Back to Search
Start Over
Apoptosis and melanoma chemoresistance.
- Source :
-
Oncogene [Oncogene] 2003 May 19; Vol. 22 (20), pp. 3138-51. - Publication Year :
- 2003
-
Abstract
- Melanoma is the most aggressive form of skin cancer and is notoriously resistant to all current modalities of cancer therapy. A large set of genetic, functional and biochemical studies suggest that melanoma cells become 'bullet proof' against a variety of chemotherapeutic drugs by exploiting their intrinsic resistance to apoptosis and by reprogramming their proliferation and survival pathways during melanoma progression. In recent years, the identification of molecules involved in the regulation and execution of apoptosis, and their alteration in melanoma, have provided new insights into the molecular basis for melanoma chemoresistance. With this knowledge in hand, the challenge is now to devise strategies potent enough to compensate or bypass these cell death defects and improve the actual poor prognosis of patients at late stages of the disease.
- Subjects :
- Animals
Antineoplastic Agents pharmacology
Apoptosis drug effects
Apoptotic Protease-Activating Factor 1
Caspase 9
Caspases drug effects
Caspases metabolism
Cell Survival drug effects
Cell Survival physiology
Disease Progression
Humans
Inhibitor of Apoptosis Proteins
Melanocytes drug effects
Microtubule-Associated Proteins drug effects
Microtubule-Associated Proteins metabolism
Mitochondria drug effects
Mitochondria metabolism
NF-kappa B drug effects
NF-kappa B metabolism
Neoplasm Proteins
PTEN Phosphohydrolase
Phosphoric Monoester Hydrolases metabolism
Proteins drug effects
Proteins metabolism
Proto-Oncogene Proteins c-bcl-2 drug effects
Proto-Oncogene Proteins c-bcl-2 metabolism
Signal Transduction
Survivin
Tumor Suppressor Protein p14ARF drug effects
Tumor Suppressor Protein p14ARF metabolism
Tumor Suppressor Proteins metabolism
Apoptosis physiology
Drug Resistance, Neoplasm physiology
Melanoma drug therapy
Melanoma pathology
Skin Neoplasms drug therapy
Skin Neoplasms pathology
Subjects
Details
- Language :
- English
- ISSN :
- 0950-9232
- Volume :
- 22
- Issue :
- 20
- Database :
- MEDLINE
- Journal :
- Oncogene
- Publication Type :
- Academic Journal
- Accession number :
- 12789290
- Full Text :
- https://doi.org/10.1038/sj.onc.1206454