Resumen Objectivos La leucemia mieloide aguda (AML, por sus siglas en inglés) es una enfermedad muy heterogénea. Aunque se puede clasificar a los pacientes en grupos de riesgo según sus mutaciones genéticas, el pronóstico dentro de cada categoría varía sustancialmente. Es perentorio identificar nuevos marcadores moleculares de la AML. Recientemente, se ha descrito la elevación del inhibidor de la serina peptidasa Kazal tipo 2 (SPINK2) en la AML, habiendo sido relacionada con peores resultados clínicos en metaanálisis, así como en un número limitado de pacientes con AML. Métodos Analizamos la expresión de SPINK2 en 62 pacientes (45 adultos y 17 niños) con AML y en 11 líneas celulares mediante PCR cuantitativa (qRT-PCR). Los niveles de la proteína SPINK2 se determinaron en líneas celulares mediante ELISA. Resultados Observamos un aumento de expresión del ARNm de SPINK2 y de los niveles de la proteína en las líneas celulares de AML (HL60 y NB4), frente a otras líneas celulares (K562, Jurkat y NALM6, MCF7, HeLa, HUVEC, hFOB, 293T, U87). Los pacientes con AML mostraron una expresión elevada de ARNm de SPINK2 frente a los controles (p=0,004) y esta fue significativamente menor en los pacientes t(8;21) positivos, frente a los pacientes negativos (p=0,0006). Conclusions Estos resultados sugieren que el gen SPINK2 tiene un papel relevante en el desarrollo de la AML. Son necesarios más estudios para evaluar la expresión de SPINK2 en los pacientes con AML con la mutación t(8.21) e investigar su valor pronóstico en varios subgrupos de pacientes con AML.
Objectives Acute myeloid leukemia (AML) is a highly heterogeneous disease. Although patients can be classified into risk groups based on their genetic changes, the prognosis of disease within these categories varies widely. This situation raises the need to search for new molecular markers related to AML. Serine peptidase inhibitor Kazal type 2 (SPINK2) has recently been reported to be upregulated in AML and associated with poor outcomes by meta-analysis and in a limited number of AML patients. Methods We analyzed SPINK2 mRNA expression in 62 patients (45 adult and 17 pediatric) with AML and 11 cell lines using quantitative Real-Time PCR (qRT-PCR). SPINK2 protein level was determined using ELISA in cell lines. Results We found that the expression of SPINK2 mRNA and protein levels in AML cell lines (HL60 and NB4) have increased compared to other cell lines (K562, Jurkat and NALM6, MCF7, HeLa, HUVEC, hFOB, 293T, U87). SPINK2 mRNA expression was upregulated in patients with AML compared to controls (p=0.004) and significantly lower in t(8;21)-positive patients compared to negative patients (p=0.0006). Conclusions Our results suggest that SPINK2 serves an important role in AML development. Further studies are needed to evaluate SPINK2 expression in AML patients with t(8.21) and investigate to clarify its prognostic value in various subgroups of AML.
Purpose: Plasma Cell Dyscrasias are a heterogeneous group of hematological diseases. The candidate ten genes identified from our transcriptome data are highly valuable and specific. Methods: We investigated the prognostic biomarker status of these genes in Plasma Cell Dyscrasias. Expression levels of ISG20, EEF2, TRIB1, RRBP1, TMED9, KDELR1, DNAJC1, DPP7, COPE and LMAN2 genes were measured via qRT-PCR from bone marrow samples of 38 Multiple Myeloma, 23 MGUS and 16 control groups. Results: According to our results, in the Multiple Myeloma group, all genes were more highly expressed than control and MGUS groups (p<0.05) In addition, the striking correlation with anemia factors, calcium and Durie Salmon Staging indicates that DNAJC1 is an important risk factor for MM (p<0.05). TMED9 was another prominent gene that showed higher expression in Multiple Myeloma compared to other groups. Also, there was strong association between TMED9 gene expression and clinical parameters of urea, Ca, albumin, LDH, and IGA levels (p<0.05) Moreover, TMED9gene in our results sheds light on myeloma genesis. Conclusion: This study contributed significantly to the search on prognostic biomarkers for Multiple Myeloma progression from MGUS and for starting early treatment in MGUS.
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