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Molecular analysis of transferrin receptor mRNA expression in acute myeloid leukaemia

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Autor
Kollia, P.; Stavroyianni, N.; Stamatopoulos, K.; Zoi, K.; Viniou, N.; Mantzourani, M.; Noguchi, C. T.; Paterakis, G.; Abazis, D.; Pangalos, C.; Loukopoulos, D.; Yataganas, X.
Fecha
2001
DOI
10.1046/j.1365-2141.2001.03065.x
Materia
transferrin receptor
mRNA
acute myeloid leukaemia
IRON UPTAKE
CELLS
LEUKEMIA
PCR
MECHANISMS
GROWTH
Hematology
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Resumen
Transferrin receptor (TfR, CD71) is an integral membrane glycoprotein that mediates cellular uptake of iron. In most tissues, TfR expression is correlated positively with proliferation and regulated at the post-transcriptional level. The available data regarding the pattern of TfR gene expression in haematological malignancies are very Limited. In the present study, we evaluated TfR gene expression at the molecular level in bone marrow (BM) samples of 44 patients with de novo acute myeloid leukaemia (AXIL) at diagnosis with BM blasts > 85%. TfR mRNA levels were determined by densitometric analysis of quantitative reverse transcription polymerase chain reaction products corresponding to TfR exons 15-17. Each sample was tested in at least two independent experiments. In 13/44 patients, TfR messages were not detected (this is probably an underestimate as some positive results may be attributed to residual normal erythroid cells present in the samples). In 17/44, TfR mRNA levels were low-intermediate, and were high in the remaining patients (14/44). TfR mRNA positivity was significantly associated with older age. No statistically significant correlations were found either with specific French-American-British (FAB) subtypes or attainment of complete remission, incidence of relapse and survival (after adjusting accordingly for age and FAB subtype). The absence of TfR mRNA transcripts in a significant minority of cases suggests that alternative mechanisms of iron uptake may function in AML blast cells.
URI
http://hdl.handle.net/11615/29538
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  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ. [19735]
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