Genomes and Genes
Affiliation: Fred Hutchinson Cancer Research Center
- Tumors induce coordinate growth of artery, vein, and lymphatic vessel triadsAlanna Ruddell
Fred Hutchinson Cancer Research Center, Seattle, WA, USA
BMC Cancer 14:354. 2014..These processes have generally been studied separately, so that it is not known how peritumoral blood and lymphatic vessels grow relative to each other...
- CTCF haploinsufficiency destabilizes DNA methylation and predisposes to cancerChristopher J Kemp
Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA Electronic address
Cell Rep 7:1020-9. 2014..These findings establish CTCF as a prominent tumor-suppressor gene and point to CTCF-mediated epigenetic stability as a major barrier to neoplastic progression...
- Plasma proteome profiles associated with inflammation, angiogenesis, and cancerKaren S Kelly-Spratt
Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America
PLoS ONE 6:e19721. 2011..This approach provides a basis for distinguishing between protein changes in plasma that are cancer-related and those that are part of a non-specific host response...
- p19Arf suppresses growth, progression, and metastasis of Hras-driven carcinomas through p53-dependent and -independent pathwaysKaren S Kelly-Spratt
Fred Hutchinson Cancer Research Center, Seattle, Washington, USA
PLoS Biol 2:E242. 2004..This indicates that selection for p53 mutations is a direct result of signaling from the initiating oncogenic lesion, Hras, acting through p19(Arf)...
- Resistance to skin tumorigenesis in DNAPK-deficient SCID mice is not due to immunodeficiency but results from hypersensitivity to TPA-induced apoptosisC J Kemp
Fred Hutchinson Cancer Research Center C1 015, 1100 Fairview Avenue North, PO Box 19024, Seattle, WA 98109 1024, USA
Carcinogenesis 20:2051-6. 1999..This hypersensitivity of SCID (severe combined immunodeficient) cells to TPA indicates that the resistance to skin tumor formation in scid/scid mice is due to loss of initiated cells through TPA-induced cell killing...
- Multistep skin cancer in mice as a model to study the evolution of cancer cellsChristopher J Kemp
Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N, Seattle, WA 98109, USA
Semin Cancer Biol 15:460-73. 2005..This indicates that tumor cells have an inherent reduced capacity to buffer against perturbations. Reduced buffering may play an important role in both tumor evolution and therapy response and may be a hallmark of cancer cells...
- The murine gene Cdkn1b (p27(Kip1)) maps to distal chromosome 6 and is excluded as Pas1C J Kemp
Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N, Seattle, Washington 98109, USA
Mamm Genome 11:402-4. 2000
- p53 induction and apoptosis in response to radio- and chemotherapy in vivo is tumor-type-dependentC J Kemp
Fred Hutchinson Cancer Research Center, Seattle, Washington 90109 1024, USA
Cancer Res 61:327-32. 2001..This variation provides one explanation for the tissue specificity of tumor suppression by p53. It also indicates that the role of apoptosis in the response of tumors to therapy varies significantly among tumor types...
- Pathway-specific tumor suppression. Reduction of p27 accelerates gastrointestinal tumorigenesis in Apc mutant mice, but not in Smad3 mutant miceJeannette Philipp-Staheli
Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 90109, USA
Cancer Cell 1:355-68. 2002..These results indicate that reduction of p27 cooperates with mutations in Apc but not in Smad3 during GI tumorigenesis. Thus, tumor suppression by p27 is contingent on the specific oncogenic pathway that drives tumor development...
- Ataxia-telangiectasia mutated is not required for p53 induction and apoptosis in irradiated epithelial tissuesKay E Gurley
Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, C1 015, Seattle, WA 90109 1024, USA
Mol Cancer Res 5:1312-8. 2007..This indicates that marked differences in DNA damage signaling pathways exist between tissues, which could explain some of the tissue-specific phenotypes, especially tumor suppression, associated with Atm deficiency...
- Distinct roles for p53, p27Kip1, and p21Cip1 during tumor developmentJeannette Philipp-Staheli
Fred Hutchinson Cancer Research Center, C1 015, 1100 Fairview Ave N, Seattle, WA 90109 1024, USA
Oncogene 23:905-13. 2004..Although p21 is functionally similar to both p53 and p27, it plays a lesser role in tumor suppression. These results further highlight the highly cooperative nature of p27 and its central role in tumor suppression...
- Deficiency in the gap junction protein connexin32 alters p27Kip1 tumor suppression and MAPK activation in a tissue-specific mannerTimothy J King
Cancer Prevention Research Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA
Oncogene 24:1718-26. 2005..This study demonstrates that tissues dependent on Cx32 tumor suppression, such as the liver and lung, exhibit altered tumorigenesis and tumor biology (MAPK pathway activation) related to p27 status...
- Plasma proteome profiling of a mouse model of breast cancer identifies a set of up-regulated proteins in common with human breast cancer cellsSharon J Pitteri
Fred Hutchinson Cancer Research Center, Seattle, Washington 98109 1024, USA
J Proteome Res 7:1481-9. 2008....
- Endocrine dysfunction in p27Kip1 deficient mice and susceptibility to Wnt-1 driven breast cancerCynthia E Glover
Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA
Carcinogenesis 30:1058-63. 2009..This study shows that while not a significant inhibitor of Wnt-1-driven breast cancer, p27 inhibits gastric tumors, whose latency is modulated by sex steroids...
- Tumor suppression by p53 in the absence of AtmS Lawrence Bailey
Fred Hutchinson Cancer Research Center, Seattle, WA 90109 1024, USA
Mol Cancer Res 6:1185-92. 2008..In conclusion, in these models of oncogene- or DNA damage-induced tumors, p53 retains tumor suppressor activity in the absence of Atm...
- p27kip1 deficiency impairs G2/M arrest in response to DNA damage, leading to an increase in genetic instabilityShannon R Payne
Fred Hutchinson Cancer Research Center C1 015, 1100 Fairview Ave N, Seattle, WA 90109 1024, USA
Mol Cell Biol 28:258-68. 2008..The second is by transient inhibition of cell cycle progression following genotoxic insult, thereby minimizing chromosome damage and fixation of mutations...
- p27(Kip1) (Cdkn1b)-deficient mice are susceptible to chemical carcinogenesis and may be a useful model for carcinogen screeningShannon R Payne
Fred Hutchinson Cancer Research Center C1 015, PO Box 19024, 1100 Fairview Ave N, Seattle, Washington 90109 1024, USA
Toxicol Pathol 31:355-63. 2003....
- High throughput quantitative analysis of serum proteins using glycopeptide capture and liquid chromatography mass spectrometryHui Zhang
Institute for Systems Biology, Seattle, WA 98103, USA
Mol Cell Proteomics 4:144-55. 2005..We further identify, by tandem mass spectrometry, some of the peptides that were consistently elevated in cancer mice compared with their control littermates...
- Integrated pipeline for mass spectrometry-based discovery and confirmation of biomarkers demonstrated in a mouse model of breast cancerJeffrey R Whiteaker
Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA
J Proteome Res 6:3962-75. 2007..Furthermore, the approach can be extended to find biomarkers relevant to human disease...
- Tumor suppressor geneticsShannon R Payne
Fred Hutchinson Cancer Research Center, Seattle, WA 90109, USA
Carcinogenesis 26:2031-45. 2005..Incorporating these new findings into existing models of the clonal evolution will be a challenge for the future...
- A pathway in quiescent cells that controls p27Kip1 stability, subcellular localization, and tumor suppressionArnaud Besson
Howard Hughes Medical Institute, Division of Basic Sciences, Seattle, Washington 98109, USA
Genes Dev 20:47-64. 2006..Thus, phosphorylation of p27 on Ser10 is an important event in the regulation of the tumor suppressor function of p27...
- DNA-PK suppresses a p53-independent apoptotic response to DNA damageKay E Gurley
Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA
EMBO Rep 10:87-93. 2009..This shows that there are two separate, but equally effective, apoptotic responses to DNA damage: one is p53 dependent and the other, engaged in the absence of DNA-PK, does not require p53...
- Non-invasive imaging of carcinogen-induced early neoplasia using ultrahigh-resolution optical coherence tomographyMichael J Cobb
Department of Bioengineering, University of Washington, Seattle, WA 98195, USA
Cancer Biomark 2:163-73. 2006....
- TRAIL-R deficiency in mice enhances lymph node metastasis without affecting primary tumor developmentAnne Grosse-Wilde
Human Biology Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA
J Clin Invest 118:100-10. 2008..Hence, treatment of cancer patients with agonists of the apoptosis-inducing receptors for TRAIL may prove useful in reducing the incidence of metastasis...
- Estradiol-dependent decrease in the orexigenic potency of ghrelin in female ratsDeborah J Clegg
Department of Psychiatry, University of Cincinnati, P O Box 670559, Cincinnati, OH 45267 0559, USA
Diabetes 56:1051-8. 2007....
- Role of epidermal growth factor and its receptor in chemotherapy-induced intestinal injuryFrederick S Huang
Division of Hematology Oncology, Children s Hospital Medical Center, Cincinnati, Ohio 45229, USA
Am J Physiol Gastrointest Liver Physiol 282:G432-42. 2002..These findings do not support a critical role for EGF or its receptor in chemotherapy-induced intestinal injury...
- A mouse model repository for cancer biomarker discoveryKaren S Kelly-Spratt
Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA
J Proteome Res 7:3613-8. 2008..We present the overall design of this resource and its potential use by the research community for biomarker discovery...
- The Role of Double Strand Breaks in CarcinogenesisCHRISTOPHER KEMP; Fiscal Year: 2006..Understanding the functional interaction of the P13 Ks, in regulating p53, apoptosis, development and carcinogenesis at the level of the whole animal is a necessary link to apply knowledge gained from cell culture models to the clinic. ..
- Mouse Models of Tumor Progression and Therapy ResponseCHRISTOPHER KEMP; Fiscal Year: 2007..These experiments will reveal the molecular and cellular basis for the poor clinical outcome associated with p27 deficient tumors. This knowledge can then be applied to improve treatment design and regimen in the clinical setting. ..