Research Topics
| KWOK KIN contact WONGSummaryAffiliation: Massachusetts General Hospital Country: USA Publications
Research Grants
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Detail Information
Publications
PF00299804, an irreversible pan-ERBB inhibitor, is effective in lung cancer models with EGFR and ERBB2 mutations that are resistant to gefitinibJeffrey A Engelman
Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA, USA
Cancer Res 67:11924-32. 2007..These preclinical evaluations support further clinical development of PF00299804 for cancers with mutations and/or amplifications of ERBB family members...
Hsp90 inhibition suppresses mutant EGFR-T790M signaling and overcomes kinase inhibitor resistanceTakeshi Shimamura
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215, USA
Cancer Res 68:5827-38. 2008..Nonetheless, these findings suggest that Hsp90 inhibitors may be effective in T790M-expressing cells and offer an alternative therapeutic strategy for this subset of lung cancers...- NF-kappaB fans the flames of lung carcinogenesisKWOK KIN WONG
Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
Cancer Prev Res (Phila) 3:403-5. 2010..Our growing understanding of the tumor-promoting NF-kappaB downstream effector pathways could lead to the development of novel approaches for lung cancer therapy and chemoprevention... 
A phase I study with neratinib (HKI-272), an irreversible pan ErbB receptor tyrosine kinase inhibitor, in patients with solid tumorsKwok K Wong
Dana Farber Cancer Institute, and Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
Clin Cancer Res 15:2552-8. 2009..The dose-limiting toxicities, maximum tolerated dose, pharmacokinetic profile, and preliminary antitumor activity of neratinib (HKI-272), an irreversible pan ErbB inhibitor, were determined in patients with advanced solid tumors...- HKI-272 in non small cell lung cancerKWOK KIN WONG
Department of Medical Oncology, Dana Farber Cancer Institute, and Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
Clin Cancer Res 13:s4593-6. 2007..A phase II trial of HKI-272 in non-small cell lung cancer patients has been initiated. HKI-272 might offer benefits to non-small cell lung cancer patients who have relapsed after an initial response to erlotinib... - Searching for a magic bullet in NSCLC: the role of epidermal growth factor receptor mutations and tyrosine kinase inhibitorsKWOK KIN WONG
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Lung Cancer 60:S10-8. 2008..Such information may result in the design of highly specific agents that target specific mutations, which could result in more efficacious treatments... - Novel agents in the treatment of lung cancer: Fourth Cambridge ConferenceThomas J Lynch
Division of Hematology Oncology, Massachusetts General Hospital, 55 Fruit Street, Yawkey, 7th Floor, Suite 7601, Boston, MA 02114, USA
Clin Cancer Res 13:s4583-8. 2007.... - Summary statement: novel agents in the treatment of lung cancer: advances in epidermal growth factor receptor-targeted agentsThomas J Lynch
Division of Hematology/Oncology, Massachusetts General Hospital, Boston 02114, and University of Colorado Cancer Center, Aurora, USA
Clin Cancer Res 12:4365s-4371s. 2006 - Non-small-cell lung cancer and Ba/F3 transformed cells harboring the ERBB2 G776insV_G/C mutation are sensitive to the dual-specific epidermal growth factor receptor and ERBB2 inhibitor HKI-272Takeshi Shimamura
Department of Medical Oncology and Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
Cancer Res 66:6487-91. 2006..Thus, the subset of NSCLC patients with tumors carrying the ERBB2 G776insV_G/C mutation may benefit from treatment with HKI-272... - Epidermal growth factor receptor variant III mutations in lung tumorigenesis and sensitivity to tyrosine kinase inhibitorsHongbin Ji
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 103:7817-22. 2006..These findings suggest a therapeutic strategy for cancers harboring the EGFRvIII mutation... - Telomere shortening and mood disorders: preliminary support for a chronic stress model of accelerated agingNaomi M Simon
Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA
Biol Psychiatry 60:432-5. 2006..We propose that chronic stress associated with mood disorders may contribute to excess vulnerability for diseases of aging such as cardiovascular disease and possibly some cancers through accelerated organismal aging... - Proapoptotic BH3-only BCL-2 family protein BIM connects death signaling from epidermal growth factor receptor inhibition to the mitochondrionJing Deng
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Cancer Res 67:11867-75. 2007..This finding has clear implications for overcoming resistance to erlotinib. Resistance to EGFR inhibition can be modulated by alterations in the intrinsic apoptotic pathway controlled by the BCL-2 family of proteins... - Magnetic resonance imaging of the response of a mouse model of non-small cell lung cancer to tyrosine kinase inhibitor treatmentXiangzhi Zhou
Department of Radiology, Brigham and Women s Hospital, Boston MA, USA
Comp Med 58:276-81. 2008..The MRI approaches in this work can be applied on other antitumor drug treatment evaluation in vivo when appropriate sequences are chosen... - Allele-dependent variation in the relative cellular potency of distinct EGFR inhibitorsYuki Yuza
Department of Medical Oncology, Center for Cancer Genome Discovery, Dana Farber Cancer Institute, Boston, Massachusetts, USA
Cancer Biol Ther 6:661-7. 2007..More broadly, these results imply that the development and deployment of targeted therapies should focus on inhibition of specific cancer-causing mutations, not only on the mutated target... - The impact of human EGFR kinase domain mutations on lung tumorigenesis and in vivo sensitivity to EGFR-targeted therapiesHongbin Ji
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA
Cancer Cell 9:485-95. 2006..These data suggest that persistent EGFR signaling is required for tumor maintenance in human lung adenocarcinomas expressing EGFR mutants... - EGFR targeted therapy: view from biological standpointHongbin Ji
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA
Cell Cycle 5:2072-6. 2006.... - Bronchial and peripheral murine lung carcinomas induced by T790M-L858R mutant EGFR respond to HKI-272 and rapamycin combination therapyDanan Li
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Cancer Cell 12:81-93. 2007..However, the combination of HKI-272 and rapamycin resulted in significant regression of both types of lung tumors. This combination therapy may potentially benefit lung cancer patients with the EGFR T790M mutation... - High-resolution genomic profiles of human lung cancerGiovanni Tonon
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 102:9625-30. 2005..Integrated DNA-RNA analyses identified WHSC1L1 and TPX2 as two candidates likely targeted for amplification in both pancreatic ductal adenocarcinoma and non-small-cell lung cancer... - Telomere dysfunction promotes genome instability and metastatic potential in a K-ras p53 mouse model of lung cancerSamanthi A Perera
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Carcinogenesis 29:747-53. 2008..Furthermore, these findings clearly demonstrate (in an in vivo model system) the dual nature of telomere shortening as both a tumor-suppressive and tumor-promoting mechanism in lung cancer, dependent on p53 status... - Telomere dysfunction and Atm deficiency compromises organ homeostasis and accelerates ageingKWOK KIN WONG
Department of Adult Oncology, Dana Farber Cancer Institute Boston, Massachusetts 02115, USA
Nature 421:643-8. 2003.... - LKB1 modulates lung cancer differentiation and metastasisHongbin Ji
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Nature 448:807-10. 2007..These studies establish LKB1 as a critical barrier to pulmonary tumorigenesis, controlling initiation, differentiation and metastasis... - Therapeutic anti-EGFR antibody 806 generates responses in murine de novo EGFR mutant-dependent lung carcinomasDanan Li
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
J Clin Invest 117:346-52. 2007..Taken together, these data support the hypothesis that mAb806 may lead to significant advancements in the treatment of the population of NSCLC patients with these 2 classes of EGFR mutations... - Mouse models of lung cancerAmit Dutt
Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, and Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA
Clin Cancer Res 12:4396s-4402s. 2006..We present here a brief overview of the existing mouse models of lung cancers and the challenges and opportunities for building the next generation of lung cancer mouse models... - The age of cancer: telomeres, checkpoints, and longevityRonald A Depinho
Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA
J Clin Invest 111:S9-14. 2003 - DNA-dependent protein kinase catalytic subunit is not required for dysfunctional telomere fusion and checkpoint response in the telomerase-deficient mouseRichard S Maser
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Mol Cell Biol 27:2253-65. 2007.... - BAC consensus conference, November 4-6, 2004: epidemiology, pathogenesis, and preclinical modelsDavid C Christiani
Harvard University Schools of Medicine and Public Health, Boston, MA, USA
J Thorac Oncol 1:S2-7. 2006..CONCLUSIONS: Elucidation of molecular events involved in BAC tumorigenesis will allow for more precise epidemiologic studies and improved animal models, which will enable development of more effective treatments against the disease... - The T790M mutation in EGFR kinase causes drug resistance by increasing the affinity for ATPCai Hong Yun
Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, 25 Shattuck Street, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 105:2070-5. 2008.... - Mutations in BRAF and KRAS converge on activation of the mitogen-activated protein kinase pathway in lung cancer mouse modelsHongbin Ji
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Cancer Res 67:4933-9. 2007..These results unveil a potential common vulnerability of BRAF and KRas mutant lung tumors that potentially affects rational deployment of MEK targeted therapies to non-small-cell lung cancer patients... - Alu elements mediate MYB gene tandem duplication in human T-ALLJennifer O'Neil
Department of Pediatric Oncology, Belfer Foundation Institute for Innovative Cancer Science, Dana Farber Cancer Institute, Boston, MA 02115, USA
J Exp Med 204:3059-66. 2007..We conclude that Alu-mediated MYB tandem duplication occurs at low frequency during normal thymocyte development and is clonally selected during the molecular pathogenesis of human T-ALL... - Walking the telomere plank into cancerKwok-Kin Wong
J Natl Cancer Inst 95:1184-6. 2003 - An alternative inhibitor overcomes resistance caused by a mutation of the epidermal growth factor receptorSusumu Kobayashi
Division of Hematology/Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School
Cancer Res 65:7096-101. 2005..These data also support the notion that clinical investigations of compounds similar to CL-387,785 may be useful as a treatment strategy for patients with resistance to EGFR inhibitor therapy caused by the T790M mutation... - Chromosomal end fusion resulting from telomere erosion increases susceptibility to radiation via multinucleation: effect of p53Yeun-Jin Ju
Laboratory of Molecular Oncology, Korea Institute of Radiological and Medical Sciences, Seoul 139-706, Korea
Int J Oncol 29:753-63. 2006..Thus, the suggested anticancer radiotherapeutic strategy combined with telomerase inhibition could clinically be applicable to cancers, irrespective of p53 status... - Differential roles of telomere attrition in type I and II endometrial carcinogenesisEsra A Akbay
Department of Pathology, UT Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, TX 75390 9072, USA
Am J Pathol 173:536-44. 2008..Based on this and previous studies, we propose a model in which telomere attrition contributes to the initiation of TII and progression of TI endometrial cancers...
Research Grants
- Inhibition of P13k and MEK Pathways in the Treatment of Lung CancerKWOK KIN contact WONG; Fiscal Year: 2010..Results from the experiments proposed will help guide the clinical development of these combination therapies for patients with lung cancers and other cancer types. ..
- EGFRvIII Mutation in Tumorigenesis and Sensitivity to Tyrosine Kinase InhibitorsKWOK KIN WONG; Fiscal Year: 2010....
- Dysfunctional Telomeres, Checkpoints and AgingKWOK KIN WONG; Fiscal Year: 2007....
- EGFRvIII Mutation in Tumorigenesis and Sensitivity to Tyrosine Kinase InhibitorsKWOK KIN WONG; Fiscal Year: 2007....
- Dysfunctional Telomeres, Checkpoints and AgingKWOK KIN WONG; Fiscal Year: 2010....