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GST-pi and P-170 co-expression in multiple myeloma
M Petrini1, D Di Simone, A Favati
1Department of Haematology, University of Pisa, Italy.
British Journal of Haematology
|June 1, 1995
Summary
Multiple myeloma plasma cells frequently express P-glycoprotein (P-170) and glutathione-S-transferase pi (GST-pi), indicating drug resistance mechanisms. Therapy may increase expression of these markers.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- Multiple myeloma is a plasma cell malignancy.
- Drug resistance is a major challenge in multiple myeloma treatment.
- Mechanisms of drug resistance, including P-glycoprotein (P-170) and glutathione-S-transferase pi (GST-pi) expression, are not fully understood in this context.
Purpose of the Study:
- To investigate the expression of P-glycoprotein (P-170), glutathione-S-transferase pi (GST-pi), and p-21 in plasma cells of multiple myeloma patients.
- To determine the correlation of these markers with clinical and prognostic parameters.
- To assess changes in marker expression before and after therapy.
Main Methods:
- Immunocytochemical detection was used to analyze bone marrow plasma cells from 40 multiple myeloma patients.
- Expression levels of P-170, GST-pi, and p-21 were quantified.
- Patients were categorized as treated or untreated, and samples were analyzed pre- and post-therapy.
Main Results:
- P-170 and GST-pi were expressed in a high percentage of samples (72% and 82%, respectively), irrespective of clinical or prognostic factors.
- A significant positive correlation and co-expression (91%) were observed between GST-pi and P-170.
- Expression of both markers increased after therapy, while p-21 expression showed no association with these resistance mechanisms.
Conclusions:
- Multiple myeloma exhibits diverse drug resistance mechanisms involving P-170 and GST-pi.
- These resistance markers are present in both treated and untreated patients and can be upregulated by therapy.
- Further research is needed to elucidate the role of p-21 and other factors in myeloma drug resistance.