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Article ; Online: New mechanistic insights into modifiable risk factors that promote pancreatic cancer.

Srinivasan, Supriya / Dosch, Austin R / Nagathihalli, Nagaraj S

2019 Volume 10, Issue 25, Page(s) 2417–2418

Language	English
Publishing date	2019-03-29
Publishing country	United States
Document type	Editorial
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.26813
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Article ; Online: Interleukin-1 signaling in solid organ malignancies.

Dosch, Austin R / Singh, Samara / Nagathihalli, Nagaraj S / Datta, Jashodeep / Merchant, Nipun B

Biochimica et biophysica acta. Reviews on cancer

2021 Volume 1877, Issue 1, Page(s) 188670

Abstract: As inflammation plays a critical role in the development and progression of cancer, therapeutic targeting of cytokine pathways involved in both tumorigenesis and dictating response to clinical treatments are of significant interest. Recent evidence has ... ...

Abstract	As inflammation plays a critical role in the development and progression of cancer, therapeutic targeting of cytokine pathways involved in both tumorigenesis and dictating response to clinical treatments are of significant interest. Recent evidence has highlighted the importance of the pro-inflammatory cytokine interleukin-1 (IL-1) as a key mediator of tumor growth, metastatic disease spread, immunosuppression, and drug resistance in cancer. IL-1 promotes tumorigenesis through diverse mechanisms, including the activation of oncogenic signaling pathways directly in tumor cells and via orchestrating crosstalk between the cellular constituents of the tumor microenvironment (TME), thereby driving cancer growth. This review will provide an overview of IL-1 signaling and physiology and summarize the disparate mechanisms involving IL-1 in tumorigenesis and cancer progression. Additionally, clinical studies targeting IL-1 signaling in the management of solid organ tumors will be summarized herein.
MeSH term(s)	Carcinogenesis ; Humans ; Interleukin-1 ; Neoplasms/pathology ; Signal Transduction/physiology ; Tumor Microenvironment
Chemical Substances	Interleukin-1
Language	English
Publishing date	2021-12-16
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2918802-7
ISSN	1879-2561 ; 0304-419X
ISSN (online)	1879-2561
ISSN	0304-419X
DOI	10.1016/j.bbcan.2021.188670
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Article ; Online: Tumor Cell-Intrinsic p38 MAPK Signaling Promotes IL1α-Mediated Stromal Inflammation and Therapeutic Resistance in Pancreatic Cancer.

Singh, Samara P / Dosch, Austin R / Mehra, Siddharth / De Castro Silva, Iago / Bianchi, Anna / Garrido, Vanessa T / Zhou, Zhiqun / Adams, Andrew / Amirian, Haleh / Box, Edmond W / Sun, Xiaodian / Ban, Yuguang / Datta, Jashodeep / Nagathihalli, Nagaraj S / Merchant, Nipun B

Cancer research

2024 Volume 84, Issue 8, Page(s) 1320–1332

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is characterized by a KRAS-driven inflammatory program and a desmoplastic stroma, which contribute to the profoundly chemoresistant phenotype. The tumor stroma contains an abundance of cancer-associated fibroblasts ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) is characterized by a KRAS-driven inflammatory program and a desmoplastic stroma, which contribute to the profoundly chemoresistant phenotype. The tumor stroma contains an abundance of cancer-associated fibroblasts (CAF), which engage in extensive paracrine cross-talk with tumor cells to perpetuate protumorigenic inflammation. IL1α, a pleiotropic, tumor cell-derived cytokine, plays a critical role in shaping the stromal landscape. To provide insights into the molecular mechanisms regulating IL1A expression in PDAC, we performed transcriptional profiling of The Cancer Genome Atlas datasets and pharmacologic screening in PDAC cells and identified p38α MAPK as a key positive regulator of IL1A expression. Both genetic and pharmacologic inhibition of p38 MAPK significantly diminished IL1α production in vitro. Chromatin- and coimmunoprecipitation analyses revealed that p38 MAPK coordinates the transcription factors Sp1 and the p65 subunit of NFκB to drive IL1A overexpression. Single-cell RNA sequencing of a highly desmoplastic murine PDAC model, Ptf1aCre/+; LSL-KrasG12D/+; Tgfbr2flox/flox (PKT), confirmed that p38 MAPK inhibition significantly decreases tumor cell-derived Il1a and attenuates the inflammatory CAF phenotype in a paracrine IL1α-dependent manner. Furthermore, p38 MAPK inhibition favorably modulated intratumoral immunosuppressive myeloid populations and augmented chemotherapeutic efficacy to substantially reduce tumor burden and improve overall survival in PKT mice. These findings illustrate a cellular mechanism of tumor cell-intrinsic p38-p65/Sp1-IL1α signaling that is responsible for sustaining stromal inflammation and CAF activation, offering an attractive therapeutic approach to enhance chemosensitivity in PDAC. Significance: Inhibition of p38 MAPK suppresses tumor cell-derived IL1α and attenuates the inflammatory stroma and immunosuppressive tumor microenvironment to overcome chemotherapeutic resistance in pancreatic cancer.
MeSH term(s)	Mice ; Animals ; Drug Resistance, Neoplasm/genetics ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/metabolism ; Cancer-Associated Fibroblasts/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism ; Inflammation/pathology ; Tumor Microenvironment
Chemical Substances	p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2024-01-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-23-1200
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Article ; Online: Remodeling of Stromal Immune Microenvironment by Urolithin A Improves Survival with Immune Checkpoint Blockade in Pancreatic Cancer.

Mehra, Siddharth / Garrido, Vanessa T / Dosch, Austin R / Lamichhane, Purushottam / Srinivasan, Supriya / Singh, Samara P / Zhou, Zhiqun / De Castro Silva, Iago / Joshi, Chandrashekar / Ban, Yuguang / Datta, Jashodeep / Gilboa, Eli / Merchant, Nipun B / Nagathihalli, Nagaraj S

Cancer research communications

2023 Volume 3, Issue 7, Page(s) 1224–1236

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is a significant contributor to cancer-related morbidity and mortality, and it is known for its resistance to conventional treatment regimens, including chemotherapy and immune checkpoint blockade (ICB)-based ... ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) is a significant contributor to cancer-related morbidity and mortality, and it is known for its resistance to conventional treatment regimens, including chemotherapy and immune checkpoint blockade (ICB)-based therapies. We have previously shown that Urolithin A (Uro A), a gut microbial metabolite derived from pomegranates, can target and inhibit Significance: Immunotherapeutic agents are ineffective against pancreatic cancer, mainly due to the immunosuppressive tumor microenvironment and stromal desmoplasia. Our current study demonstrates the therapeutic utility of a novel gut microbial metabolite, Uro A, to remodel the stromal-immune microenvironment and improve overall survival with anti-PD-1 therapy in pancreatic cancer.
MeSH term(s)	Mice ; Animals ; Immune Checkpoint Inhibitors/pharmacology ; CD8-Positive T-Lymphocytes/metabolism ; Phosphatidylinositol 3-Kinases/pharmacology ; Pancreatic Neoplasms/drug therapy ; Carcinoma, Pancreatic Ductal/drug therapy ; Tumor Microenvironment
Chemical Substances	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one (1143-70-0) ; Immune Checkpoint Inhibitors ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
Language	English
Publishing date	2023-07-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2767-9764
ISSN (online)	2767-9764
DOI	10.1158/2767-9764.CRC-22-0329
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Article: Emerging Role of CREB in Epithelial to Mesenchymal Plasticity of Pancreatic Cancer.

Mehra, Siddharth / Singh, Samara / Nagathihalli, Nagaraj

Frontiers in oncology

2022 Volume 12, Page(s) 925687

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is an aggressive solid malignancy with a high rate of metastasis and therapeutic resistance as its major hallmarks. Although a defining mutational event in pancreatic cancer initiation is the presence of ... ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) is an aggressive solid malignancy with a high rate of metastasis and therapeutic resistance as its major hallmarks. Although a defining mutational event in pancreatic cancer initiation is the presence of oncogenic
Language	English
Publishing date	2022-06-21
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2022.925687
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Article ; Online: Src-mediated regulation of E-cadherin and EMT in pancreatic cancer.

Nagathihalli, Nagaraj S / Merchant, Nipun B

Frontiers in bioscience (Landmark edition)

2012 Volume 17, Issue 6, Page(s) 2059–2069

Abstract: The Src family of non receptor tyrosine kinases are integrators of divergent signal transduction pathways which regulate numerous cellular processes, including tumorigenicity and angiogenesis. In pancreatic adenocarcinoma, c-Src (Src) is frequently ... ...

Abstract	The Src family of non receptor tyrosine kinases are integrators of divergent signal transduction pathways which regulate numerous cellular processes, including tumorigenicity and angiogenesis. In pancreatic adenocarcinoma, c-Src (Src) is frequently activated and results in increased tumor progression, invasion and metastasis. Dysfunction of the E-cadherin-mediated cell adhesion system plays an important role in tumor progression to invasive, metastatic carcinoma. Src has been shown to play a role in E-cadherin regulation and epithelial to mesenchymal transition (EMT). Increased Src activity promotes EMT while Src inhibition suppresses this process. Recent studies have focused on Src dependent regulation of E-cadherin and other tumor progression-related events such as EMT with the development of metastasis. Src has also been shown to be involved in chemoresistance of PDAC cells by promoting EMT. Although the molecular events associated with Src-dependent regulation of E-cadherin are becoming better defined, the cellular processes that trigger the onset of EMT remain unclear. Here we highlight recent work that advances our understanding of Src signaling as it relates to E-cadherin associated regulation and EMT in PDAC.
MeSH term(s)	Animals ; Cadherins/metabolism ; Carcinoma, Pancreatic Ductal/metabolism ; Carcinoma, Pancreatic Ductal/pathology ; Carcinoma, Pancreatic Ductal/therapy ; Epithelial-Mesenchymal Transition ; Humans ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/pathology ; Pancreatic Neoplasms/therapy ; Protein Kinase Inhibitors/therapeutic use ; Signal Transduction ; Transcription Factors/metabolism ; src-Family Kinases/antagonists & inhibitors ; src-Family Kinases/metabolism
Chemical Substances	Cadherins ; Protein Kinase Inhibitors ; Transcription Factors ; src-Family Kinases (EC 2.7.10.2)
Language	English
Publishing date	2012-06-01
Publishing country	Singapore
Document type	Journal Article ; Review
ZDB-ID	2704569-9
ISSN	2768-6698 ; 1093-9946
ISSN (online)	2768-6698
ISSN	1093-9946
DOI	10.2741/4037
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Article ; Online: Targeting Tumor-Stromal IL6/STAT3 Signaling through IL1 Receptor Inhibition in Pancreatic Cancer.

Dosch, Austin R / Singh, Samara / Dai, Xizi / Mehra, Siddharth / Silva, Iago De Castro / Bianchi, Anna / Srinivasan, Supriya / Gao, Zhen / Ban, Yuguang / Chen, Xi / Banerjee, Sulagna / Nagathihalli, Nagaraj S / Datta, Jashodeep / Merchant, Nipun B

Molecular cancer therapeutics

2021 Volume 20, Issue 11, Page(s) 2280–2290

Abstract: A hallmark of pancreatic ductal adenocarcinoma (PDAC) is the presence of a dense, desmoplastic stroma and the consequent altered interactions between cancer cells and their surrounding tumor microenvironment (TME) that promote disease progression, ... ...

Abstract	A hallmark of pancreatic ductal adenocarcinoma (PDAC) is the presence of a dense, desmoplastic stroma and the consequent altered interactions between cancer cells and their surrounding tumor microenvironment (TME) that promote disease progression, metastasis, and chemoresistance. We have previously shown that IL6 secreted from pancreatic stellate cells (PSC) stimulates the activation of STAT3 signaling in tumor cells, an established mechanism of therapeutic resistance in PDAC. We have now identified the tumor cell-derived cytokine IL1α as an upstream mediator of IL6 release from PSCs that is involved in STAT3 activation within the TME. Herein, we show that IL1α is overexpressed in both murine and human PDAC tumors and engages with its cognate receptor IL1R1, which is strongly expressed on stromal cells. Further, we show that IL1R1 inhibition using anakinra (recombinant IL1 receptor antagonist) significantly reduces stromal-derived IL6, thereby suppressing IL6-dependent STAT3 activation in human PDAC cell lines. Anakinra treatment results in significant reduction in IL6 and activated STAT3 levels in pancreatic tumors from
MeSH term(s)	Animals ; Humans ; Interleukin-6/metabolism ; Mice ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Receptors, Interleukin-1/antagonists & inhibitors ; Signal Transduction
Chemical Substances	Interleukin-6 ; Receptors, Interleukin-1
Language	English
Publishing date	2021-09-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-21-0083
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Article ; Online: Combined Blockade of MEK and CDK4/6 Pathways Induces Senescence to Improve Survival in Pancreatic Ductal Adenocarcinoma.

Willobee, Brent A / Gaidarski, Alexander A / Dosch, Austin R / Castellanos, Jason A / Dai, Xizi / Mehra, Siddharth / Messaggio, Fanuel / Srinivasan, Supriya / VanSaun, Michael N / Nagathihalli, Nagaraj S / Merchant, Nipun B

Molecular cancer therapeutics

2021 Volume 20, Issue 7, Page(s) 1246–1256

Abstract: ... ...

Abstract	Activating
MeSH term(s)	Animals ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/metabolism ; Carcinoma, Pancreatic Ductal/pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Cellular Senescence/drug effects ; Cyclin-Dependent Kinase 4/antagonists & inhibitors ; Cyclin-Dependent Kinase 4/metabolism ; Cyclin-Dependent Kinase 6/antagonists & inhibitors ; Cyclin-Dependent Kinase 6/metabolism ; Disease Models, Animal ; Drug Synergism ; Gene Expression Regulation, Neoplastic ; Genes, p16 ; Humans ; Mice ; Mice, Knockout ; Mice, Transgenic ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Signal Transduction/drug effects ; Xenograft Model Antitumor Assays
Chemical Substances	Protein Kinase Inhibitors ; CDK4 protein, human (EC 2.7.11.22) ; CDK6 protein, human (EC 2.7.11.22) ; Cyclin-Dependent Kinase 4 (EC 2.7.11.22) ; Cyclin-Dependent Kinase 6 (EC 2.7.11.22) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2)
Language	English
Publishing date	2021-05-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-19-1043
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Article ; Online: Combined MEK and STAT3 Inhibition Uncovers Stromal Plasticity by Enriching for Cancer-Associated Fibroblasts With Mesenchymal Stem Cell-Like Features to Overcome Immunotherapy Resistance in Pancreatic Cancer.

Datta, Jashodeep / Dai, Xizi / Bianchi, Anna / De Castro Silva, Iago / Mehra, Siddharth / Garrido, Vanessa T / Lamichhane, Purushottam / Singh, Samara P / Zhou, Zhiqun / Dosch, Austin R / Messaggio, Fanuel / Ban, Yuguang / Umland, Oliver / Hosein, Peter J / Nagathihalli, Nagaraj S / Merchant, Nipun B

Gastroenterology

2022 Volume 163, Issue 6, Page(s) 1593–1612

Abstract: Background & aims: We have shown that reciprocally activated rat sarcoma (RAS)/mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK) and Janus kinase/signal transducer and activator of transcription 3 (STAT3) pathways mediate ... ...

Abstract	Background & aims: We have shown that reciprocally activated rat sarcoma (RAS)/mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK) and Janus kinase/signal transducer and activator of transcription 3 (STAT3) pathways mediate therapeutic resistance in pancreatic ductal adenocarcinoma (PDAC), while combined MEK and STAT3 inhibition (MEKi+STAT3i) overcomes such resistance and alters stromal architecture. We now determine whether MEKi+STAT3i reprograms the cancer-associated fibroblast (CAF) and immune microenvironment to overcome resistance to immune checkpoint inhibition in PDAC. Methods: CAF and immune cell transcriptomes in MEKi (trametinib)+STAT3i (ruxolitinib)-treated vs vehicle-treated Ptf1a Results: MEKi+STAT3i attenuates Il6/Cxcl1-expressing proinflammatory and Lrrc15-expressing myofibroblastic CAF phenotypes while enriching for Ly6a/Cd34-expressing CAFs exhibiting mesenchymal stem cell-like features via scRNAseq in PKT mice. This CAF plasticity is associated with M2-to-M1 reprogramming of tumor-associated macrophages, and enhanced trafficking of cluster of differentiation 8 Conclusions: Combined MEKi+STAT3i mitigates stromal inflammation and enriches for CAF phenotypes with mesenchymal stem cell-like properties to overcome immunotherapy resistance in PDAC.
MeSH term(s)	Mice ; Animals ; Cancer-Associated Fibroblasts ; STAT3 Transcription Factor/genetics ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Immunotherapy ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/genetics ; Immunologic Factors ; Mesenchymal Stem Cells ; Adenocarcinoma ; Immune Checkpoint Inhibitors/pharmacology ; Immune Checkpoint Inhibitors/therapeutic use ; Tumor Microenvironment ; Pancreatic Neoplasms
Chemical Substances	ruxolitinib (82S8X8XX8H) ; STAT3 Transcription Factor ; Immunologic Factors ; Immune Checkpoint Inhibitors
Language	English
Publishing date	2022-08-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2022.07.076
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Article ; Online: Evolving 'omics' technologies for diagnostics of head and neck cancer.

Nagaraj, Nagathihalli S

Briefings in functional genomics & proteomics

2009 Volume 8, Issue 1, Page(s) 49–59

Abstract: Squamous cell carcinoma of head and neck (SCCHN) is the sixth most common malignancy and is a major cause of cancer morbidity and mortality worldwide. As with most solid cancers, the cure rate for SCCHN is excellent if tumors are diagnosed early in the ... ...

Abstract	Squamous cell carcinoma of head and neck (SCCHN) is the sixth most common malignancy and is a major cause of cancer morbidity and mortality worldwide. As with most solid cancers, the cure rate for SCCHN is excellent if tumors are diagnosed early in the course of the disease. Early diagnosis of cancer remains difficult because of the lack of specific symptoms in early disease as well as the limited understanding of etiology and oncogenesis. Advances in proteomics and genomics contribute to the understanding of the pathophysiology of neoplasia, cancer diagnosis and anticancer drug discovery. The powerful 'omics' technologies have opened new avenues towards biomarker discovery, identification of signaling molecules associated with cell growth, cell death, cellular metabolism and early detection of cancer. Analysis of tumor-specific omics profiles provided a unique opportunity to diagnose, classify, and detect malignant disease; to better understand and define the behavior of specific tumors; and to provide direct and targeted therapy. These technologies however still require integration and standardization of techniques and validation against accepted clinical and pathologic parameters. This article provides a summary of technologies, potential clinical applications, and challenges of omics in head and neck cancer.
MeSH term(s)	Biomarkers, Tumor ; Carcinoma, Squamous Cell/diagnosis ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/metabolism ; Computational Biology/methods ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genomics/methods ; Head and Neck Neoplasms/diagnosis ; Head and Neck Neoplasms/genetics ; Head and Neck Neoplasms/metabolism ; Humans ; Medical Oncology/methods ; Metabolomics/methods ; Models, Biological ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Prognosis ; Proteomics/methods ; Signal Transduction
Chemical Substances	Biomarkers, Tumor ; Neoplasm Proteins
Language	English
Publishing date	2009-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2138368-6
ISSN	1477-4062 ; 1473-9550
ISSN (online)	1477-4062
ISSN	1473-9550
DOI	10.1093/bfgp/elp004
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