Transgenic expression of Helicobacter pylori CagA induces gastrointestinal and hematopoietic neoplasms in mouse
Infection with cagA-positive Helicobacter pylori is associated with gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma of B cell origin. The cagA-encoded CagA protein is delivered into gastric epithelial cells via the bacterial type IV secretion system and, upon tyr...
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| Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 105; no. 3; pp. 1003 - 1008 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
National Academy of Sciences
22.01.2008
National Acad Sciences |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Infection with cagA-positive Helicobacter pylori is associated with gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma of B cell origin. The cagA-encoded CagA protein is delivered into gastric epithelial cells via the bacterial type IV secretion system and, upon tyrosine phosphorylation by Src family kinases, specifically binds to and aberrantly activates SHP-2 tyrosine phosphatase, a bona fide oncoprotein in human malignancies. CagA also elicits junctional and polarity defects in epithelial cells by interacting with and inhibiting partitioning-defective 1 (PAR1)/microtubule affinity-regulating kinase (MARK) independently of CagA tyrosine phosphorylation. Despite these CagA activities that contribute to neoplastic transformation, a causal link between CagA and in vivo oncogenesis remains unknown. Here, we generated transgenic mice expressing wild-type or phosphorylation-resistant CagA throughout the body or predominantly in the stomach. Wild-type CagA transgenic mice showed gastric epithelial hyperplasia and some of the mice developed gastric polyps and adenocarcinomas of the stomach and small intestine. Systemic expression of wild-type CagA further induced leukocytosis with IL-3/GM-CSF hypersensitivity and some mice developed myeloid leukemias and B cell lymphomas, the hematological malignancies also caused by gain-of-function SHP-2 mutations. Such pathological abnormalities were not observed in transgenic mice expressing phosphorylation-resistant CagA. These results provide first direct evidence for the role of CagA as a bacterium-derived oncoprotein (bacterial oncoprotein) that acts in mammals and further indicate the importance of CagA tyrosine phosphorylation, which enables CagA to deregulate SHP-2, in the development of H. pylori-associated neoplasms. |
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| AbstractList | Infection with cagA-positive Helicobacter pylori is associated with gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma of B cell origin. The cagA-encoded CagA protein is delivered into gastric epithelial cells via the bacterial type IV secretion system and, upon tyrosine phosphorylation by Src family kinases, specifically binds to and aberrantly activates SHP-2 tyrosine phosphatase, a bona fide oncoprotein in human malignancies. CagA also elicits junctional and polarity defects in epithelial cells by interacting with and inhibiting partitioning-defective 1 (PAR1)/microtubule affinity-regulating kinase (MARK) independently of CagA tyrosine phosphorylation. Despite these CagA activities that contribute to neoplastic transformation, a causal link between CagA and in vivo oncogenesis remains unknown. Here, we generated transgenic mice expressing wild-type or phosphorylation-resistant CagA throughout the body or predominantly in the stomach. Wild-type CagA transgenic mice showed gastric epithelial hyperplasia and some of the mice developed gastric polyps and adenocarcinomas of the stomach and small intestine. Systemic expression of wild-type CagA further induced leukocytosis with IL-3/GM-CSF hypersensitivity and some mice developed myeloid leukemias and B cell lymphomas, the hematological malignancies also caused by gain-of-function SHP-2 mutations. Such pathological abnormalities were not observed in transgenic mice expressing phosphorylation-resistant CagA. These results provide first direct evidence for the role of CagA as a bacterium-derived oncoprotein (bacterial oncoprotein) that acts in mammals and further indicate the importance of CagA tyrosine phosphorylation, which enables CagA to deregulate SHP-2, in the development of H. pylori-associated neoplasms. Infection with cagA-positive Helicobacter pylori is associated with gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma of B cell origin. The cagA-encoded CagA protein is delivered into gastric epithelial cells via the bacterial type IV secretion system and, upon tyrosine phosphorylation by Src family kinases, specifically binds to and aberrantly activates SHP-2 tyrosine phosphatase, a bona fide oncoprotein in human malignancies. CagA also elicits junctional and polarity defects in epithelial cells by interacting with and inhibiting partitioning-defective 1 (PAR1)/microtubule affinity-regulating kinase (MARK) independently of CagA tyrosine phosphorylation. Despite these CagA activities that contribute to neoplastic transformation, a causal link between CagA and in vivo oncogenesis remains unknown. Here, we generated transgenic mice expressing wild-type or phosphorylation-resistant CagA throughout the body or predominantly in the stomach. Wild-type CagA transgenic mice showed gastric epithelial hyperplasia and some of the mice developed gastric polyps and adenocarcinomas of the stomach and small intestine. Systemic expression of wild-type CagA further induced leukocytosis with IL-3/GM-CSF hypersensitivity and some mice developed myeloid leukemias and B cell lymphomas, the hematological malignancies also caused by gain-of-function SHP-2 mutations. Such pathological abnormalities were not observed in transgenic mice expressing phosphorylation-resistant CagA. These results provide first direct evidence for the role of CagA as a bacterium-derived oncoprotein (bacterial oncoprotein) that acts in mammals and further indicate the importance of CagA tyrosine phosphorylation, which enables CagA to deregulate SHP-2, in the development of H. pylori-associated neoplasms.Infection with cagA-positive Helicobacter pylori is associated with gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma of B cell origin. The cagA-encoded CagA protein is delivered into gastric epithelial cells via the bacterial type IV secretion system and, upon tyrosine phosphorylation by Src family kinases, specifically binds to and aberrantly activates SHP-2 tyrosine phosphatase, a bona fide oncoprotein in human malignancies. CagA also elicits junctional and polarity defects in epithelial cells by interacting with and inhibiting partitioning-defective 1 (PAR1)/microtubule affinity-regulating kinase (MARK) independently of CagA tyrosine phosphorylation. Despite these CagA activities that contribute to neoplastic transformation, a causal link between CagA and in vivo oncogenesis remains unknown. Here, we generated transgenic mice expressing wild-type or phosphorylation-resistant CagA throughout the body or predominantly in the stomach. Wild-type CagA transgenic mice showed gastric epithelial hyperplasia and some of the mice developed gastric polyps and adenocarcinomas of the stomach and small intestine. Systemic expression of wild-type CagA further induced leukocytosis with IL-3/GM-CSF hypersensitivity and some mice developed myeloid leukemias and B cell lymphomas, the hematological malignancies also caused by gain-of-function SHP-2 mutations. Such pathological abnormalities were not observed in transgenic mice expressing phosphorylation-resistant CagA. These results provide first direct evidence for the role of CagA as a bacterium-derived oncoprotein (bacterial oncoprotein) that acts in mammals and further indicate the importance of CagA tyrosine phosphorylation, which enables CagA to deregulate SHP-2, in the development of H. pylori-associated neoplasms. Infection with cagA -positive Helicobacter pylori is associated with gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma of B cell origin. The cagA -encoded CagA protein is delivered into gastric epithelial cells via the bacterial type IV secretion system and, upon tyrosine phosphorylation by Src family kinases, specifically binds to and aberrantly activates SHP-2 tyrosine phosphatase, a bona fide oncoprotein in human malignancies. CagA also elicits junctional and polarity defects in epithelial cells by interacting with and inhibiting partitioning-defective 1 (PAR1)/microtubule affinity-regulating kinase (MARK) independently of CagA tyrosine phosphorylation. Despite these CagA activities that contribute to neoplastic transformation, a causal link between CagA and in vivo oncogenesis remains unknown. Here, we generated transgenic mice expressing wild-type or phosphorylation-resistant CagA throughout the body or predominantly in the stomach. Wild-type CagA transgenic mice showed gastric epithelial hyperplasia and some of the mice developed gastric polyps and adenocarcinomas of the stomach and small intestine. Systemic expression of wild-type CagA further induced leukocytosis with IL-3/GM-CSF hypersensitivity and some mice developed myeloid leukemias and B cell lymphomas, the hematological malignancies also caused by gain-of-function SHP-2 mutations. Such pathological abnormalities were not observed in transgenic mice expressing phosphorylation-resistant CagA. These results provide first direct evidence for the role of CagA as a bacterium-derived oncoprotein (bacterial oncoprotein) that acts in mammals and further indicate the importance of CagA tyrosine phosphorylation, which enables CagA to deregulate SHP-2, in the development of H. pylori -associated neoplasms. bacterial oncoprotein transgenic mouse Infection with cagA-positive Helicobacter pylori is associated with gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma of B cell origin. The cagA-encoded CagA protein is delivered into gastric epithelial cells via the bacterial type IV secretion system and, upon tyrosine phosphorylation by Src family kinases, specifically binds to and aberrantly activates SHP-2 tyrosine phosphatase, a bona fide oncoprotein in human malignancies. CagA also elicits junctional and polarity defects in epithelial cells by interacting with and inhibiting partitioning-defective 1 (PAR1)/microtubule affinity-regulating kinase (MARK) independently of CagA tyrosine phosphorylation. Despite these CagA activities that contribute to neoplastic transformation, a causal link between CagA and in vivo oncogenesis remains unknown. Here, we generated transgenic mice expressing wild-type or phosphorylation-resistant CagA throughout the body or predominantly in the stomach. Wild-type CagA transgenic mice showed gastric epithelial hyperplasia and some of the mice developed gastric polyps and adenocarcinomas of the stomach and small intestine. Systemic expression of wild-type CagA further induced leukocytosis with IL-3/GM-CSF hypersensitivity and some mice developed myeloid leukemias and B cell lymphomas, the hematological malignancies also caused by gain-of-function SHP-2 mutations. Such pathological abnormalities were not observed in transgenic mice expressing phosphorylation-resistant CagA. These results provide first direct evidence for the role of CagA as a bacterium-derived oncoprotein (bacterial oncoprotein) that acts in mammals and further indicate the importance of CagA tyrosine phosphorylation, which enables CagA to deregulate SHP-2, in the development of H. pylori-associated neoplasms. [PUBLICATION ABSTRACT] Infection with cagA -positive Helicobacter pylori is associated with gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma of B cell origin. The cagA -encoded CagA protein is delivered into gastric epithelial cells via the bacterial type IV secretion system and, upon tyrosine phosphorylation by Src family kinases, specifically binds to and aberrantly activates SHP-2 tyrosine phosphatase, a bona fide oncoprotein in human malignancies. CagA also elicits junctional and polarity defects in epithelial cells by interacting with and inhibiting partitioning-defective 1 (PAR1)/microtubule affinity-regulating kinase (MARK) independently of CagA tyrosine phosphorylation. Despite these CagA activities that contribute to neoplastic transformation, a causal link between CagA and in vivo oncogenesis remains unknown. Here, we generated transgenic mice expressing wild-type or phosphorylation-resistant CagA throughout the body or predominantly in the stomach. Wild-type CagA transgenic mice showed gastric epithelial hyperplasia and some of the mice developed gastric polyps and adenocarcinomas of the stomach and small intestine. Systemic expression of wild-type CagA further induced leukocytosis with IL-3/GM-CSF hypersensitivity and some mice developed myeloid leukemias and B cell lymphomas, the hematological malignancies also caused by gain-of-function SHP-2 mutations. Such pathological abnormalities were not observed in transgenic mice expressing phosphorylation-resistant CagA. These results provide first direct evidence for the role of CagA as a bacterium-derived oncoprotein (bacterial oncoprotein) that acts in mammals and further indicate the importance of CagA tyrosine phosphorylation, which enables CagA to deregulate SHP-2, in the development of H. pylori -associated neoplasms. |
| Author | Miura, Motohiro Hatakeyama, Masanori Matsui, Atsushi Higashi, Hideaki Iwabuchi, Kazuya Yuasa, Hitomi Musashi, Manabu Azuma, Takeshi Sawa, Hirofumi Tanaka, Shinya Suzuki, Misao Ohnishi, Naomi Yamada, Gen |
| Author_xml | – sequence: 1 fullname: Ohnishi, Naomi – sequence: 2 fullname: Yuasa, Hitomi – sequence: 3 fullname: Tanaka, Shinya – sequence: 4 fullname: Sawa, Hirofumi – sequence: 5 fullname: Miura, Motohiro – sequence: 6 fullname: Matsui, Atsushi – sequence: 7 fullname: Higashi, Hideaki – sequence: 8 fullname: Musashi, Manabu – sequence: 9 fullname: Iwabuchi, Kazuya – sequence: 10 fullname: Suzuki, Misao – sequence: 11 fullname: Yamada, Gen – sequence: 12 fullname: Azuma, Takeshi – sequence: 13 fullname: Hatakeyama, Masanori |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/18192401$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1016/j.ejmg.2005.03.001 10.1038/nrc1433 10.1038/nm1084 10.1093/ajcp/106.5.670 10.1038/nrc703 10.1016/S0021-9258(19)74349-X 10.1126/science.1067147 10.1084/jem.20051027 10.1074/jbc.C100754200 10.1128/MCB.17.9.5499 10.1053/j.gastro.2005.12.038 10.1073/pnas.96.25.14559 10.1136/gut.40.3.297 10.1182/blood.V97.4.911 10.1158/0008-5472.CAN-04-1923 10.1002/bies.10286 10.1182/blood-2004-11-4207 10.1016/S1470-2045(01)00486-7 10.1073/pnas.92.1.160 10.1038/nature05765 10.1053/j.gastro.2005.02.064 10.1016/S1097-2765(02)00681-0 10.1146/annurev.biochem.75.103004.142702 10.1083/jcb.200208039 10.1101/gad.1211604 10.1074/jbc.M309964200 10.1038/sj.onc.1210251 10.1016/S0016-5085(98)70143-X 10.1038/ng1156 10.1016/S0022-3565(24)36411-0 10.1038/sj.onc.1210139 10.1128/MCB.26.1.261-276.2006 10.1093/jnci/87.23.1777 10.1111/j.1572-0241.1998.00375.x 10.1056/NEJM199405053301803 10.1073/pnas.222375399 10.1016/0168-9525(96)10016-0 |
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| References | e_1_3_3_17_2 e_1_3_3_16_2 Musashi M (e_1_3_3_40_2) 1991; 280 e_1_3_3_19_2 e_1_3_3_38_2 Blaser MJ (e_1_3_3_6_2) 1995; 55 e_1_3_3_18_2 e_1_3_3_39_2 e_1_3_3_13_2 e_1_3_3_36_2 e_1_3_3_12_2 e_1_3_3_37_2 e_1_3_3_15_2 e_1_3_3_34_2 e_1_3_3_14_2 Honda S (e_1_3_3_23_2) 1998; 58 e_1_3_3_35_2 e_1_3_3_32_2 e_1_3_3_33_2 e_1_3_3_11_2 e_1_3_3_10_2 e_1_3_3_31_2 e_1_3_3_5_2 e_1_3_3_8_2 e_1_3_3_7_2 e_1_3_3_28_2 e_1_3_3_9_2 e_1_3_3_27_2 Correa P (e_1_3_3_30_2) 1992; 52 e_1_3_3_29_2 e_1_3_3_24_2 e_1_3_3_26_2 e_1_3_3_25_2 e_1_3_3_2_2 e_1_3_3_20_2 e_1_3_3_1_2 e_1_3_3_4_2 e_1_3_3_22_2 e_1_3_3_3_2 e_1_3_3_21_2 12719469 - J Cell Biol. 2003 Apr 28;161(2):249-55 16354697 - Mol Cell Biol. 2006 Jan;26(1):261-76 9766647 - Cancer Res. 1998 Oct 1;58(19):4255-9 8984731 - Trends Genet. 1996 May;12(5):171-5 14963045 - J Biol Chem. 2004 Apr 23;279(17):17205-16 8996200 - J Pharmacol Exp Ther. 1997 Jan;280(1):225-31 11902583 - Nat Rev Cancer. 2002 Jan;2(1):28-37 15273746 - Nat Med. 2004 Aug;10(8):849-57 9517643 - Am J Gastroenterol. 1998 Mar;93(3):375-9 9271425 - Mol Cell Biol. 1997 Sep;17(9):5499-507 15604238 - Cancer Res. 2004 Dec 15;64(24):8816-20 1458460 - Cancer Res. 1992 Dec 15;52(24):6735-40 7743510 - Cancer Res. 1995 May 15;55(10):2111-5 11743164 - Science. 2002 Jan 25;295(5555):683-6 11905707 - Lancet Oncol. 2001 Sep;2(9):533-43 8253786 - J Biol Chem. 1993 Dec 15;268(35):26559-70 7816809 - Proc Natl Acad Sci U S A. 1995 Jan 3;92(1):160-4 12419219 - Mol Cell. 2002 Oct;10(4):745-55 16756488 - Annu Rev Biochem. 2006;75:137-63 12766944 - Bioessays. 2003 Jun;25(6):542-53 12391297 - Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14428-33 15314019 - Genes Dev. 2004 Aug 15;18(16):1909-25 16618412 - Gastroenterology. 2006 Apr;130(4):1181-90 8929480 - Am J Clin Pathol. 1996 Nov;106(5):670-5 17507984 - Nature. 2007 May 17;447(7142):330-3 16275761 - J Exp Med. 2005 Nov 7;202(9):1235-47 16053901 - Eur J Med Genet. 2005 Apr-Jun;48(2):81-96 17237808 - Oncogene. 2007 Jul 12;26(32):4617-26 11159516 - Blood. 2001 Feb 15;97(4):911-4 7473834 - J Natl Cancer Inst. 1995 Dec 6;87(23):1777-80 15887107 - Gastroenterology. 2005 May;128(5):1229-42 12717436 - Nat Genet. 2003 Jun;34(2):148-50 15761018 - Blood. 2005 Jul 1;106(1):311-7 15343275 - Nat Rev Cancer. 2004 Sep;4(9):688-94 9721161 - Gastroenterology. 1998 Sep;115(3):642-8 11788577 - J Biol Chem. 2002 Mar 1;277(9):6775-8 9135515 - Gut. 1997 Mar;40(3):297-301 10588744 - Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14559-64 17160020 - Oncogene. 2007 May 24;26(24):3462-72 8145781 - N Engl J Med. 1994 May 5;330(18):1267-71 |
| References_xml | – ident: e_1_3_3_13_2 doi: 10.1016/j.ejmg.2005.03.001 – ident: e_1_3_3_14_2 doi: 10.1038/nrc1433 – ident: e_1_3_3_35_2 doi: 10.1038/nm1084 – ident: e_1_3_3_36_2 doi: 10.1093/ajcp/106.5.670 – ident: e_1_3_3_2_2 doi: 10.1038/nrc703 – ident: e_1_3_3_29_2 doi: 10.1016/S0021-9258(19)74349-X – volume: 52 start-page: 6735 year: 1992 ident: e_1_3_3_30_2 article-title: Human gastric carcinogenesis: a multistep and multifactorial process–First American Cancer Society Award Lecture on Cancer Epidemiology and Prevention. publication-title: Cancer Res – ident: e_1_3_3_9_2 doi: 10.1126/science.1067147 – ident: e_1_3_3_19_2 doi: 10.1084/jem.20051027 – ident: e_1_3_3_11_2 doi: 10.1074/jbc.C100754200 – ident: e_1_3_3_32_2 doi: 10.1128/MCB.17.9.5499 – ident: e_1_3_3_26_2 doi: 10.1053/j.gastro.2005.12.038 – ident: e_1_3_3_8_2 doi: 10.1073/pnas.96.25.14559 – volume: 58 start-page: 4255 year: 1998 ident: e_1_3_3_23_2 article-title: Development of Helicobacter pylori-induced gastric carcinoma in Mongolian gerbils. publication-title: Cancer Res – ident: e_1_3_3_7_2 doi: 10.1136/gut.40.3.297 – ident: e_1_3_3_33_2 doi: 10.1182/blood.V97.4.911 – ident: e_1_3_3_37_2 doi: 10.1158/0008-5472.CAN-04-1923 – ident: e_1_3_3_38_2 doi: 10.1002/bies.10286 – ident: e_1_3_3_31_2 doi: 10.1182/blood-2004-11-4207 – ident: e_1_3_3_1_2 doi: 10.1016/S1470-2045(01)00486-7 – ident: e_1_3_3_28_2 doi: 10.1073/pnas.92.1.160 – ident: e_1_3_3_20_2 doi: 10.1038/nature05765 – ident: e_1_3_3_25_2 doi: 10.1053/j.gastro.2005.02.064 – ident: e_1_3_3_18_2 doi: 10.1016/S1097-2765(02)00681-0 – ident: e_1_3_3_39_2 doi: 10.1146/annurev.biochem.75.103004.142702 – ident: e_1_3_3_17_2 doi: 10.1083/jcb.200208039 – ident: e_1_3_3_22_2 doi: 10.1101/gad.1211604 – ident: e_1_3_3_15_2 doi: 10.1074/jbc.M309964200 – ident: e_1_3_3_21_2 doi: 10.1038/sj.onc.1210251 – ident: e_1_3_3_24_2 doi: 10.1016/S0016-5085(98)70143-X – ident: e_1_3_3_34_2 doi: 10.1038/ng1156 – volume: 280 start-page: 225 year: 1991 ident: e_1_3_3_40_2 article-title: Phorbol ester enhancement of IL-3-dependent proliferation of primitive hematopoietic progenitors of mice. publication-title: J Pharmacol Exp Ther doi: 10.1016/S0022-3565(24)36411-0 – ident: e_1_3_3_12_2 doi: 10.1038/sj.onc.1210139 – ident: e_1_3_3_16_2 doi: 10.1128/MCB.26.1.261-276.2006 – volume: 55 start-page: 2111 year: 1995 ident: e_1_3_3_6_2 article-title: Infection with Helicobacter pylori strains possessing cagA is associated with an increased risk of developing adenocarcinoma of the stomach. publication-title: Cancer Res – ident: e_1_3_3_4_2 doi: 10.1093/jnci/87.23.1777 – ident: e_1_3_3_5_2 doi: 10.1111/j.1572-0241.1998.00375.x – ident: e_1_3_3_3_2 doi: 10.1056/NEJM199405053301803 – ident: e_1_3_3_10_2 doi: 10.1073/pnas.222375399 – ident: e_1_3_3_27_2 doi: 10.1016/0168-9525(96)10016-0 – reference: 16275761 - J Exp Med. 2005 Nov 7;202(9):1235-47 – reference: 8145781 - N Engl J Med. 1994 May 5;330(18):1267-71 – reference: 12719469 - J Cell Biol. 2003 Apr 28;161(2):249-55 – reference: 15604238 - Cancer Res. 2004 Dec 15;64(24):8816-20 – reference: 7473834 - J Natl Cancer Inst. 1995 Dec 6;87(23):1777-80 – reference: 15887107 - Gastroenterology. 2005 May;128(5):1229-42 – reference: 1458460 - Cancer Res. 1992 Dec 15;52(24):6735-40 – reference: 15314019 - Genes Dev. 2004 Aug 15;18(16):1909-25 – reference: 11902583 - Nat Rev Cancer. 2002 Jan;2(1):28-37 – reference: 16756488 - Annu Rev Biochem. 2006;75:137-63 – reference: 8253786 - J Biol Chem. 1993 Dec 15;268(35):26559-70 – reference: 11743164 - Science. 2002 Jan 25;295(5555):683-6 – reference: 11788577 - J Biol Chem. 2002 Mar 1;277(9):6775-8 – reference: 12391297 - Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14428-33 – reference: 7816809 - Proc Natl Acad Sci U S A. 1995 Jan 3;92(1):160-4 – reference: 17507984 - Nature. 2007 May 17;447(7142):330-3 – reference: 8984731 - Trends Genet. 1996 May;12(5):171-5 – reference: 10588744 - Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14559-64 – reference: 16053901 - Eur J Med Genet. 2005 Apr-Jun;48(2):81-96 – reference: 15343275 - Nat Rev Cancer. 2004 Sep;4(9):688-94 – reference: 11905707 - Lancet Oncol. 2001 Sep;2(9):533-43 – reference: 16354697 - Mol Cell Biol. 2006 Jan;26(1):261-76 – reference: 9135515 - Gut. 1997 Mar;40(3):297-301 – reference: 17237808 - Oncogene. 2007 Jul 12;26(32):4617-26 – reference: 12717436 - Nat Genet. 2003 Jun;34(2):148-50 – reference: 9721161 - Gastroenterology. 1998 Sep;115(3):642-8 – reference: 9766647 - Cancer Res. 1998 Oct 1;58(19):4255-9 – reference: 12419219 - Mol Cell. 2002 Oct;10(4):745-55 – reference: 14963045 - J Biol Chem. 2004 Apr 23;279(17):17205-16 – reference: 15273746 - Nat Med. 2004 Aug;10(8):849-57 – reference: 8996200 - J Pharmacol Exp Ther. 1997 Jan;280(1):225-31 – reference: 9517643 - Am J Gastroenterol. 1998 Mar;93(3):375-9 – reference: 16618412 - Gastroenterology. 2006 Apr;130(4):1181-90 – reference: 15761018 - Blood. 2005 Jul 1;106(1):311-7 – reference: 12766944 - Bioessays. 2003 Jun;25(6):542-53 – reference: 7743510 - Cancer Res. 1995 May 15;55(10):2111-5 – reference: 8929480 - Am J Clin Pathol. 1996 Nov;106(5):670-5 – reference: 9271425 - Mol Cell Biol. 1997 Sep;17(9):5499-507 – reference: 11159516 - Blood. 2001 Feb 15;97(4):911-4 – reference: 17160020 - Oncogene. 2007 May 24;26(24):3462-72 |
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| Snippet | Infection with cagA-positive Helicobacter pylori is associated with gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma of B... Infection with cagA -positive Helicobacter pylori is associated with gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma of B... Infection with cagA -positive Helicobacter pylori is associated with gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma of B... |
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| SubjectTerms | Adenocarcinoma Animals Antigens, Bacterial - genetics Antigens, Bacterial - metabolism Bacteria Bacterial proteins Bacterial Proteins - genetics Bacterial Proteins - metabolism Biological Sciences Bone marrow cells carcinogenesis Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Cell Transformation, Neoplastic - pathology Epithelial cells Gastrointestinal Neoplasms - genetics Gastrointestinal Neoplasms - metabolism Gastrointestinal Neoplasms - pathology Gene expression Gene Expression Regulation, Neoplastic Helicobacter pylori Helicobacter pylori - genetics Helicobacter pylori - metabolism Helicobacter pylori - pathogenicity Hematologic Neoplasms - genetics Hematologic Neoplasms - metabolism Hematologic Neoplasms - pathology humans hyperplasia Hypersensitivity Infections Kinases Leukocytes Lymphoma Mice Mice, Transgenic Mutation oncogene proteins Phosphorylation phosphotransferases (kinases) Phosphotyrosine - metabolism polyps (pathological conditions) Rodents small intestine Stomach Transgenic animals Tumors type IV secretion system tyrosine |
| Title | Transgenic expression of Helicobacter pylori CagA induces gastrointestinal and hematopoietic neoplasms in mouse |
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