Abstract
Background: The objective of our research was to clarify the role of genetic polymorphisms in GST (T1 and M1) in the development of Ph-ve CML.
Materials and methods: We report on a case-control study, with 126 participants, divided into 26 patients with Ph-ve CML (57.7% male, 42.3% female) and 100 healthy volunteers (51% male, 49% female) with no medical history of cancer as a control population. All Ph-ve CML patients were diagnosed according to standard hematologic and cytogenetic criteria based on CBC, confirmed by Reverse Transcriptase Polymerase Chain Reaction (RT-PCR) to determine the presence or absence of the BCR-ABL gene, followed by bone marrow (BM) examination.
Results: Of the 26 studied cases, 50% had the GSTT1 null genotype against 21% of the control group, a statistically significant difference (CI= 1.519 - 9.317; p-value= 0.004). The GSTM1 null genotype was detected in 23.1% of cases and 35% of controls, a difference not statistically significant (OR= 0.557; CI= 0.205-1.515; p-value= 0.252). Distribution of GSTT1 and GSTM1 polymorphisms was also examined according to gender, age and ethnic grouping, these findings revealing no statistically significant differences.
Conclusion: Our study reveals a strong correlation between GSTT1 polymorphism and Ph-ve CML, whereas the data for GSTM1 polymorphisms indicates no role in the initial development of the disease. More studies are required to further clarify the roles that these and other genes may play in disease development.
Materials and methods: We report on a case-control study, with 126 participants, divided into 26 patients with Ph-ve CML (57.7% male, 42.3% female) and 100 healthy volunteers (51% male, 49% female) with no medical history of cancer as a control population. All Ph-ve CML patients were diagnosed according to standard hematologic and cytogenetic criteria based on CBC, confirmed by Reverse Transcriptase Polymerase Chain Reaction (RT-PCR) to determine the presence or absence of the BCR-ABL gene, followed by bone marrow (BM) examination.
Results: Of the 26 studied cases, 50% had the GSTT1 null genotype against 21% of the control group, a statistically significant difference (CI= 1.519 - 9.317; p-value= 0.004). The GSTM1 null genotype was detected in 23.1% of cases and 35% of controls, a difference not statistically significant (OR= 0.557; CI= 0.205-1.515; p-value= 0.252). Distribution of GSTT1 and GSTM1 polymorphisms was also examined according to gender, age and ethnic grouping, these findings revealing no statistically significant differences.
Conclusion: Our study reveals a strong correlation between GSTT1 polymorphism and Ph-ve CML, whereas the data for GSTM1 polymorphisms indicates no role in the initial development of the disease. More studies are required to further clarify the roles that these and other genes may play in disease development.
| Original language | English |
|---|---|
| Pages (from-to) | 319-324 |
| Journal | Current Cancer Drug Targets |
| Volume | 23 |
| Issue number | 4 |
| Early online date | 27 Oct 2022 |
| DOIs | |
| Publication status | Published - 21 Nov 2022 |
Keywords
- GSTT1
- GSTM1
- CML
- Philadelphia Negative and Sudan
