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pten (601) 601
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1. Full Text A Small-Molecule Inhibitor for Phosphatase and Tensin Homologue Deleted on Chromosome 10 (PTEN)
by Rosivatz, Erika and Matthews, Jonathan G and McDonald, Neil Q and Mulet, Xavier and Ho, Ka Kei and Lossi, Nadine and Schmid, Annette C and Mirabelli, Marianna and Pomeranz, Karen M and Erneux, Christophe and Lam, Eric W.-F and Vilar, Ramón and Woscholski, Rüdiger
ACS Chemical Biology, ISSN 1554-8929, 11/2006, Volume 1, Issue 12, pp. 780 - 790
Phosphatase and tensin homologue deleted on chromosome 10 (PTEN), a phosphoinositide 3-phosphatase, is an important regulator of insulin-dependent signaling.... 
3T3-L1 ADIPOCYTES | LIPID PHOSPHATASES | PHOSPHOINOSITIDE PHOSPHATASE | PHOSPHATIDYLINOSITOL 3-KINASE/AKT PATHWAY | BIOCHEMISTRY & MOLECULAR BIOLOGY | PANCREATIC BETA-CELLS | GLUCOSE-TRANSPORT | TYROSINE PHOSPHATASES | TUMOR-SUPPRESSOR PTEN | PROTEIN-KINASE B | NUCLEAR TRANSLOCATION | Fibroblasts - enzymology | Phosphorylation | Humans | Molecular Sequence Data | Adipocytes - enzymology | Structure-Activity Relationship | Adipocytes - drug effects | Dose-Response Relationship, Drug | PTEN Phosphohydrolase - antagonists & inhibitors | Drug Design | Vanadium - chemistry | Proto-Oncogene Proteins c-akt - metabolism | Binding Sites | Cell Membrane - drug effects | Amino Acid Sequence | Cell Line | PTEN Phosphohydrolase - genetics | Hypoglycemic Agents - chemistry | Hypoglycemic Agents - pharmacology | Cell Membrane - enzymology | Animals | Adipocytes - metabolism | Fibroblasts - drug effects | Glucose - metabolism | Ligands | Organometallic Compounds - chemistry | Mice | Organometallic Compounds - pharmacology
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2. Full Text Nuclear-cytoplasmic partitioning of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) differentially regulates the cell cycle and apoptosis
by Chung, Ji-Hyun and Eng, Charis
Cancer Research, ISSN 0008-5472, 09/2005, Volume 65, Issue 18, pp. 8096 - 8100
Phosphatase and tensin homologue deleted on chromosome 10 (PTEN), a tumor suppressor phosphatase that dephosphorylates both protein and lipid substrates, is... 
PATHWAYS | G ARREST | PROTEIN | ONCOLOGY | PHOSPHORYLATION | KINASE | SUBCELLULAR-LOCALIZATION | BREAST | Cyclin D1 - metabolism | Phosphorylation | Down-Regulation | Humans | PTEN Phosphohydrolase - metabolism | Cytoplasm - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Phosphatidylinositol 3-Kinases - metabolism | G1 Phase - physiology | Disease Progression | Cyclin-Dependent Kinase Inhibitor p27 - metabolism | Breast Neoplasms - enzymology | Cell Nucleus - metabolism | Breast Neoplasms - pathology | Resting Phase, Cell Cycle - physiology | Cell Cycle - physiology | Cell Line, Tumor | Apoptosis - physiology | Proto-Oncogene Proteins c-akt - metabolism | Mitogen-Activated Protein Kinases - metabolism
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3. Full Text WWP2 is an E3 ubiquitin ligase for PTEN
by Pokorny, Jenny L and Sarkaria, Jann N and Maddika, Subbareddy and Chen, Junjie and Palicharla, Vivek Reddy and Kavela, Sridhar and Rani, Neelam
Nature Cell Biology, ISSN 1465-7392, 06/2011, Volume 13, Issue 6, pp. 730 - 735
PTEN, a lipid phosphatase, is one of the most frequently mutated tumour suppressors in human cancer. Several recent studies have highlighted the importance of... 
STEM-CELLS | PHOSPHATASE | PROSTATE-CANCER | TRANSCRIPTION | TUMOR-SUPPRESSOR GENE | GERMLINE MUTATIONS | CELL-SURVIVAL | BREAST | P53 | DELETION | CELL BIOLOGY | Signal Transduction | Humans | Ubiquitin-Protein Ligases - metabolism | Cell Line, Tumor | Neoplasms - enzymology | PTEN Phosphohydrolase - metabolism | Male | Neoplasms - physiopathology | Ubiquitin-Protein Ligases - physiology | Ubiquitin | Ligases | Physiological aspects | Genetic aspects | Research | Embryonic stem cells | Tumors
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4. Full Text Deubiquitylation and stabilization of PTEN by USP13
by Zhang, Jinsong and Zhang, Jinsong and Zhang, Peijing and Zhang, Peijing and Wei, Yongkun and Wei, Yongkun and Piao, Hai-Long and Piao, Hai-Long and Wang, Wenqi and Wang, Wenqi and Maddika, Subbareddy and Maddika, Subbareddy and Wang, Min and Wang, Min and Chen, Dahu and Chen, Dahu and Sun, Yutong and Sun, Yutong and Hung, Mien-Chie and Hung, Mien-Chie and Chen, Junjie and Chen, Junjie and Ma, Li and Ma, L
Nature Cell Biology, ISSN 1465-7392, 2013, Volume 15, Issue 12, pp. 1486 - 1494
The tumour suppressor PTEN is frequently lost in human cancers. In addition to gene mutations and deletions, recent studies have revealed the importance of... 
BREAST-CANCER | UBIQUITINATION | CELLS | GENE | PIK3CA | PATHWAY | TUMOR-SUPPRESSOR | MUTATIONS | LIGASE | CELL BIOLOGY | Neoplasm Transplantation | Cell Proliferation | Humans | Carcinogenesis - metabolism | Breast Neoplasms - metabolism | Ubiquitination | Tumor Suppressor Proteins - genetics | HEK293 Cells | Female | Protein Stability | Proto-Oncogene Proteins c-akt - metabolism | Endopeptidases - metabolism | Gene Expression | Tumor Suppressor Proteins - metabolism | Signal Transduction | PTEN Phosphohydrolase - metabolism | Tumor Burden | Protein Transport | Carcinogenesis - pathology | Animals | Endopeptidases - genetics | Breast Neoplasms - pathology | Mice, Nude | Cell Line, Tumor | Glycolysis | Mice | Tumor suppressor genes | Research | Ubiquitin-proteasome system | Properties | Proteases | Identification and classification
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5. Full Text Reactive nitrogen species induced by hyperglycemia suppresses Akt signaling and triggers apoptosis by upregulating phosphatase PTEN (phosphatase and tensin homologue deleted on chromosome 10) in an LKB1-dependent manner
by Song, Ping and Wu, Yong and Xu, Jian and Xie, Zhonglin and Dong, Yunzhou and Zhang, Miao and Zou, Ming-Hui
Circulation, ISSN 0009-7322, 10/2007, Volume 116, Issue 14, pp. 1585 - 1595
Background - Oxidative stress plays a causal role in vascular injury in diabetes mellitus, but the mechanisms and targets remain poorly understood. Methods and... 
Endothelium-derived factors | Hyperglycemia | Peroxynitrite | Apoptosis | Endothelium | endothelium | AORTIC ENDOTHELIAL-CELLS | CARDIAC & CARDIOVASCULAR SYSTEMS | peroxynitrite | ACTIVATED PROTEIN-KINASE | PHOSPHORYLATION | NITRIC-OXIDE SYNTHASE | apoptosis | endothelium-derived factors | hyperglycemia | HIGH GLUCOSE | TUMOR-SUPPRESSOR | INSULIN HYPERSENSITIVITY | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | TYROSINE NITRATION | EXPRESSION | Diabetes Mellitus, Experimental - drug therapy | Phosphorylation | Humans | Male | Endothelium, Vascular - enzymology | Threonine - metabolism | Hyperglycemia - drug therapy | Up-Regulation - physiology | Hyperglycemia - pathology | Diabetes Mellitus, Experimental - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Umbilical Veins - cytology | Protein-Serine-Threonine Kinases - metabolism | Insulin - pharmacology | Reactive Nitrogen Species - metabolism | Cells, Cultured | PTEN Phosphohydrolase - metabolism | Serine - metabolism | Hypoglycemic Agents - pharmacology | Hyperglycemia - metabolism | Animals | Signal Transduction - drug effects | Peroxynitrous Acid - metabolism | Diabetes Mellitus, Experimental - pathology | Endothelium, Vascular - pathology | Signal Transduction - physiology | Mice | Apoptosis - physiology | Oxidative stress | Blood circulation disorders | Diabetics | Blood sugar | Physiological aspects | Research | Health aspects | Protein kinases | Risk factors
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6. Full Text Phosphatase of regenerating liver 2 (PRL2) is essential for placental development by down-regulating PTEN (phosphatase and tensin homologue deleted on chromosome 10) and activating Akt protein
by Dong, Yuanshu and Zhang, Lujuan and Zhang, Sheng and Bai, Yunpeng and Chen, Hanying and Sun, Xiaoxin and Yong, Weidong and Li, Wei and Colvin, Stephanie C and Rhodes, Simon J and Shou, Weinian and Zhang, Zhong-Yin
Journal of Biological Chemistry, ISSN 0021-9258, 09/2012, Volume 287, Issue 38, pp. 32172 - 32179
The PRL (phosphatase of regenerating liver) phosphatases are implicated in the control of cell proliferation and invasion. Aberrant PRL expression is... 
INVASION | METASTASIS | CELL-MIGRATION | STABILITY | BIOCHEMISTRY & MOLECULAR BIOLOGY | TUMOR-SUPPRESSOR | GLYCOGEN CELLS | EXPRESSION | BINDING | TYROSINE-PHOSPHATASE | Angiogenic Proteins | Pregnancy, Animal | Cell Proliferation | Embryonic Stem Cells - cytology | Trophoblasts - metabolism | Immediate-Early Proteins - physiology | Humans | Mice, Inbred C57BL | Oncogene Proteins - metabolism | PTEN Phosphohydrolase - metabolism | Cycloheximide - pharmacology | Mice, Knockout | Placenta - metabolism | Pregnancy | Protein Tyrosine Phosphatases - genetics | Animals | Immediate-Early Proteins - genetics | Alleles | HEK293 Cells | Female | Mice | Proto-Oncogene Proteins c-akt - metabolism | Cell Movement | Protein Tyrosine Phosphatases - physiology | Protein Phosphatase | Molecular Bases of Disease | Placenta | Oncogene | PRL Phosphatases | Cell Growth | Akt | Pten | PRL2
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7. Full Text Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) has nuclear localization signal-like sequences for nuclear import mediated by major vault protein
by Chung, Ji-Hyun and Ginn-Pease, Margaret E and Eng, Charis
Cancer Research, ISSN 0008-5472, 05/2005, Volume 65, Issue 10, pp. 4108 - 4116
Although phosphatase and tensin homologue deleted on chromosome 10 (PTEN) localization in the nucleus and cytoplasm is established, the mechanism is unknown.... 
DOMAIN | TRANSPORT | MELANOMA | GENE | MECHANISM | ONCOLOGY | TUMOR-SUPPRESSOR | CELL-CYCLE ARREST | EXPRESSION | BREAST | P53 | Phosphoric Monoester Hydrolases - genetics | Phosphorylation | Tumor Suppressor Proteins - metabolism | Mutagenesis, Site-Directed | Nuclear Localization Signals - genetics | Humans | Nuclear Localization Signals - metabolism | Cytoplasm - metabolism | Structure-Activity Relationship | Breast Neoplasms - metabolism | Breast Neoplasms - genetics | Cell Nucleus - metabolism | Karyopherins - metabolism | Transfection | Cell Nucleus - genetics | PTEN Phosphohydrolase | Tumor Suppressor Proteins - genetics | Vault Ribonucleoprotein Particles - metabolism | Cell Line, Tumor | Mutation | Phosphoric Monoester Hydrolases - metabolism
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8. Full Text Potential value of PTEN in predicting cetuximab response in colorectal cancer: An exploratory study
by Razis, Evangelia and Briasoulis, Evangelos and Vrettou, Eleni and Skarlos, Dimosthenis V and Papamichael, Dimitrios and Kostopoulos, Ioannis and Samantas, Epaminontas and Xanthakis, Ioannis and Bobos, Mattheos and Galanidi, Eleni and Bai, Maria and Gikonti, Ioanna and Koukouma, Alona and Kafiri, Georgia and Papakostas, Pavlos and Kalogeras, Konstantine T and Kosmidis, Paris and Fountzilas, George
BMC Cancer, ISSN 1471-2407, 08/2008, Volume 8, Issue 1, pp. 234 - 234
Background: The epidermal growth factor receptor (EGFR) is over-expressed in 70-75% of colorectal adenocarcinomas (CRC). The anti-EGFR monoclonal antibody... 
ONCOLOGY | EPIDERMAL-GROWTH-FACTOR | KRAS MUTATION | IN-SITU HYBRIDIZATION | PHASE-II | GENE AMPLIFICATION | FACTOR RECEPTOR EXPRESSION | MOLECULAR DETERMINANTS | KINASE INHIBITORS | CARCINOMA | EGFR | Colorectal Neoplasms - mortality | PTEN Phosphohydrolase - genetics | Predictive Value of Tests | Colorectal Neoplasms - enzymology | Adenocarcinoma - pathology | Humans | Middle Aged | Adenocarcinoma - enzymology | Antibodies, Monoclonal - therapeutic use | In Situ Hybridization, Fluorescence | Male | Survival Rate | Antineoplastic Agents - therapeutic use | Adenocarcinoma - drug therapy | Antibodies, Monoclonal, Humanized | Receptor, Epidermal Growth Factor - metabolism | Colorectal Neoplasms - drug therapy | Gene Deletion | Adult | Female | Aged | Cetuximab | Colorectal Neoplasms - pathology | Adenocarcinoma - mortality | Physiological aspects | Diagnosis | Drug therapy | Identification and classification | Oncogenes | Colorectal cancer
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9. Full Text PTEN genomic deletion predicts prostate cancer recurrence and is associated with low AR expression and transcriptional activity
by Choucair, Khalil and Ejdelman, Joshua and Brimo, Fadi and Aprikian, Armen and Chevalier, Simone and Lapointe, Jacques
BMC Cancer, ISSN 1471-2407, 11/2012, Volume 12, Issue 1, pp. 543 - 543
Background: Prostate cancer (PCa), a leading cause of cancer death in North American men, displays a broad range of clinical outcome from relatively indolent... 
PTEN | Prostate cancer | Prognosis | ANDROGEN RECEPTOR | CELLS | RESPONSIVENESS | IN-SITU HYBRIDIZATION | FISH ANALYSIS | RADICAL PROSTATECTOMY | CASTRATION | GENE | ONCOLOGY | TUMOR-SUPPRESSOR | PROGRESSION | PTEN Phosphohydrolase - genetics | Prostatic Neoplasms - pathology | Sequence Deletion | Gene Expression | Genetic Predisposition to Disease | Follow-Up Studies | Signal Transduction | Humans | Middle Aged | Transcriptional Activation | Kaplan-Meier Estimate | Male | DNA Copy Number Variations | Neoplasm Recurrence, Local - pathology | Prostatic Neoplasms - genetics | Receptors, Androgen - genetics | Receptors, Androgen - biosynthesis | Neoplasm Recurrence, Local - genetics | Transcription, Genetic | Aged | Immunohistochemistry | Usage | Physiological aspects | Genetic aspects | Cellular signal transduction | Diagnosis | Research | Protein kinases | AR
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10. Full Text Bioinformatics prediction of miR-30a targets and its inhibition of cell proliferation of osteosarcoma by up-regulating the expression of PTEN
by Zhong, Biao and Guo, Shang and Zhang, Wei and Zhang, Chi and Wang, Yukai and Zhang, Changqing
BMC Medical Genomics, ISSN 1755-8794, 11/2017, Volume 10, Issue 1, pp. 64 - 8
Background: MiRNAs are frequently abnormally expressed in the progression of human osteosarcoma. Phosphatase and tensin homologue deleted on chromosome 10... 
MiR-30a | PTEN | Anti-tumor | Osteosarcoma | MIRNA | GENETICS & HEREDITY | TUMOR-GROWTH | CARCINOMA | Genetic aspects | MicroRNA | Research | Gene expression
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11. Full Text Phosphatase and tensin homologue deleted on chromosome ten (PTEN) as a molecular target in lung epithelial wound repair
by Lai, J‐P and Dalton, J T and Knoell, D L
British Journal of Pharmacology, ISSN 0007-1188, 12/2007, Volume 152, Issue 8, pp. 1172 - 1184
Background and purpose: Epithelial injury contributes to lung pathogenesis. Our work and that of others have identified the phosphoinositide‐3 kinase... 
lung | PTEN | epithelium | wound remodelling | Wound remodelling | Epithelium | Lung | CELLS | ACTIVATION | FREQUENT | PROTEIN | KINASE | TUMOR-SUPPRESSOR PTEN | CANCER | INHIBITION | GROWTH | PHARMACOLOGY & PHARMACY | EXPRESSION | L-Lactate Dehydrogenase - metabolism | PTEN Phosphohydrolase - drug effects | Phosphorylation | Epithelial Cells - drug effects | Humans | Phosphatidylinositol 3-Kinases - metabolism | Lung - cytology | L-Lactate Dehydrogenase - drug effects | Drug Delivery Systems | Dose-Response Relationship, Drug | Protein Tyrosine Phosphatases - antagonists & inhibitors | Phenanthrolines - pharmacology | Phenanthrolines - administration & dosage | Time Factors | Phosphatidylinositol 3-Kinases - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Wound Healing - drug effects | Cell Line | Lung - pathology | Signal Transduction | Organometallic Compounds - adverse effects | Epithelial Cells - pathology | Glucose-6-Phosphatase - antagonists & inhibitors | Lung - drug effects | Wound Healing - physiology | Phenanthrolines - adverse effects | Organometallic Compounds - pharmacology | Organometallic Compounds - administration & dosage | Proto-Oncogene Proteins c-akt - drug effects | Research Papers
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12. Full Text Phosphorylation of PTEN (phosphatase and tensin homologue deleted on chromosome ten) protein is enhanced in human fibromyomatous uteri
by Kovács, Kálmán A and Lengyel, Ferenc and Vértes, Marietta and Vértes, Zsuzsanna and Környei, József L and Gőcze, Péter M and Sumegi, Balazs and Szabó, István
Journal of Steroid Biochemistry and Molecular Biology, ISSN 0960-0760, 2007, Volume 103, Issue 2, pp. 196 - 199
PTEN phosphatase, a product of PTEN tumor suppressor gene, exists in cells in phosphorylated and unphosphorylated form and has a central role in regulation of... 
Leiomyoma | Enhanced PTEN phosphorylation | Impaired PTEN/Akt signalling | impaired PTEN/Akt signalling | ACTIVATION | enhanced PTEN phosphorylation | BIOCHEMISTRY & MOLECULAR BIOLOGY | GROWTH | ENDOCRINOLOGY & METABOLISM | MYOMETRIUM | AKT/PROTEIN KINASE-B | HUMAN LEIOMYOMA | EXPRESSION | leiomyoma | ESTROGEN-RECEPTOR | Protein Kinases - metabolism | Gene Expression | Phosphorylation | Uterine Neoplasms - metabolism | Humans | Middle Aged | PTEN Phosphohydrolase - metabolism | Adult | Female | Leiomyoma - metabolism | Oncogene Protein v-akt - metabolism | Case-Control Studies | Proteins | Genetic research | Physiological aspects
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13. 日本鰻魚紅體與卵巢組織在發育過程中其PTEN(phosphatase and tensin homologue deleted on chromosome 10)Homolog和EDF-1(Endothelial differentiation-related factor-1)表現與影響其表現因子之研究
by Ya-Mai Chen and 陳雅玫
摘要 PTEN (phosphatase and Tensin homolog deleted on chromosome 10，亦稱MMAC1 or TEP1)為一種磷酸酶，擷抗磷脂酰肌醇激酶（PI3K；phosphoinositide 3-kinase）所引起的生理活性。內皮分化因子(Endothlial... 
鹼性纖維母細胞 | endothelial cells | 生長因子補充劑 | gas glands | insulin | 類胰島素生長因子 | EDF-1 | PTEN | IGF-1 | bFGF | 過氧化體增殖劑活化受器 | PI3K | PPAR | 睪固酮 | 胰島素增敏劑 | steroids | 卵巢發育指數 | GSI | 紅體發育指數
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14. Full Text Curcumin up‐regulates phosphatase and tensin homologue deleted on chromosome 10 through microRNA‐mediated control of DNA methylation – a novel mechanism suppressing liver fibrosis
by Zheng, Jianjian and Wu, Cunzao and Lin, Zhuo and Guo, Yong and Shi, Liang and Dong, Peihong and Lu, Zhongqiu and Gao, Shenmeng and Liao, Yi and Chen, Bicheng and Yu, Fujun
The FEBS Journal, ISSN 1742-464X, 01/2014, Volume 281, Issue 1, pp. 88 - 103
Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) has been reported to play a role in the suppression of activated hepatic stellate cells... 
DNA methylation | microRNA‐29b | DNA methyltransferase | hepatic stellate cells | phosphatase and tensin homologue deleted on chromosome 10 | microRNA-29b | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | RECEPTOR | IN-VITRO | INHIBITION | METHYLTRANSFERASES | GROWTH | TUMORIGENESIS | EXPRESSION | PROGRESSION | RNA, Small Interfering - genetics | Luciferases - metabolism | Apoptosis - drug effects | Humans | Male | DNA (Cytosine-5-)-Methyltransferases - antagonists & inhibitors | Liver Cirrhosis - chemically induced | Proto-Oncogene Proteins c-akt - genetics | DNA (Cytosine-5-)-Methyltransferases - metabolism | PTEN Phosphohydrolase - antagonists & inhibitors | Antineoplastic Agents - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Liver Cirrhosis - genetics | Real-Time Polymerase Chain Reaction | Hepatic Stellate Cells - pathology | Hepatic Stellate Cells - drug effects | Chromosome Deletion | PTEN Phosphohydrolase - genetics | Promoter Regions, Genetic | Liver Cirrhosis - prevention & control | RNA, Messenger - genetics | Cells, Cultured | Curcumin - pharmacology | Gene Expression Regulation | PTEN Phosphohydrolase - metabolism | Rats | Carbon Tetrachloride - toxicity | Reverse Transcriptase Polymerase Chain Reaction | Rats, Sprague-Dawley | Blotting, Western | DNA (Cytosine-5-)-Methyltransferases - genetics | Animals | Cell Proliferation - drug effects | MicroRNAs - genetics | Chromosomes, Human, Pair 10 - genetics | DNA Methylation - drug effects | Liver diseases | Phosphatases | MicroRNA | Liver | DNA | Fibrosis | Genetic research | Genetic transcription | Methylation | Epigenetics | MicroRNAs | Apoptosis
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15. Full Text Loss of Phosphatase and tensin homologue deleted on chromosome 10 engages ErbB3 and insulin-like growth factor-I receptor signaling to promote antiestrogen resistance in breast cancer
by Miller, Todd W and Pérez-Torres, Marianela and Narasanna, Archana and Guix, Marta and Stål, Olle and Pérez-Tenorio, Gizeh and Gonzalez-Angulo, Ana M and Hennessy, Bryan T and Mills, Gordon B and Kennedy, J. Phillip and Lindsley, Craig W and Arteaga, Carlos L and Linköpings universitet and Institutionen för klinisk och experimentell medicin and Onkologi and Hälsouniversitetet
Cancer Research, ISSN 0008-5472, 05/2009, Volume 69, Issue 10, pp. 4192 - 4201
Knockdown of the tumor suppressor phosphatase Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) with shRNA in three estrogen receptor... 
ACTIVATED PROTEIN-KINASE | PIK3CA MUTATIONS | ONCOLOGY | CELL-MIGRATION | TYROSINE KINASE | GENE-EXPRESSION | PROGESTERONE-RECEPTOR | TUMOR-SUPPRESSOR PTEN | 26S PROTEASOME | VIVO ANTITUMOR-ACTIVITY | ESTROGEN-RECEPTOR | Chromosome Deletion | PTEN Phosphohydrolase - deficiency | Humans | Drug Resistance, Neoplasm | Receptor, ErbB-2 - physiology | Receptor, ErbB-3 - physiology | Chromosomes, Human, Pair 19 | Estrogen Receptor Modulators - therapeutic use | Breast Neoplasms - genetics | Breast Neoplasms - pathology | Cell Division | Receptor, IGF Type 1 - physiology | Cell Line, Tumor | Female | Transcription, Genetic | Genes, Reporter | Medical and Health Sciences | MEDICINE | Medicin och hälsovetenskap | MEDICIN
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16. Full Text Lapatinib antitumor activity is not dependent upon phosphatase and tensin homologue deleted on chromosome 10 in ErbB2-overexpressing breast cancers
by Xia, Wenle and Husain, Intisar and Liu, Leihua and Bacus, Sarah and Saini, Shermini and Spohn, Janice and Pry, Karen and Westlund, Ron and Stein, Steven H and Spector, Neil L
Cancer Research, ISSN 0008-5472, 02/2007, Volume 67, Issue 3, pp. 1170 - 1175
Trastuzumab antitumor activity in ErbB2-overexpressing breast cancers seems to be dependent upon the presence of phosphatase and tensin homologue deleted on... 
CELLS | TRASTUZUMAB | ONCOLOGY | ERBB2 TYROSINE KINASES | GW572016 | PTEN | CARCINOMAS | EGFR/ERBB2 | AKT | INHIBITOR | TUMOR-GROWTH | PTEN Phosphohydrolase - genetics | PTEN Phosphohydrolase - deficiency | Phosphorylation | Receptor, ErbB-2 - biosynthesis | Apoptosis - drug effects | Humans | Receptor, ErbB-2 - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Breast Neoplasms - drug therapy | Breast Neoplasms - enzymology | Breast Neoplasms - genetics | Signal Transduction - drug effects | Cell Line, Tumor | Antineoplastic Agents - pharmacology | Receptor, ErbB-2 - antagonists & inhibitors | Apoptosis - physiology | Proto-Oncogene Proteins c-akt - metabolism | Quinazolines - pharmacology
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17. Full Text Phosphatase and tensin homologue deleted on chromosome ten (PTEN) gene mutations in haematological malignancies
by Welbourn, John T
2007
PTEN is a tumour suppressor protein named after its homology with phosphatase and tensin and its frequent deletion on chromosome 10. PTEN was discovered to be... 
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