6
Vogelstein, B.7
Clevers, H.8
-
20
-
-
0030949463
-
Activation of β-catenin-Tcf signaling in colon cancer by mutations in β-catenin or APC
-
of outstanding interest. This paper and the report by Korinek [19] use cell lines derived from human-colon-carcinoma to demonstrate that mutations in APC are associated with transcriptional activation of a reporter gene containing a DNA-binding site recognized by all Tcf family members. Important evidence is presented that Apc affects the availability of β-catenin for partnering with Tcf-4.
-
Morin PJ, Sparks AB, Korinek V, Barker N, Clevers H, Vogelstein B, Kinzler KW. Activation of β-catenin-Tcf signaling in colon cancer by mutations in β-catenin or APC. of outstanding interest Science. 275:1997;1787-1790 This paper and the report by Korinek [19] use cell lines derived from human-colon-carcinoma to demonstrate that mutations in APC are associated with transcriptional activation of a reporter gene containing a DNA-binding site recognized by all Tcf family members. Important evidence is presented that Apc affects the availability of β-catenin for partnering with Tcf-4.
-
(1997)
Science
, vol.275
, pp. 1787-1790
-
-
Morin, P.J.1
Sparks, A.B.2
Korinek, V.3
Barker, N.4
Clevers, H.5
Vogelstein, B.6
Kinzler, K.W.7
-
21
-
-
0032482198
-
Effects of forced expression of an N-terminal truncated β-catenin on mouse intestinal epithelial homeostasis
-
of special interest. An in vivo experiment showing that augmenting β-catenin levels in the intestinal epithelium of chimeric mice enhances proliferation in the crypt. An accompanying induction of E-cadherin expression produces a slowing of cell migration, and illustrates how β-catenin affects both proliferation and adhesion.
-
Wong MH, Rubinfeld B, Gordon JI. Effects of forced expression of an N-terminal truncated β-catenin on mouse intestinal epithelial homeostasis. of special interest J Cell Biol. 141:1998;765-777 An in vivo experiment showing that augmenting β-catenin levels in the intestinal epithelium of chimeric mice enhances proliferation in the crypt. An accompanying induction of E-cadherin expression produces a slowing of cell migration, and illustrates how β-catenin affects both proliferation and adhesion.
-
(1998)
J Cell Biol
, vol.141
, pp. 765-777
-
-
Wong, M.H.1
Rubinfeld, B.2
Gordon, J.I.3
-
22
-
-
0031848068
-
Depletion of epithelial stem cell compartments in the small intestine of mice lacking Tcf-4
-
-/- mice but by E16.5, the intervillus epithelium lacks proliferating cells; what remains are cells that resemble the differentiated cells on the villus. In conclusion, Tcf-4 is needed to sustain epithelial proliferation. Unfortunately, mice die by postnatal day 1 so the role of Tcf-4 in adult crypts will have to be defined by conditional targeting. Colonic crypts in the knockout animals appeared normal, but, unlike small intestinal crypts, colonic crypts also have Tcf-3.
-
-/- mice but by E16.5, the intervillus epithelium lacks proliferating cells; what remains are cells that resemble the differentiated cells on the villus. In conclusion, Tcf-4 is needed to sustain epithelial proliferation. Unfortunately, mice die by postnatal day 1 so the role of Tcf-4 in adult crypts will have to be defined by conditional targeting. Colonic crypts in the knockout animals appeared normal, but, unlike small intestinal crypts, colonic crypts also have Tcf-3.
-
(1998)
Nat Genet
, vol.19
, pp. 379-383
-
-
Korinek, V.1
Barker, N.2
Moerer, P.3
Van Donselaar, E.4
Huls, G.5
Peters, P.J.6
Clevers, H.7
-
23
-
-
0030771851
-
Accumulation of Armadillo induced by Wingless, Dishevelled and dominant negative Zeste-white 3 leads to elevated DE-cadherin in Drosophila clone 8 wing disc cells
-
Yanagawa S-I, Lee J-S, Haruna T, Oda H, Uemura T, Takeichi M, Ishimoto A. Accumulation of Armadillo induced by Wingless, Dishevelled and dominant negative Zeste-white 3 leads to elevated DE-cadherin in Drosophila clone 8 wing disc cells. J Biol Chem. 272:1997;25243-25251.
-
(1997)
J Biol Chem
, vol.272
, pp. 25243-25251
-
-
Yanagawa S-I1
Lee J-S2
Haruna, T.3
Oda, H.4
Uemura, T.5
Takeichi, M.6
Ishimoto, A.7
-
24
-
-
0031937635
-
Two members of the Tcf family implicated in Wnt/β-catenin signaling during embryogenesis in the mouse
-
Korinek V, Barker N, Willert K, Molenaar M, Roose J, Wagenaar G, Markman M, Lamers W, Destree O, Clevers H. Two members of the Tcf family implicated in Wnt/β-catenin signaling during embryogenesis in the mouse. Mol Cell Biol. 18:1998;1248-1256.
-
(1998)
Mol Cell Biol
, vol.18
, pp. 1248-1256
-
-
Korinek, V.1
Barker, N.2
Willert, K.3
Molenaar, M.4
Roose, J.5
Wagenaar, G.6
Markman, M.7
Lamers, W.8
Destree, O.9
Clevers, H.10
-
26
-
-
0030797904
-
Secretory phospholipase Pla2g2a confers resistance to intestinal tumorigenesis
-
Min/+ littermates with just the endogenous B6 Pla2g2a allele. This experiment, which kept the genetic background constant, provides very strong evidence that Pla2g2a is Mom1 (modifier of Min). The big question: what is the mechanism by which this phospholipase affects tumorigenesis?
-
Min/+ littermates with just the endogenous B6 Pla2g2a allele. This experiment, which kept the genetic background constant, provides very strong evidence that Pla2g2a is Mom1 (modifier of Min). The big question: what is the mechanism by which this phospholipase affects tumorigenesis?
-
(1997)
Nat Genet
, vol.17
, pp. 88-91
-
-
Cornier, R.T.1
Hong, K.H.2
Halberg, R.B.3
Hawkins, T.L.4
Richardson, P.5
Mulherkar, R.6
Dove, W.F.7
Lander, E.S.8
-
27
-
-
0030606299
-
Δ716 knockout mice by inhibition of cyclooxygenase 2 (Cox-2)
-
Δ716 knockout mice by inhibition of cyclooxygenase 2 (Cox-2). Cell. 87:1996;803-809.
-
(1996)
Cell
, vol.87
, pp. 803-809
-
-
Oshima, M.1
Dinchuk, J.E.2
Kargman, S.L.3
Oshima, H.4
Hancock, B.5
Kwong, E.6
Trzaskos, J.M.7
Evans, J.F.8
Taketo, M.M.9
-
29
-
-
0031440118
-
Key role of the Cdx2 homeobox gene in extracellular matrix-mediated intestinal cell differentiation
-
Lorentz O, Duluc I, De Arcangelis A, Simon-Assmann P, Kedinger M, Freund J-N. Key role of the Cdx2 homeobox gene in extracellular matrix-mediated intestinal cell differentiation. J Cell Biol. 139:1997;1553-1565.
-
(1997)
J Cell Biol
, vol.139
, pp. 1553-1565
-
-
Lorentz, O.1
Duluc, I.2
De Arcangelis, A.3
Simon-Assmann, P.4
Kedinger, M.5
Freund J-N6
-
32
-
-
0028305431
-
Fetal endoderm primarily holds the temporal and positional information required for mammalian intestinal development
-
Duluc I, aiFreund J-N, Leberquier C, Kedinger M. Fetal endoderm primarily holds the temporal and positional information required for mammalian intestinal development. J Cell Biol. 126:1994;211-221.
-
(1994)
J Cell Biol
, vol.126
, pp. 211-221
-
-
Duluc, I.1
Aifreund J-N2
Leberquier, C.3
Kedinger, M.4
-
33
-
-
0016296248
-
Morphology and cell proliferation of subepithelial fibroblasts in adult mouse jejenum
-
Marsh MN, Trier JS. Morphology and cell proliferation of subepithelial fibroblasts in adult mouse jejenum. Gastroenterology. 67:1974;622-645.
-
(1974)
Gastroenterology
, vol.67
, pp. 622-645
-
-
Marsh, M.N.1
Trier, J.S.2
-
34
-
-
0029016752
-
Homeostatic regulation of intestinal epithelia by intraepithelial γδ T cells
-
Komano H, Fujiura Y, Kawaguchi M, Matsumoto S, Hashimoto Y, Obana S, Mombaerts P, Tonegawa S, Yamamoto H, Itohara S, et al. Homeostatic regulation of intestinal epithelia by intraepithelial γδ T cells. Proc Natl Acad Sci USA. 92:1995;6147-6151.
-
(1995)
Proc Natl Acad Sci USA
, vol.92
, pp. 6147-6151
-
-
Komano, H.1
Fujiura, Y.2
Kawaguchi, M.3
Matsumoto, S.4
Hashimoto, Y.5
Obana, S.6
Mombaerts, P.7
Tonegawa, S.8
Yamamoto, H.9
Itohara, S.10
-
35
-
-
0029999782
-
Clustered arrangement of winged helix genes Fkh6 and Mfh1: Possible implications for mesoderm development
-
Kaestner KH, Bleckmann SC, Monaghan AP, Schlöndorff J, Mincheva A, Lichter P, Schütz G. Clustered arrangement of winged helix genes Fkh6 and Mfh1: Possible implications for mesoderm development. Development. 122:1996;1751-1758.
-
(1996)
Development
, vol.122
, pp. 1751-1758
-
-
Kaestner, K.H.1
Bleckmann, S.C.2
Monaghan, A.P.3
Schlöndorff, J.4
Mincheva, A.5
Lichter, P.6
Schütz, G.7
-
36
-
-
0030907001
-
The mesenchymal winged helix transcription factor Fkh6 is required for the control of gastrointestinal proliferation and differentiation
-
of outstanding interest. Loss of forkhead 6 homolog (Fkh6) from the gut mesoderm produces a prominent phenotype in late fetal life. Mesenchymal invagination is delayed, thereby delaying formation of villi and proliferation is not restricted to the intervillus epithelium. Most knockout mice die during the first three postnatal weeks. Those that survive have increased crypt proliferation, elongated villi (but no dividing cells in the villus epithelium), and goblet- cell hyperplasia. These results indicate that Fkh6 is involved in mesenchymal-epithelial signaling and negatively regulates proliferation. An interesting issue is why there are differences in the distribution of dividing cells in the fetal versus adult intestine.
-
Kaestner KH, Silberg DG, Traber PG, Schutz G. The mesenchymal winged helix transcription factor Fkh6 is required for the control of gastrointestinal proliferation and differentiation. of outstanding interest Genes Dev. 11:1997;1583-1595 Loss of forkhead 6 homolog (Fkh6) from the gut mesoderm produces a prominent phenotype in late fetal life. Mesenchymal invagination is delayed, thereby delaying formation of villi and proliferation is not restricted to the intervillus epithelium. Most knockout mice die during the first three postnatal weeks. Those that survive have increased crypt proliferation, elongated villi (but no dividing cells in the villus epithelium), and goblet- cell hyperplasia. These results indicate that Fkh6 is involved in mesenchymal-epithelial signaling and negatively regulates proliferation. An interesting issue is why there are differences in the distribution of dividing cells in the fetal versus adult intestine.
-
(1997)
Genes Dev
, vol.11
, pp. 1583-1595
-
-
Kaestner, K.H.1
Silberg, D.G.2
Traber, P.G.3
Schutz, G.4
-
37
-
-
0031438047
-
TGF-β signalling from cell membrane to nucleus through SMAD proteins
-
Heldin C-H, Miyazono K, ten Dijke P. TGF-β signalling from cell membrane to nucleus through SMAD proteins. Nature. 390:1997;465-471.
-
(1997)
Nature
, vol.390
, pp. 465-471
-
-
Heldin C-H1
Miyazono, K.2
Ten Dijke, P.3
-
38
-
-
0030593038
-
Kern SE: DPC4, a candidate tumor suppressor gene at human chromosome 18q21.1.
-
Hahn SA, Schutte M, Shamsul Hoque ATM, Moskaluk CA, da Costa LT, Rozenblum E, Weinstein CL, Fischer A, Yeo CJ, Hruban RH, Kern SE: DPC4, a candidate tumor suppressor gene at human chromosome 18q21.1. Science 271:350-353.
-
Science
, vol.271
, pp. 350-353
-
-
Hahn, S.A.1
Schutte, M.2
Shamsul Hoque, A.T.M.3
Moskaluk, C.A.4
Da Costa, L.T.5
Rozenblum, E.6
Weinstein, C.L.7
Fischer, A.8
Yeo, C.J.9
Hruban, R.H.10
-
39
-
-
0032478143
-
Targeted deletion of Smad4 shows it is required for transforming growth factor β and activin signaling in colorectal cancer cells
-
of outstanding interest. Homologous recombination was used in colorectal cancer cells to disrupt SMAD4. Smad4-deficient cells are unable to transduce signals from transforming growth factor β (TGFβ) or activin. This study provided direct evidence in human cells that Smad4 mediates pathway-specific signaling by TGFβ-family members.
-
Zhou S, Buckhaults P, Zawel L, Bunz F, Riggins G, Le Dai J, Kern SE, Kinzler KW, Vogelstein B. Targeted deletion of Smad4 shows it is required for transforming growth factor β and activin signaling in colorectal cancer cells. of outstanding interest Proc Natl Acad Sci USA. 95:1998;2412-2416 Homologous recombination was used in colorectal cancer cells to disrupt SMAD4. Smad4-deficient cells are unable to transduce signals from transforming growth factor β (TGFβ) or activin. This study provided direct evidence in human cells that Smad4 mediates pathway-specific signaling by TGFβ-family members.
-
(1998)
Proc Natl Acad Sci USA
, vol.95
, pp. 2412-2416
-
-
Zhou, S.1
Buckhaults, P.2
Zawel, L.3
Bunz, F.4
Riggins, G.5
Le Dai, J.6
Kern, S.E.7
Kinzler, K.W.8
Vogelstein, B.9
-
40
-
-
0032489508
-
Intestinal tumorigenesis in compound mutant mice of both Dpc4 (Smad4) and Apc genes
-
Δ716/+ mice, the compound heterozygotes develop adenomas with pronounced stromal hyperplasia. By 20 weeks of age >50% of the lesions have progressed to adenocarcinoma. Note that Smad4 is absent from the epithelial component of these adenomas, due to loss of the wild-type allele, but remains detectable in the mesenchymal component. Is the epithelium driving the mesenchymal response? Desmoplasia refers to the excessive production of connective tissue surrounding the leading edges of invasive carcinomas. These mice may represent a model for studying the origins of desmoplasia.
-
Δ716/+ mice, the compound heterozygotes develop adenomas with pronounced stromal hyperplasia. By 20 weeks of age >50% of the lesions have progressed to adenocarcinoma. Note that Smad4 is absent from the epithelial component of these adenomas, due to loss of the wild-type allele, but remains detectable in the mesenchymal component. Is the epithelium driving the mesenchymal response? Desmoplasia refers to the excessive production of connective tissue surrounding the leading edges of invasive carcinomas. These mice may represent a model for studying the origins of desmoplasia.
-
(1998)
Cell
, vol.92
, pp. 645-656
-
-
Takaku, K.1
Oshima, M.2
Miyoshi, H.3
Matsui, M.4
Seldin, M.F.5
Taketo, M.M.6
-
41
-
-
15444348295
-
The tumor suppressor gene Smad4/Dpc4 is required for gastrulation and later for anterior development of the mouse embryo
-
-/- mice die by embryonic day 7.5 without detectable mesoderm, and with abnormalities in development of their visceral endoderm.
-
-/- mice die by embryonic day 7.5 without detectable mesoderm, and with abnormalities in development of their visceral endoderm.
-
(1998)
Genes Dev
, vol.12
, pp. 107-119
-
-
Sirard, C.1
De La Pompa, J.L.2
Elia, A.3
Itie, A.4
Mirtsos, C.5
Cheung, A.6
Hahn, S.7
Wakeham, A.8
Schwartz, L.9
Kern, S.E.10
-
42
-
-
0032524069
-
Mutations in the SMAD4/DPC4 gene in juvenile polyposis
-
of special interest. Families with an autosomal dominant disease, juvenile polyposis, develop hamartomous polyps in their gut and are also predisposed to carcinoma. This study shows that in certain juvenile polyposis kindreds, these neoplasms are due to germline mutations in SMAD4.
-
Howe JR, Roth S, Ringold JC, Summers RW, Järvinen HJ, Sistonen P, Tomlinson IPM, Houlston RS, Bevan S, Mitros FA, et al. Mutations in the SMAD4/DPC4 gene in juvenile polyposis. of special interest Science. 280:1998;1086-1088 Families with an autosomal dominant disease, juvenile polyposis, develop hamartomous polyps in their gut and are also predisposed to carcinoma. This study shows that in certain juvenile polyposis kindreds, these neoplasms are due to germline mutations in SMAD4.
-
(1998)
Science
, vol.280
, pp. 1086-1088
-
-
Howe, J.R.1
Roth, S.2
Ringold, J.C.3
Summers, R.W.4
Järvinen, H.J.5
Sistonen, P.6
Tomlinson, I.P.M.7
Houlston, R.S.8
Bevan, S.9
Mitros, F.A.10
-
43
-
-
6844252284
-
Mutation spectrum and genotype-phenotype analyses in Cowden disease and Bannayan-Zonana syndrome, two hamartoma syndromes with germline PTEN mutation
-
Marsh DJ, Coulon V, Lunetta KL, Rocca-Serra P, Dahia PLM, Zheng Z, Liaw D, Caron S, Duboue B, Lin AY, et al. Mutation spectrum and genotype-phenotype analyses in Cowden disease and Bannayan-Zonana syndrome, two hamartoma syndromes with germline PTEN mutation. Hum Mol Genet. 7:1998;507-515.
-
(1998)
Hum Mol Genet
, vol.7
, pp. 507-515
-
-
Marsh, D.J.1
Coulon, V.2
Lunetta, K.L.3
Rocca-Serra, P.4
Dahia, P.L.M.5
Zheng, Z.6
Liaw, D.7
Caron, S.8
Duboue, B.9
Lin, A.Y.10
-
44
-
-
0031870959
-
Pten is essential for embryonic development and tumour suppression
-
+/- embryonic stem cells and wild-type blastocysts exhibit colonic hyperplasia, dysplasia and neoplasia. Increased numbers of fibroblasts surround crypts in areas of hyperplasia or dysplasia, raising the question of whether the proliferative abnormalities in the gut are a reflection of disorders in mesenchymal-epithelial cross talk.
-
+/- embryonic stem cells and wild-type blastocysts exhibit colonic hyperplasia, dysplasia and neoplasia. Increased numbers of fibroblasts surround crypts in areas of hyperplasia or dysplasia, raising the question of whether the proliferative abnormalities in the gut are a reflection of disorders in mesenchymal-epithelial cross talk.
-
(1998)
Nat Genet
, vol.19
, pp. 348-355
-
-
Dicristofano, A.1
Pesce, B.2
Cordon-Cardo, C.3
Pandolfi, P.P.4
-
45
-
-
0030046511
-
Hlx homeobox gene is essential for an inductive tissue interaction that drives expansion of embryonic liver and gut
-
Hentsch B, Lyons I, Li R, Hartley L, Lints TJ, Adams JM, Harvey RP. Hlx homeobox gene is essential for an inductive tissue interaction that drives expansion of embryonic liver and gut. Genes Dev. 10:1996;70-79.
-
(1996)
Genes Dev
, vol.10
, pp. 70-79
-
-
Hentsch, B.1
Lyons, I.2
Li, R.3
Hartley, L.4
Lints, T.J.5
Adams, J.M.6
Harvey, R.P.7
-
46
-
-
0031260579
-
Sonic hedgehog directs specialized mesoderm differentiation in the intestine and pancreas
-
of special interest. Sonic hedgehog (Shh) is secreted throughout the fetal gut endoderm but is normally absent from the pancreatic endoderm. Forced expression of Shh in the pancreatic endoderm changes the identity of its associated mesoderm so that it resembles the intestinal mesoderm.
-
Apelqvist Å, Ahlgren U, Edlund H. Sonic hedgehog directs specialized mesoderm differentiation in the intestine and pancreas. of special interest Curr Biol. 7:1997;804-810 Sonic hedgehog (Shh) is secreted throughout the fetal gut endoderm but is normally absent from the pancreatic endoderm. Forced expression of Shh in the pancreatic endoderm changes the identity of its associated mesoderm so that it resembles the intestinal mesoderm.
-
(1997)
Curr Biol
, vol.7
, pp. 804-810
-
-
Apelqvist, Å.1
Ahlgren, U.2
Edlund, H.3
-
47
-
-
0029784320
-
Biochemistry and genetics of eukaryotic mismatch repair
-
Kolodner R. Biochemistry and genetics of eukaryotic mismatch repair. Genes Dev. 10:1996;1433-1442.
-
(1996)
Genes Dev
, vol.10
, pp. 1433-1442
-
-
Kolodner, R.1
-
48
-
-
0030465237
-
HMSH2 forms specific mispair-binding complexes with hMSH3 and hMSH6
-
Acharya S, Wilson T, Gradia S, Kane MF, Guerrette S, Marsischky GT, Kolodner R, Fishel R. hMSH2 forms specific mispair-binding complexes with hMSH3 and hMSH6. Proc Natl Acad Sci USA. 93:1996;13629-13634.
-
(1996)
Proc Natl Acad Sci USA
, vol.93
, pp. 13629-13634
-
-
Acharya, S.1
Wilson, T.2
Gradia, S.3
Kane, M.F.4
Guerrette, S.5
Marsischky, G.T.6
Kolodner, R.7
Fishel, R.8
-
49
-
-
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
-
50
-
-
0029111463
-
Msh2 deficient mice are viable and susceptible to lymphoid tumors
-
Reitmair A, Schmits R, Ewel A, Bapat B, Redston M, Mitri A, Waterhouse P, Mittrücker H-W, Wakeham A, Liu B, et al. Msh2 deficient mice are viable and susceptible to lymphoid tumors. Nat Genet. 11:1995;64-70.
-
(1995)
Nat Genet
, vol.11
, pp. 64-70
-
-
Reitmair, A.1
Schmits, R.2
Ewel, A.3
Bapat, B.4
Redston, M.5
Mitri, A.6
Waterhouse, P.7
Mittrücker H-W8
Wakeham, A.9
Liu, B.10
-
51
-
-
8944232867
-
Involvement of mouse Mlh1 in DNA mismatch repair and meiotic crossing over
-
Baker SM, Plug AW, Prolla TA, Bronner CE, Harris AC, Yao X, Christie D-M, Monell C, Arnheim N, Bradley A, et al. Involvement of mouse Mlh1 in DNA mismatch repair and meiotic crossing over. Nat Genet. 13:1996;336-342.
-
(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-M7
Monell, C.8
Arnheim, N.9
Bradley, A.10
-
52
-
-
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, Chagnati 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
Chagnati, R.10
-
53
-
-
9444271133
-
Spontaneous intestinal carcinomas and skin neoplasms in Msh2-deficient mice
-
Reitmair AH, Redston M, Cai JC, Chuang TCY, 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.Y.4
Bjerknes, M.5
Cheng, H.6
Hay, K.7
Gallinger, S.8
Bapat, B.9
Mak, T.W.10
-
54
-
-
0031882250
-
Tumor susceptibility and spontaneous mutation in mice deficient in Mlh1, Pms1 and Pms2 DNA mismatch repair
-
of outstanding interest. The authors compare tumorigenesis in mice deficient for various mismatch repair enzymes and find remarkable differences. Pms1 knockout mice do not develop any tumors. Pms2 knockouts develop lymphomas but not gut tumors. Mlh1 knockout mice develop lymphomas as well as intestinal adenomas and adenocarcinomas.
-
Prolla TA, Baker SM, Harris AC, Tsao J-L, Yao X, Bronner CE, Zheng B, Gordon M, Reneker J, Arnheim N, et al. Tumor susceptibility and spontaneous mutation in mice deficient in Mlh1, Pms1 and Pms2 DNA mismatch repair. of outstanding interest Nat Genet. 18:1998;276-279 The authors compare tumorigenesis in mice deficient for various mismatch repair enzymes and find remarkable differences. Pms1 knockout mice do not develop any tumors. Pms2 knockouts develop lymphomas but not gut tumors. Mlh1 knockout mice develop lymphomas as well as intestinal adenomas and adenocarcinomas.
-
(1998)
Nat Genet
, vol.18
, pp. 276-279
-
-
Prolla, T.A.1
Baker, S.M.2
Harris, A.C.3
Tsao J-L4
Yao, X.5
Bronner, C.E.6
Zheng, B.7
Gordon, M.8
Reneker, J.9
Arnheim, N.10
-
55
-
-
8944262831
-
MSH2 deficiency contributes to accelerated APC-mediated intestinal tumorigenesis
-
Reitmair AH, Cai J-C, Bjerknes M, Redston M, Cheng H, Pind MTL, Hay K, Mitri A, Bapat BV, Mak TW, Gallinger S. MSH2 deficiency contributes to accelerated APC-mediated intestinal tumorigenesis. Cancer Res. 56:1996;2922-2926.
-
(1996)
Cancer Res
, vol.56
, pp. 2922-2926
-
-
Reitmair, A.H.1
Cai J-C2
Bjerknes, M.3
Redston, M.4
Cheng, H.5
Pind, M.T.L.6
Hay, K.7
Mitri, A.8
Bapat, B.V.9
Mak, T.W.10
Gallinger, S.11
-
56
-
-
0030709433
-
Mutation in the mismatch repair gene Msh6 causes cancer susceptibility
-
-/- are unable to repair single base pair mismatches, although they can repair insertion or deletion mutations. Mice derived from these embryonic stem cells develop lymphoid and gut tumors.
-
-/- are unable to repair single base pair mismatches, although they can repair insertion or deletion mutations. Mice derived from these embryonic stem cells develop lymphoid and gut tumors.
-
(1997)
Cell
, vol.91
, pp. 467-477
-
-
Edelman, W.1
Yang, K.2
Umar, A.3
Heyer, J.4
Lau, K.5
Fan, K.6
Liedtke, W.7
Cohen, P.8
Kane, M.F.9
Lipford, J.R.10
Yu, N.11
-
57
-
-
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, Robatzel M, Warren G, Elliott EA, Yu J, Ashley T, Arnheim N, et al. 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
Robatzel, M.5
Warren, G.6
Elliott, E.A.7
Yu, J.8
Ashley, T.9
Arnheim, N.10
-
58
-
-
0030965212
-
Elevated levels of mutation in multiple tissues of mice deficient in the DNA mismatch repair gene Pms2
-
Narayanan L, Fritzell JA, Baker SM, Liskay RM, Glazer PM. Elevated levels of mutation in multiple tissues of mice deficient in the DNA mismatch repair gene Pms2. Proc Natl Acad Sci USA. 94:1997;3122-3127.
-
(1997)
Proc Natl Acad Sci USA
, vol.94
, pp. 3122-3127
-
-
Narayanan, L.1
Fritzell, J.A.2
Baker, S.M.3
Liskay, R.M.4
Glazer, P.M.5
-
60
-
-
0010945939
-
APC mutations in colorectal tumors with mismatch repair deficiency
-
Huang J, Papadopoulos N, McKinley AJ, Farrington SM, Curtis LJ, Wyllie AH, Zheng S, Willson JKV, Markowitz SD, Morin P, et al. APC mutations in colorectal tumors with mismatch repair deficiency. Proc Natl Acad Sci USA. 93:1996;9049-9054.
-
(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.V.8
Markowitz, S.D.9
Morin, P.10
-
61
-
-
0029066689
-
Inactivation of the type II TGF-β 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-β 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
-
62
-
-
0031018674
-
Somatic frameshift mutations in the BAX gene in colon cancers of the microsatellite mutator phenotype
-
of special interest. Demonstrates of the effects of microsatellite instability on the functional integrity of a gene likely to be involved in tumorigenesis: over 50% of colorectal cancers with unstable microsatellite sequences contained frameshift mutations in an 8 basepair tract of guanosines in BAX.
-
Rampino N, Yamamoto H, Ionov Y, Li Y, Sawai H, Reed JC, Perucho M. Somatic frameshift mutations in the BAX gene in colon cancers of the microsatellite mutator phenotype. of special interest Science. 275:1997;967-969 Demonstrates of the effects of microsatellite instability on the functional integrity of a gene likely to be involved in tumorigenesis: over 50% of colorectal cancers with unstable microsatellite sequences contained frameshift mutations in an 8 basepair tract of guanosines in BAX.
-
(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
-
63
-
-
0032483439
-
Identification of c-MYC as a target of the APC pathway
-
He TC, Sparks AB, Rago C, Hermeking H, Zawel L, da Costa LT, Morin PJ, Vogelstein B, Kinzler KW. Identification of c-MYC as a target of the APC pathway. Science. 281:1998;1509-1512.
-
(1998)
Science
, vol.281
, pp. 1509-1512
-
-
He, T.C.1
Sparks, A.B.2
Rago, C.3
Hermeking, H.4
Zawel, L.5
Da Costa, L.T.6
Morin, P.J.7
Vogelstein, B.8
Kinzler, K.W.9
|