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Literature DB >> 21986108

Targeting heat shock response pathways to treat pancreatic cancer.

Yi Xia¹, Palma Rocchi, Juan L Iovanna, Ling Peng.

Abstract

Pancreatic cancer belongs to the group of extremely aggressive human cancers; conventional cancer treatments have little impact. Increasing understanding of the pathways associated with pancreatic cancer progression has enabled the development of targeted therapy on this cancer. Heat shock proteins (HSPs) and related heat shock response (HSR) pathways control multiple important oncogenic pathways for pancreatic cancer development. Consequently, they represent promising novel targets for pancreatic cancer therapy. Various strategies have been proposed and elaborated to target HSPs/HSR in pancreatic cancer with the corresponding modulators, the details of which are highlighted in this review.

Entities: Disease Species

Mesh：

Year: 2011 PMID： 21986108 DOI： 10.1016/j.drudis.2011.09.016

Source DB: PubMed Journal: Drug Discov Today ISSN： 1359-6446 Impact factor: 7.851

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Cited

11 in total

1. A comparison of cell survival and heat shock protein expression after radiation in normal dermal fibroblasts, microvascular endothelial cells, and different head and neck squamous carcinoma cell lines.

Authors: Dominique Muschter; Fabian Geyer; Richard Bauer; Tobias Ettl; Stephan Schreml; Frank Haubner
Journal: Clin Oral Investig Date: 2018-01-06 Impact factor: 3.573

Review 2. Radiosensitizers in pancreatic cancer--preclinical and clinical exploits with molecularly targeted agents.

Authors: Amanda J Walker; Sara R Alcorn; Amol K Narang; Katriana M Nugent; Aaron T Wild; Joseph M Herman; Phuoc T Tran
Journal: Curr Probl Cancer Date: 2013-10-05 Impact factor: 3.187

3. Novel role of VMP1 as modifier of the pancreatic tumor cell response to chemotherapeutic drugs.

Authors: Marine Gilabert; Maria Inés Vaccaro; Martin E Fernandez-Zapico; Ezequiel L Calvo; Olivier Turrini; Véronique Secq; Stéphane Garcia; Vincent Moutardier; Gwen Lomberk; Nelson Dusetti; Raul Urrutia; Juan L Iovanna
Journal: J Cell Physiol Date: 2013-09 Impact factor: 6.384

4. A network-based approach for predicting Hsp27 knock-out targets in mouse skeletal muscles.

Authors: Malek Kammoun; Brigitte Picard; Joëlle Henry-Berger; Isabelle Cassar-Malek
Journal: Comput Struct Biotechnol J Date: 2013-08-14 Impact factor: 7.271

5. Curaxin CBL0137 eradicates drug resistant cancer stem cells and potentiates efficacy of gemcitabine in preclinical models of pancreatic cancer.

Authors: Catherine Burkhart; Daria Fleyshman; Rachael Kohrn; Mairead Commane; Jennifer Garrigan; Vadim Kurbatov; Ilya Toshkov; Rajesh Ramachandran; Laura Martello; Katerina V Gurova
Journal: Oncotarget Date: 2014-11-30

Review 6. Small Molecule Inhibitors to Disrupt Protein-protein Interactions of Heat Shock Protein 90 Chaperone Machinery.

Authors: Young Ho Seo
Journal: J Cancer Prev Date: 2015-03

Targeting heat shock response pathways to treat pancreatic cancer.

1. A comparison of cell survival and heat shock protein expression after radiation in normal dermal fibroblasts, microvascular endothelial cells, and different head and neck squamous carcinoma cell lines.

Review 2. Radiosensitizers in pancreatic cancer--preclinical and clinical exploits with molecularly targeted agents.

3. Novel role of VMP1 as modifier of the pancreatic tumor cell response to chemotherapeutic drugs.

4. A network-based approach for predicting Hsp27 knock-out targets in mouse skeletal muscles.

5. Curaxin CBL0137 eradicates drug resistant cancer stem cells and potentiates efficacy of gemcitabine in preclinical models of pancreatic cancer.

Review 6. Small Molecule Inhibitors to Disrupt Protein-protein Interactions of Heat Shock Protein 90 Chaperone Machinery.

Review 7. Targeting Heat Shock Proteins in Cancer: A Promising Therapeutic Approach.

8. Synergistic activity of Hsp90 inhibitors and anticancer agents in pancreatic cancer cell cultures.

Review 9. AlphaB-crystallin and breast cancer: role and possible therapeutic strategies.

10. New HSP27 inhibitors efficiently suppress drug resistance development in cancer cells.