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Targeting ER-Golgi Homeostasis in an Advantageous Therapeutic Strategy in Lung Cancer

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Clalit Health Services

Status

Unknown

Conditions

The Combined Effect of Hsp90 Inhibitor and HDAC/Proteasome Inhibitors on Lung Cancer Cell Fate and ER-Golgi Homeostasis Will be Examined.

Study type

Observational

Funder types

Other

Identifiers

NCT01270399
MMC10160-2010CTIL

Details and patient eligibility

About

Lung cancer remains the most common cause of cancer-related death in the world. The major advances in treatment of lung cancer have brought only minor improvements in survival therefore novel systemic treatment methods are urgently needed.

Protein levels are regulated by the protein homeostasis network that generates and protects the protein fold (ER and Golgi included).

The heat shock protein 90 (Hsp90) is an essential molecular chaperon involved in the posttranslational folding and stability of proteins. Hsp90 inhibition leads to accumulation of unfolded proteins and ER stress. The therapeutic efficacy of such inhibition may be augmented by co-administering it with other drugs that disrupt ER-Golgi homeostasis like histone deacetylase (HDAC) or proteasome inhibitors. ER-Golgi homeostasis disruption affects a wide network of proteins and pathways as such affords a systemic target. Thus, the investigators aimed to examine the effect of combined treatment of Hsp90 antagonist with proteasome or HDAC inhibitors on human lung cancer cell lines and primary cells.

Enrollment

20 estimated patients

Sex

All

Ages

18+ years old

Volunteers

No Healthy Volunteers

Inclusion criteria

  • PATIENTS WITH PROVED DIAGNOSIS OF LUNG CARCINOMA THAT ARE CANDIDATS FOR RADICAL SURGICAL TREATMENT

Exclusion criteria

  • PATIENTS WITH SUSPICION FOR LUNG CARCINOMA WITHOUT PATHOLOGYCAL DIAFNOSIS BEFORE SURGERY

Trial design

20 participants in 2 patient groups

malignant neoplasm's cells
natural cells

Trial contacts and locations

1

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Data sourced from clinicaltrials.gov

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