105 research outputs found
Amifostine can differentially modulate DNA double-strand breaks and apoptosis induced by idarubicin in normal and cancer cells
We have previously shown that amifostine differentially modulated the DNA-damaging action of idarubicin in normal and cancer cells and that the presence of p53 protein and oncogenic tyrosine kinases might play a role in this diversity. Aim: To investigate further this effect we have studied the influence of amifostine on idarubicin-induced DNA double-strand breaks (DSBs) and apoptosis. Methods: We employed pulse-field gel electrophoresis () for the detection of DSBs and assessment of their repair in human normal lymphocytes and chronic myelogenous leukaemia K562 cells lacking p53 activity and expressing the BCR/ABL tyrosine kinase. Apoptosis was evaluated by caspase-3 activity assay assisted by the alkaline comet assay and DAPI staining. Results: Idarubicin induced DSBs in a dose-independent manner in normal and cancer cells. Both types of the cells did not repair these lesions in 120 min and amifostine differentially modulated their level β decreased it in the lymphocytes and increased in K562 cells. In contrast to control cells, amifostine potentated apoptotic DNA fragmentation, chromatin condensation and the activity of caspase-3 in leukaemia cells. Conclusion: Amifostine can differentially modulate DSBs and apoptosis induced by idarubicin in normal and cancer cells. It can protect normal cells against drug-induced DNA damage and it can potentate the action of the drug in leukaemic cells. Further studies on link between amifostine-induced modulation of DSBs and apoptosis of cancer cells will bring a deeper insight into molecular mechanism of amifostine action.Π Π°Π½Π΅Π΅ Π½Π°ΠΌΠΈ Π±ΡΠ»ΠΎ ΠΏΠΎΠΊΠ°Π·Π°Π½ΠΎ, ΡΡΠΎ Π°ΠΌΠΈΡΠΎΡΡΠΈΠ½ Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΠ°Π»ΡΠ½ΠΎ ΠΌΠΎΠ΄ΡΠ»ΠΈΡΡΠ΅Ρ ΠΠΠ-ΠΏΠΎΠ²ΡΠ΅ΠΆΠ΄Π°ΡΡΠ΅Π΅ Π΄Π΅ΠΉΡΡΠ²ΠΈΠ΅ ΠΈΠ΄Π°ΡΡΠ±ΠΈΡΠΈΠ½Π° Π²
Π½ΠΎΡΠΌΠ°Π»ΡΠ½ΡΡ
ΠΈ Π·Π»ΠΎΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
ΠΊΠ»Π΅ΡΠΊΠ°Ρ
, ΠΈ ΡΡΠΎ Π½Π°Π»ΠΈΡΠΈΠ΅ Π±Π΅Π»ΠΊΠ° Ρ53 ΠΈ ΠΎΠ½ΠΊΠΎΠ³Π΅Π½Π½ΡΡ
ΡΠΈΡΠΎΠ·ΠΈΠ½ ΠΊΠΈΠ½Π°Π· ΠΌΠΎΠΆΠ΅Ρ ΠΈΠΌΠ΅ΡΡ Π·Π½Π°ΡΠ΅Π½ΠΈΠ΅ Π΄Π»Ρ
ΡΡΠΈΡ
ΡΠ°Π·Π»ΠΈΡΠΈΠΉ. Π¦Π΅Π»Ρ: ΠΈΠ·ΡΡΠΈΡΡ Π²Π»ΠΈΡΠ½ΠΈΠ΅ Π°ΠΌΠΈΡΠΎΡΡΠΈΠ½Π° Π½Π° ΠΈΠ΄Π°ΡΡΠ±ΠΈΡΠΈΠ½-ΠΎΠΏΠΎΡΡΠ΅Π΄ΠΎΠ²Π°Π½Π½ΡΠ΅ Π΄Π²ΡΡ
Π½ΠΈΡΠ΅Π²ΡΠ΅ ΡΠ°Π·ΡΡΠ²Ρ ΠΠΠ (DSBs)
ΠΈ Π°ΠΏΠΎΠΏΡΠΎΠ·. ΠΠ΅ΡΠΎΠ΄Ρ: ΠΌΡ ΠΏΡΠΈΠΌΠ΅Π½ΠΈΠ»ΠΈ Π³Π΅Π»Ρ-ΡΠ»Π΅ΠΊΡΡΠΎΡΠΎΡΠ΅Π· Π² ΠΏΡΠ»ΡΡΠΈΡΡΡΡΠ΅ΠΌ ΠΏΠΎΠ»Π΅ (PFGE) Π΄Π»Ρ Π²ΡΡΠ²Π»Π΅Π½ΠΈΡ DSBs ΠΈ ΠΈΠ·ΡΡΠ΅Π½ΠΈΡ
ΠΈΡ
ΡΠ΅ΠΏΠ°ΡΠ°ΡΠΈΠΈ Π² Π½ΠΎΡΠΌΠ°Π»ΡΠ½ΡΡ
Π»ΠΈΠΌΡΠΎΡΠΈΡΠ°Ρ
ΡΠ΅Π»ΠΎΠ²Π΅ΠΊΠ° ΠΈ ΠΊΠ»Π΅ΡΠΊΠ°Ρ
K562 Ρ
ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΌΠΈΠ΅Π»ΠΎΠΈΠ΄Π½ΠΎΠΉ Π»Π΅ΠΉΠΊΠ΅ΠΌΠΈΠΈ, Ρ ΠΊΠΎΡΠΎΡΡΡ
Ρ53
Π½Π΅Π°ΠΊΡΠΈΠ²Π΅Π½ ΠΈ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡΠΎΠ²Π°Π½Π° BCR/ABL-ΡΠΈΡΠΎΠ·ΠΈΠ½ ΠΊΠΈΠ½Π°Π·Π°. ΠΠΏΠΎΠΏΡΠΎΠ· ΠΎΡΠ΅Π½ΠΈΠ²Π°Π»ΠΈ Ρ ΠΏΠΎΠΌΠΎΡΡΡ ΡΠ΅Π°ΠΊΡΠΈΠ²ΠΎΠ² Π΄Π»Ρ Π²ΡΡΠ²Π»Π΅Π½ΠΈΡ
Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΠΈ ΠΊΠ°ΡΠΏΠ°Π·Ρ-3, ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ΠΈΡ ΡΠ΅Π»ΠΎΡΠ½ΠΎΠ³ΠΎ Π³Π΅Π»Ρ-ΡΠ»Π΅ΠΊΡΡΠΎΡΠΎΡΠ΅Π·Π° ΠΎΠ΄ΠΈΠ½ΠΎΡΠ½ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ ΠΈ DAPI-ΠΎΠΊΡΠ°ΡΠΈΠ²Π°Π½ΠΈΡ. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ:
ΠΈΠ΄Π°ΡΡΠ±ΠΈΡΠΈΠ½ Π²ΡΠ·ΡΠ²Π°Π΅Ρ ΠΎΠ±ΡΠ°Π·ΠΎΠ²Π°Π½ΠΈΠ΅ DSBs Π² Π½ΠΎΡΠΌΠ°Π»ΡΠ½ΡΡ
ΠΈ Π·Π»ΠΎΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
ΠΊΠ»Π΅ΡΠΊΠ°Ρ
Π½Π΅Π·Π°Π²ΠΈΡΠΈΠΌΠΎ ΠΎΡ Π΄ΠΎΠ·Ρ. ΠΠ±Π° ΡΠΈΠΏΠ° ΠΊΠ»Π΅ΡΠΎΠΊ Π½Π΅
ΡΠ΅ΠΏΠ°ΡΠΈΡΠΎΠ²Π°Π»ΠΈ ΡΡΠΈ ΠΏΠΎΠ²ΡΠ΅ΠΆΠ΄Π΅Π½ΠΈΡ Π·Π° 120 ΠΌΠΈΠ½, ΠΏΡΠΈ ΡΡΠΎΠΌ Π°ΠΌΠΈΡΠΎΡΡΠΈΠ½ Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΠ°Π»ΡΠ½ΠΎ ΠΌΠΎΠ»ΡΠ»ΠΈΡΠΎΠ²Π°Π» ΡΡΠΎΠ²Π΅Π½Ρ DSBs β ΡΠΌΠ΅Π½ΡΡΠ°Π»
Π² Π»ΠΈΠΌΡΠΎΡΠΈΡΠ°Ρ
ΠΈ ΡΠ²Π΅Π»ΠΈΡΠΈΠ²Π°Π» Π² K562-ΠΊΠ»Π΅ΡΠΊΠ°Ρ
. Π ΠΎΡΠ»ΠΈΡΠΈΠ΅ ΠΎΡ ΠΊΠΎΠ½ΡΡΠΎΠ»ΡΠ½ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ Π°ΠΌΠΈΡΠΎΡΡΠΈΠ½ ΠΏΠΎΡΠ΅Π½ΡΠΈΠΈΡΠΎΠ²Π°Π» Π°ΠΏΠΎΠΏΡΠΈΡΠ΅ΡΠΊΡΡ
ΡΡΠ°Π³ΠΌΠ΅Π½ΡΠ°ΡΠΈΡ ΠΠΠ, ΠΊΠΎΠ½Π΄Π΅Π½ΡΠ°ΡΠΈΡ Ρ
ΡΠΎΠΌΠ°ΡΠΈΠ½Π° ΠΈ Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΡ ΠΊΠ°ΡΠΏΠ°Π·Ρ-3 Π² Π»Π΅ΠΉΠΊΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΊΠ»Π΅ΡΠΊΠ°Ρ
. ΠΡΠ²ΠΎΠ΄Ρ: Π°ΠΌΠΈΡΠΎΡΡΠΈΠ½ ΠΌΠΎΠΆΠ΅Ρ
Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΠ°Π»ΡΠ½ΠΎ ΠΌΠΎΠ΄ΡΠ»ΠΈΡΠΎΠ²Π°ΡΡ DSBs ΠΈ Π°ΠΏΠΎΠΏΡΠΎΠ·, Π²ΡΠ·Π²Π°Π½Π½ΡΠ΅ ΠΈΠ΄Π°ΡΡΠ±ΠΈΡΠΈΠ½ΠΎΠΌ Π² Π½ΠΎΡΠΌΠ°Π»ΡΠ½ΡΡ
ΠΈ Π·Π»ΠΎΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
ΠΊΠ»Π΅ΡΠΊΠ°Ρ
. ΠΠ½
ΠΌΠΎΠΆΠ΅Ρ Π·Π°ΡΠΈΡΠΈΡΡ Π½ΠΎΡΠΌΠ°Π»ΡΠ½ΡΠ΅ ΠΊΠ»Π΅ΡΠΊΠΈ ΠΎΡ ΠΏΠΎΠ²ΡΠ΅ΠΆΠ΄Π΅Π½ΠΈΡ ΠΠΠ, Π²ΡΠ·Π²Π°Π½Π½ΠΎΠ³ΠΎ Ρ
ΠΈΠΌΠΈΠΎΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠΎΠΌ, ΠΈ Π² ΡΠΎ ΠΆΠ΅ Π²ΡΠ΅ΠΌΡ ΠΏΠΎΡΠ΅Π½ΡΠΈΠΈΡΠΎΠ²Π°ΡΡ
Π΄Π΅ΠΉΡΡΠ²ΠΈΠ΅ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ° Π½Π° Π»Π΅ΠΉΠΊΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΊΠ»Π΅ΡΠΊΠΈ. ΠΠ°Π»ΡΠ½Π΅ΠΉΡΠΈΠ΅ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ ΡΠ²ΡΠ·ΠΈ ΠΌΠ΅ΠΆΠ΄Ρ Π²ΡΠ·Π²Π°Π½Π½ΠΎΠΉ Π°ΠΌΠΈΡΠΎΡΡΠΈΠ½ΠΎΠΌ ΠΌΠΎΠ΄ΡΠ»ΡΡΠΈΠ΅ΠΉ
DSBs ΠΈ Π°ΠΏΠΎΠΏΡΠΎΠ·Π° ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ ΠΏΠΎΠ·Π²ΠΎΠ»ΠΈΡ Π»ΡΡΡΠ΅ ΠΏΠΎΠ½ΡΡΡ ΠΌΠΎΠ»Π΅ΠΊΡΠ»ΡΡΠ½ΡΠ΅ ΠΌΠ΅Ρ
Π°Π½ΠΈΠ·ΠΌΡ Π΄Π΅ΠΉΡΡΠ²ΠΈΡ Π°ΠΌΠΈΡΠΎΡΡΠΈΠ½Π°
Promoter methylation of cancer-related genes in gastric carcinoma
Genetic changes associated with gastric cancer are not completely known, but epigenetic mechanisms involved in this disease seem to play an important role in its pathophysiology. One of these mechanisms, an aberrant methylation in the promoter regions of genes involved in cancer induction and promotion, may be of particular importance in gastric cancer. Aim: To analyze the methylation status of eight genes: Apaf-1, Casp8, CDH1, MDR1, GSTP1, BRCA1, hMLH1, Fas in gastric cancer patients. Methods: The methylation pattern of the genes was assessed by methylation specific restriction enzyme PCR (MSRE-PCR) in gastric tumors taken during surgery of 27 patients and compared with the methylation pattern in material obtained from biopsy in 25 individuals without cancer and pre-cancerous lesions. Results: We observed a promoter hypermethylation in the Casp8, hMLH1, CDH1 and MDR1 in gastric cancer patients as compared with the controls. Additionally, we investigated the relationship between promoter hypermethylation and age, gender, smoking and gastric cancer family history. The hypermethylation of the hMLH1 gene occurred more frequently in female than in men, and the hypermethylation of the CDH1 gene was observed preferentially in smoking than in non-smoking individuals. Conclusion: The data obtained indicate that changes in DNA methylation may contribute to gastric carcinogenesis.ΠΠ΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ, Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π½ΡΠ΅ Ρ ΠΎΠΏΡΡ
ΠΎΠ»ΡΡ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ°, ΠΈΠ·ΡΡΠ΅Π½Ρ Π½Π΅ Π² ΠΏΠΎΠ»Π½ΠΎΠΉ ΠΌΠ΅ΡΠ΅. Π ΡΠΎ ΠΆΠ΅ Π²ΡΠ΅ΠΌΡ ΡΠΏΠΈΠ³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΠ΅
ΠΌΠ΅Ρ
Π°Π½ΠΈΠ·ΠΌΡ ΡΠΊΠΎΡΠ΅Π΅ Π²ΡΠ΅Π³ΠΎ ΠΈΠ³ΡΠ°ΡΡ ΠΊΠ»ΡΡΠ΅Π²ΡΡ ΡΠΎΠ»Ρ ΠΈ Π»Π΅ΠΆΠ°Ρ Π² ΠΎΡΠ½ΠΎΠ²Π΅ Π²ΠΎΠ·Π½ΠΈΠΊΠ½ΠΎΠ²Π΅Π½ΠΈΡ ΡΡΠΎΠ³ΠΎ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ. ΠΠ΄ΠΈΠ½ ΠΈΠ· ΡΠ°ΠΊΠΈΡ
ΠΌΠ΅Ρ
Π°Π½ΠΈΠ·ΠΌΠΎΠ²β
Π½Π°ΡΡΡΠ΅Π½ΠΈΡΠΌΠ΅ΡΠΈΠ»ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΏΡΠΎΠΌΠΎΡΠΎΡΠΎΠ² Π³Π΅Π½ΠΎΠ², ΠΊΠΎΡΠΎΡΡΠ΅ ΡΠ΅Π³ΡΠ»ΠΈΡΡΡΡ Π·Π»ΠΎΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡΡΡΠ°Π½ΡΡΠΎΡΠΌΠ°ΡΠΈΡΠΈ ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅
ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΠΎΠ³ΠΎ ΠΏΡΠΎΡΠ΅ΡΡΠ°, ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎ Π²Π°ΠΆΠ½ΡΠΌ Π² ΡΠ°Π·Π²ΠΈΡΠΈΠΈ ΡΠ°ΠΊΠ° ΠΆΠ΅Π»ΡΠ΄ΠΊΠ°. Π¦Π΅Π»Ρ: ΠΏΡΠΎΠ°Π½Π°Π»ΠΈΠ·ΠΈΡΠΎΠ²Π°ΡΡ ΡΡΠ°ΡΡΡ ΠΌΠ΅ΡΠΈΠ»ΠΈΡΠΎΠ²Π°Π½ΠΈΡ
ΠΏΡΠΎΠΌΠΎΡΠΎΡΠΎΠ² Π²ΠΎΡΡΠΌΠΈ Π³Π΅Π½ΠΎΠ²: Apaf-1, Casp8, CDH1, MDR1, GSTP1, BRCA1, hMLH1, Fas Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
ΡΠ°ΠΊΠΎΠΌ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ°. ΠΠ΅ΡΠΎΠ΄Ρ: ΠΌΠ΅ΡΠΈΠ»ΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅
ΠΏΡΠΎΠΌΠΎΡΠΎΡΠΎΠ² Π³Π΅Π½ΠΎΠ² ΠΈΠ·ΡΡΠ°Π»ΠΈ Ρ ΠΏΠΎΠΌΠΎΡΡΡΡΠΏΠ΅ΡΠΈΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΊ ΡΠ°ΠΉΡΠ°ΠΌΠΌΠ΅ΡΠΈΠ»ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΡΠ΅ΡΡΡΠΈΠΊΡΠΈΠ΅ΠΉ Ρ ΠΠ¦Π (MSRE-PCR)
Π½Π° Ρ
ΠΈΡΡΡΠ³ΠΈΡΠ΅ΡΠΊΠΎΠΌΠΌΠ°ΡΠ΅ΡΠΈΠ°Π»Π΅ (ΠΎΠΏΡΡ
ΠΎΠ»ΠΈ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ°) 27 ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ². ΠΠΊΠ°ΡΠ΅ΡΡΠ²Π΅ ΠΊΠΎΠ½ΡΡΠΎΠ»Ρ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π»ΠΈ ΠΈΠΎΠΏΡΠΈΠΉΠ½ΡΠΉΠΌΠ°ΡΠ΅ΡΠΈΠ°Π», ΠΏΠΎΠ»ΡΡΠ΅Π½Π½ΡΠΉ
ΠΎΡ 25 Π±ΠΎΠ»ΡΠ½ΡΡ
, Ρ ΠΊΠΎΡΠΎΡΡΡ
Π½Π΅ Π±ΡΠ»ΠΎ Π²ΡΡΠ²Π»Π΅Π½ΠΎ ΡΠ°ΠΊΠ° ΠΈΠ»ΠΈ ΠΏΡΠ΅Π΄ΡΠ°ΠΊΠΎΠ²ΡΡ
ΡΠΎΡΡΠΎΡΠ½ΠΈΠΉ. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ: ΠΎΡΠΌΠ΅ΡΠ°Π»ΠΈ Π³ΠΈΠΏΠ΅ΡΠΌΠ΅ΡΠΈΠ»ΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅
ΠΏΡΠΎΠΌΠΎΡΠΎΡΠΎΠ² Π³Π΅Π½ΠΎΠ² Casp8, hMLH1, CDH1 ΠΈ MDR1 Π² ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ° ΠΏΠΎ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ Ρ ΠΊΠΎΠ½ΡΡΠΎΠ»ΡΠ½ΡΠΌΠΈ ΠΎΠ±ΡΠ°Π·ΡΠ°ΠΌΠΈ.
ΠΡΠΎΠΌΠ΅ ΡΠΎΠ³ΠΎ, Π½Π°ΠΌΠΈ Π±ΡΠ»Π° ΠΏΡΠΎΡΠ»Π΅ΠΆΠ΅Π½Π° Π²Π·Π°ΠΈΠΌΠΎΡΠ²ΡΠ·Ρ ΠΌΠ΅ΠΆΠ΄Ρ Π³ΠΈΠΏΠ΅ΡΠΌΠ΅ΡΠΈΠ»ΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ΠΌ ΠΏΡΠΎΠΌΠΎΡΠΎΡΠΎΠ² Π³Π΅Π½ΠΎΠ² ΠΈ Π²ΠΎΠ·ΡΠ°ΡΡΠΎΠΌ, ΠΏΠΎΠ»ΠΎΠΌ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ²,
ΠΊΡΡΠ΅Π½ΠΈΠ΅ΠΌ ΠΈ ΡΠ΅ΠΌΠ΅ΠΉΠ½ΠΎΠΉ ΠΈΡΡΠΎΡΠΈΠ΅ΠΉ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ ΡΠ°ΠΊΠΎΠΌ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ°. ΠΠΈΠΏΠ΅ΡΠΌΠ΅ΡΠΈΠ»ΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ Π³Π΅Π½Π° hMLH1 Π²ΡΡΠ²Π»ΡΠ»ΠΈ ΡΠ°ΡΠ΅ Ρ ΠΆΠ΅Π½ΡΠΈΠ½, ΡΠ΅ΠΌ Ρ
ΠΌΡΠΆΡΠΈΠ½, Π° Π³ΠΈΠΏΠ΅ΡΠΌΠ΅ΡΠΈΠ»ΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ Π³Π΅Π½Π° CDH1 β Π² ΠΎΡΠ½ΠΎΠ²Π½ΠΎΠΌ Ρ ΠΊΡΡΠΈΠ»ΡΡΠΈΠΊΠΎΠ². ΠΡΠ²ΠΎΠ΄Ρ: ΠΏΠΎΠ»ΡΡΠ΅Π½Π½ΡΠ΅ Π΄Π°Π½Π½ΡΠ΅ ΡΠ²ΠΈΠ΄Π΅ΡΠ΅Π»ΡΡΡΠ²ΡΡΡ ΠΎ ΡΠΎΠΌ,
ΡΡΠΎ ΠΌΠ΅ΡΠΈΠ»ΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ ΠΠΠ ΠΌΠΎΠΆΠ΅Ρ ΠΈΠ³ΡΠ°ΡΡ Π²Π°ΠΆΠ½ΡΡ ΡΠΎΠ»Ρ ΠΏΡΠΈ ΡΠ°Π·Π²ΠΈΡΠΈΠΈ ΡΠ°ΠΊΠ° ΠΆΠ΅Π»ΡΠ΄ΠΊΠ°
Serum levels of IL-6 type cytokines and soluble IL-6 receptors in active B-cell chronic lymphocytic leukemia and in cladribine induced remission.
We have investigated the serum concentrations of interleukin-6 (IL-6) and two IL-6 family cytokines-oncostatin M (OSM) and leukemia inhibitory factor (LIF)-in 63 patients with B-cell chronic lymphocytic leukemia (B-CLL) and 17 healthy controls using the enzyme-linked immunosorbent assay (ELISA) method. Simultaneously, we measured the serum levels of the soluble forms of two subunits of the IL-6 receptor complex-ligand binding glycoprotein 80 (sIL-6R) and glycoprotein 130 (sgp130). The cytokines and receptors were evaluated in 25 untreated patients and 38 patients treated with cladribine (2-CdA), as well as in 17 healthy controls. We have correlated the serum levels of these proteins with Rai's clinical stage of the disease, the response to 2-CdA treatment and some hematological parameters. We have also evaluated the correlation of the IL-6 serum level with the concentration of OSM and IL-6 soluble receptors. IL-6 was measurable in 62/63 (98.4%), OSM in 20/25 (80%) of untreated and 14/38 (37.8%) of the treated patients. sIL-6R and sgp130 were detectable in all 63 patients and LIF in none of the CLL patients. IL-6 serum level in untreated patients was not significantly different as compared to its concentration in the control group (P>0.05). However, in the patients treated with 2-CdA the IL-6 level was significantly lower (P<0.02), and the lowest concentration was found in the patients with complete remission (CR; median 1.4pg/ml; P<0.02). The concentration of sIL-6R was significantly higher in untreated (median 61.8 ng/ml) and treated (median 50.1 ng/ml) CLL patients when compared to normal persons (median 41.2 ng/ml; P=0.04; P<0.001, respectively). There was no difference between the sIL-6R levels in the patients with CR and the healthy controls. In non-responders sIL-6R concentration was the highest and similar to its level in the untreated patients. OSM level was higher in the untreated patients (median 1.8pg/ml) than in the normal controls (median 0.0pg/ml; P<0.001) and in the CR patients (median 0.0pg/ml; P<0.03). The serum concentration of sgp130 was similar in the untreated (median 480 pg/ml) and treated (median 470 pg/ml) patients, as well as in the healthy persons (median 420 pg/ml; P>0.05). We have found significant positive correlation between the levels of sIL-6R and the lymphocytes count in CLL patients (p=0.423; P<0.001). In addition, sIL-6R and OSM serum concentrations correlated also with CLL Rai stage. In conclusion, the serum level of IL-6, OSM and sIL-6R, but not LIF and sgp130, are useful indicators of CLL activity
Anisotropic elasticity in confocal studies of colloidal crystals
We consider the theory of fluctuations of a colloidal solid observed in a
confocal slice. For a cubic crystal we study the evolution of the projected
elastic properties as a function of the anisotropy of the crystal using
numerical methods based on the fast Fourier transform. In certain situations of
high symmetry we find exact analytic results for the projected fluctuations.Comment: 6 pages, 7 figure
On a functional equation involving iterates and powers
We present a complete list of all continuous solutions f : (0,+β)β(0,+β) of the equation f 2(x) = Ξ³ [f (x)]Ξ±xΞ², where Ξ±, Ξ² and Ξ³ > 0 are given real numbers
Human breast tissue cancer diagnosis by Raman spectroscopy
Abstract. Differences between Raman spectra of normal, malignant and benign tissues have been recorded and analyzed as a method for the early detection of cancer. To the best of our knowledge, this is one of the most statistically reliable research (67 patients) on Raman spectroscopy-based diagnosis of breast cancers among the world women population. The paper demonstrates that Raman spectroscopy is a promising new tool for real-time diagnosis of tissue abnormalities
Polish 2010 growth references for school-aged children and adolescents
Growth references are useful in monitoring a child's growth, which is an essential part of child care. The aim of this paper was to provide updated growth references for Polish school-aged children and adolescents and show the prevalence of overweight and obesity among them. Growth references for height, weight, and body mass index (BMI) were constructed with the lambda, mu, sigma (LMS) method using data from a recent, large, population-representative sample of school-aged children and adolescents in Poland (nβ=β17,573). The prevalence of overweight and obesity according to the International Obesity Taskforce definition was determined with the use of LMSGrowth software. Updated growth references for Polish school-aged children and adolescents were compared with Polish growth references from the 1980s, the Warsaw 1996β1999 reference, German, and 2000 CDC references. A positive secular trend in height was observed in children and adolescents from 7 to 15Β years of age. A significant shift of the upper tail of the BMI distribution occurred, especially in Polish boys at younger ages. The prevalence of overweight or obesity was 18.7% and 14.1% in school-aged boys and girls, respectively. The presented height, weight, and BMI references are based on a current, nationally representative sample of Polish children and adolescents without known disorders affecting growth. Changes in the body size of children and adolescents over the last three decades suggest an influence of the changing economical situation on anthropometric indices
Polymorphisms in RAD51, XRCC2 and XRCC3 genes of the homologous recombination repair in colorectal cancerβa case control study
XRCC2 and XRCC3 proteins are structurally and functionally related to RAD51 which play an important role in the homologous recombination, the process frequently involved in cancer transformation. In our previous work we show that the 135G>C polymorphism (rs1801320) of the RAD51 gene can modify the effect of the Thr241Met polymorphism (rs861539) of the XRCC3 gene. We tested the association between the 135G>C polymorphism of the RAD51 gene, the Thr241Met polymorphism of the XRCC3 gene and the Arg188His polymorphism (rs3218536) of the XRCC2 gene and colorectal cancer risk and clinicopathological parameters. Polymorphisms were evaluated by restriction fragment length polymorphism polymerase chain reaction (RFLP-PCR) in 100 patients with invasive adenocarcinoma of the colon and in 100 sex, age and ethnicity matched cancerβfree controls. We stratified the patients by genotypes, tumour Dukeβs and TNM stage and calculated the linkage of each genotype with each stratum. Carriers of Arg188Arg/Me241tMet, His188His/Thr241Thr and His188His/G135G genotypes had an increased risk of colorectal cancer occurrence (OR 5.70, 95% CI 1.10β29.5; OR 12.4, 95% CI 1.63β94.9; OR 5.88, 95% CI 1.21β28.5, respectively). The C135C genotype decreased the risk of colorectal cancer singly (OR 0.06, 95% CI 0.02β0.22) as well as in combination with other two polymorphisms. TNM and Dukeβs staging were not related to any of these polymorphisms. Our results suggest that the 135G>C polymorphism of the RAD51 gene can be an independent marker of colorectal cancer risk. The Thr241Met polymorphism of the XRCC3 gene and the Arg188His polymorphism of the XRCC2 gene can modify the risk of colorectal cancer
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