Objectives: Recently, hyperactivation of the Wnt signaling pathway has been implicated in leukomogenesis, so we studied the epigenetic dysfunction of SFRP1,2 and expression of interleukin2 receptor α chain (IL2Rα, also known as CD25) and its prognostic impact in acute myeloblastic leukemia (AML). Methods: We studied the methylation profile of SFRP1,2 in AML cells by methylation-specific polymerase chain reaction (MSP) and the hyper expression of IL2Rα (CD25) by flowcytometry. Results: We analyzed the methylation profile of SFRP1,2 in 40 de novo AML patients. The percentage of hypermethylation in the patient samples were 37.5% for SFRP1, 12.5% for SFRP2. CD25 was positive in 12(30%) of 40 patients AML. We found that in patients whom 60 years and younger with intermediate risk cytogenetics in de novo AML, hypermethylation of SFRP1 and CD25 were accompanied with relapse (P=0.024). Conclusion: Our data indicates that in a subgroup of AML patients, hypermethylation of SFRP1 and high expression of CD25 predict relapse.

Objectives: As we noted that CD30 is a valuable molecule in regulation of growth and death of lymphocytes in malignant lymphomas, we decided to analyze CD30 expression and serum soluble CD30 (sCD30) molecule level in patients with acute lymphocytic leukemia (ALL) to assess their role as a prognostic markers and to examine the possibility of anti-CD30 to be a targeted therapy in these patients. Methods: We studied CD30 expression by Multicolor flow cytometry immunophenotypic analysis on bone marrow aspirates of 90 ALL patients(51 T-ALL and 39 B-ALL). Serum sCD30 level was measured by Enzyme Linked Immunosrbent Assay(ELSA). We correlate CD30 and sCD30 values with all of white blood cell counts, Hemoglobin, platelets, bone marrow blasts and cytogenetics. Results: Our study conducted on 90 ALL patients. The 90 ALL patients included 51 patients with T-ALL and 39 with B-ALL. Of the 51 T-ALL patients, 29 (56.8%) were males and 22 (43.2%) were females. Mean age was 42.4±19.1 years old (10-78 years), and of 39 B-ALL patients, 23(59%) were males and 16 (41%) were females. Mean age was 44.4±18.6 years old (9-70 years). In T-ALL, 33.3% ( 17 out of 51 patients) have high CD30-expression and 27.4℅ (14 out of 51 patients) have elevated serum sCD30.We found that there was a significant correlation between both CD30 expression and sCD30 level with WBCs count, BM blasts, Adverse risk cytogenetics, BCR/ABL and with relapse for CD30 expression, complete remission failure with elevated serum sCD30 level. While in B-ALL, CD30 expression (>20%) was detected in 20.5% ( 8 out of 39 patients) and elevated sCD30 was detected in 15.4℅ (6 out of 39 patients). However, we did not found significant relation between both CD30 expression and sCD30 level and BCR/ABL, relapse and failure of treatment. Conclusions: CD30 is expressed by lymphoblasts in ALL patients. We found that high CD30 expression and elevated sCD30 level can be used as prognostic markers for relapse and complete remission failure respectively in only T-ALL subtype not in B-ALL subtybe. Furthermore, These patients with adverse risk cytogenetics have not too many treatment options, so the use anti-CD30 targeted therapy may be a possible alternative for this patient group.

Objectives: As we noted that CD30 is a valuable molecule in regulation of growth and death of lymphocytes in malignant lymphomas, we decided to analyze CD30 expression and serum soluble CD30 (sCD30) molecule level in patients with acute lymphocytic leukemia (ALL) to assess their role as a prognostic markers and to examine the possibility of anti-CD30 to be a targeted therapy in these patients. Methods: We studied CD30 expression by Multicolor flow cytometry immunophenotypic analysis on bone marrow aspirates of 90 ALL patients(51 T-ALL and 39 B-ALL). Serum sCD30 level was measured by Enzyme Linked Immunosrbent Assay(ELSA). We correlate CD30 and sCD30 values with all of white blood cell counts, Hemoglobin, platelets, bone marrow blasts and cytogenetics. Results: Our study conducted on 90 ALL patients. The 90 ALL patients included 51 patients with T-ALL and 39 with B-ALL. Of the 51 T-ALL patients, 29 (56.8%) were males and 22 (43.2%) were females. Mean age was 42.4±19.1 years old (10-78 years), and of 39 B-ALL patients, 23(59%) were males and 16 (41%) were females. Mean age was 44.4±18.6 years old (9-70 years). In T-ALL, 33.3% ( 17 out of 51 patients) have high CD30-expression and 27.4℅ (14 out of 51 patients) have elevated serum sCD30.We found that there was a significant correlation between both CD30 expression and sCD30 level with WBCs count, BM blasts, Adverse risk cytogenetics, BCR/ABL and with relapse for CD30 expression, complete remission failure with elevated serum sCD30 level. While in B-ALL, CD30 expression (>20%) was detected in 20.5% ( 8 out of 39 patients) and elevated sCD30 was detected in 15.4℅ (6 out of 39 patients). However, we did not found significant relation between both CD30 expression and sCD30 level and BCR/ABL, relapse and failure of treatment. Conclusions: CD30 is expressed by lymphoblasts in ALL patients. We found that high CD30 expression and elevated sCD30 level can be used as prognostic markers for relapse and complete remission failure respectively in only T-ALL subtype not in B-ALL subtybe. Furthermore, These patients with adverse risk cytogenetics have not too many treatment options, so the use anti-CD30 targeted therapy may be a possible alternative for this patient group.

Objectives: As we noted that CD30 is a valuable molecule in regulation of growth and death of lymphocytes in malignant lymphomas, we decided to analyze CD30 expression and serum soluble CD30 (sCD30) molecule level in patients with acute lymphocytic leukemia (ALL) to assess their role as a prognostic markers and to examine the possibility of anti-CD30 to be a targeted therapy in these patients. Methods: We studied CD30 expression by Multicolor flow cytometry immunophenotypic analysis on bone marrow aspirates of 90 ALL patients(51 T-ALL and 39 B-ALL). Serum sCD30 level was measured by Enzyme Linked Immunosrbent Assay(ELSA). We correlate CD30 and sCD30 values with all of white blood cell counts, Hemoglobin, platelets, bone marrow blasts and cytogenetics. Results: Our study conducted on 90 ALL patients. The 90 ALL patients included 51 patients with T-ALL and 39 with B-ALL. Of the 51 T-ALL patients, 29 (56.8%) were males and 22 (43.2%) were females. Mean age was 42.4±19.1 years old (10-78 years), and of 39 B-ALL patients, 23(59%) were males and 16 (41%) were females. Mean age was 44.4±18.6 years old (9-70 years). In T-ALL, 33.3% ( 17 out of 51 patients) have high CD30-expression and 27.4℅ (14 out of 51 patients) have elevated serum sCD30.We found that there was a significant correlation between both CD30 expression and sCD30 level with WBCs count, BM blasts, Adverse risk cytogenetics, BCR/ABL and with relapse for CD30 expression, complete remission failure with elevated serum sCD30 level. While in B-ALL, CD30 expression (>20%) was detected in 20.5% ( 8 out of 39 patients) and elevated sCD30 was detected in 15.4℅ (6 out of 39 patients). However, we did not found significant relation between both CD30 expression and sCD30 level and BCR/ABL, relapse and failure of treatment. Conclusions: CD30 is expressed by lymphoblasts in ALL patients. We found that high CD30 expression and elevated sCD30 level can be used as prognostic markers for relapse and complete remission failure respectively in only T-ALL subtype not in B-ALL subtybe. Furthermore, These patients with adverse risk cytogenetics have not too many treatment options, so the use anti-CD30 targeted therapy may be a possible alternative for this patient group.

Objectives: As we noted that CD30 is a valuable molecule in regulation of growth and death of lymphocytes in malignant lymphomas, we analyzed CD30 expression and serum soluble CD30 (sCD30) molecule level in patients with acute myeloid leukemia (AML) to assess their role as a prognostic markers and to examine the possibility of anti-CD30 to be a targeted therapy in these patients. Methods: We studied CD30 expression by Multicolor flow cytometry immunophenotypic analysis on bone marrow aspirates of 50 AML patients. Serum sCD30 level was measured by Enzyme Linked Immunosrbent Assay (ELSA). We correlate CD30 and sCD30 values with all of white blood cell counts, Hemoglobin, platelets, bone marrow blasts and cytogenetics. The Fisher’s exact test or chi-square was used for comparison of categorical variables and the ttest or one-way analysis of variance (ANOVA) was applied for numerical comparisons using SPSS version 20. A p value of 0.05 was considered to be statistically significant. Results: Our study conducted on 50 AML patients, the mean patients’ age was 47.4 ± 18.1 years (range, 17-77), 11 (22%) were males and 39 (78%) were females. 16 (32%) patients have high CD30-expression and 11 (22%) have elevated serum sCD30. We found that there was a significant correlation between both CD30 expression and sCD30 level with WBCs count, BM blasts, Adverse risk cytogenetics, FLT3/ITD and with relapse for CD30 expression, complete remission failure with elevated serum sCD30 level. Conclusions: CD30 is expressed by myeloblasts in AML patients. We found that high CD30 expression and elevated sCD30 level can be used as prognostic markers for relapse and complete remission failure respectively. Furthermore, these patients with adverse risk cytogenetics have not too many treatment options, so the use antiCD30 targeted therapy may be a possible alternative for this patient group which need further studies.

Objectives: As we noted that CD30 is a valuable molecule in regulation of growth and death of lymphocytes in malignant lymphomas, we analyzed CD30 expression and serum soluble CD30 (sCD30) molecule level in patients with acute myeloid leukemia (AML) to assess their role as a prognostic markers and to examine the possibility of anti-CD30 to be a targeted therapy in these patients. Methods: We studied CD30 expression by Multicolor flow cytometry immunophenotypic analysis on bone marrow aspirates of 50 AML patients. Serum sCD30 level was measured by Enzyme Linked Immunosrbent Assay (ELSA). We correlate CD30 and sCD30 values with all of white blood cell counts, Hemoglobin, platelets, bone marrow blasts and cytogenetics. The Fisher’s exact test or chi-square was used for comparison of categorical variables and the ttest or one-way analysis of variance (ANOVA) was applied for numerical comparisons using SPSS version 20. A p value of 0.05 was considered to be statistically significant. Results: Our study conducted on 50 AML patients, the mean patients’ age was 47.4 ± 18.1 years (range, 17-77), 11 (22%) were males and 39 (78%) were females. 16 (32%) patients have high CD30-expression and 11 (22%) have elevated serum sCD30. We found that there was a significant correlation between both CD30 expression and sCD30 level with WBCs count, BM blasts, Adverse risk cytogenetics, FLT3/ITD and with relapse for CD30 expression, complete remission failure with elevated serum sCD30 level. Conclusions: CD30 is expressed by myeloblasts in AML patients. We found that high CD30 expression and elevated sCD30 level can be used as prognostic markers for relapse and complete remission failure respectively. Furthermore, these patients with adverse risk cytogenetics have not too many treatment options, so the use antiCD30 targeted therapy may be a possible alternative for this patient group which need further studies.

Objectives: As we noted that CD30 is a valuable molecule in regulation of growth and death of lymphocytes in malignant lymphomas, we analyzed CD30 expression and serum soluble CD30 (sCD30) molecule level in patients with acute myeloid leukemia (AML) to assess their role as a prognostic markers and to examine the possibility of anti-CD30 to be a targeted therapy in these patients. Methods: We studied CD30 expression by Multicolor flow cytometry immunophenotypic analysis on bone marrow aspirates of 50 AML patients. Serum sCD30 level was measured by Enzyme Linked Immunosrbent Assay (ELSA). We correlate CD30 and sCD30 values with all of white blood cell counts, Hemoglobin, platelets, bone marrow blasts and cytogenetics. The Fisher’s exact test or chi-square was used for comparison of categorical variables and the ttest or one-way analysis of variance (ANOVA) was applied for numerical comparisons using SPSS version 20. A p value of 0.05 was considered to be statistically significant. Results: Our study conducted on 50 AML patients, the mean patients’ age was 47.4 ± 18.1 years (range, 17-77), 11 (22%) were males and 39 (78%) were females. 16 (32%) patients have high CD30-expression and 11 (22%) have elevated serum sCD30. We found that there was a significant correlation between both CD30 expression and sCD30 level with WBCs count, BM blasts, Adverse risk cytogenetics, FLT3/ITD and with relapse for CD30 expression, complete remission failure with elevated serum sCD30 level. Conclusions: CD30 is expressed by myeloblasts in AML patients. We found that high CD30 expression and elevated sCD30 level can be used as prognostic markers for relapse and complete remission failure respectively. Furthermore, these patients with adverse risk cytogenetics have not too many treatment options, so the use antiCD30 targeted therapy may be a possible alternative for this patient group which need further studies.

The biological mechanism underlying cryosurgical treatment of keloids remains unclear. Transforming growth factor-beta1 (TGF-β1) has been implicated in the pathogenesis of keloids and was reported to be the target of several therapeutic modalities. However, the effect of cryosurgery on its expression in keloid tissue has not been yet investigated. In this study, 26 consecutive keloid patients were treated with cryosurgery for 2–6 sessions. Keloids were biopsied before starting cryosurgery and after two treatment sessions for the immunohistochemical evaluation of TGF-β1 expression. The average volume reduction, after two treatment sessions (in 22 patients completing the study) was 68.77 ± 15.82%. Dermal overexpression of TGF-β1 was demonstrated in all keloid specimens before treatment. Following therapy, significant reduction of that expression was detected in all keloid specimens (P = 0.016). In addition to attesting the clinical efficacy of cryosurgery, our findings indicate that cryosurgery effectively suppressed TGF-β1 expression, possibly contributing to keloid regression.

The biological mechanism underlying cryosurgical treatment of keloids remains unclear. Transforming growth factor-beta1 (TGF-β1) has been implicated in the pathogenesis of keloids and was reported to be the target of several therapeutic modalities. However, the effect of cryosurgery on its expression in keloid tissue has not been yet investigated. In this study, 26 consecutive keloid patients were treated with cryosurgery for 2–6 sessions. Keloids were biopsied before starting cryosurgery and after two treatment sessions for the immunohistochemical evaluation of TGF-β1 expression. The average volume reduction, after two treatment sessions (in 22 patients completing the study) was 68.77 ± 15.82%. Dermal overexpression of TGF-β1 was demonstrated in all keloid specimens before treatment. Following therapy, significant reduction of that expression was detected in all keloid specimens (P = 0.016). In addition to attesting the clinical efficacy of cryosurgery, our findings indicate that cryosurgery effectively suppressed TGF-β1 expression, possibly contributing to keloid regression.

The biological mechanism underlying cryosurgical treatment of keloids remains unclear. Transforming growth factor-beta1 (TGF-β1) has been implicated in the pathogenesis of keloids and was reported to be the target of several therapeutic modalities. However, the effect of cryosurgery on its expression in keloid tissue has not been yet investigated. In this study, 26 consecutive keloid patients were treated with cryosurgery for 2–6 sessions. Keloids were biopsied before starting cryosurgery and after two treatment sessions for the immunohistochemical evaluation of TGF-β1 expression. The average volume reduction, after two treatment sessions (in 22 patients completing the study) was 68.77 ± 15.82%. Dermal overexpression of TGF-β1 was demonstrated in all keloid specimens before treatment. Following therapy, significant reduction of that expression was detected in all keloid specimens (P = 0.016). In addition to attesting the clinical efficacy of cryosurgery, our findings indicate that cryosurgery effectively suppressed TGF-β1 expression, possibly contributing to keloid regression.