Monokine induced by interferon gamma (MIG/CXCL9) is an independent prognostic factor in newly diagnosed myeloma.

Leuk Lymphoma

a Wilhelminen Cancer Research Institute, Department of Medicine I, Center for Oncology and Hematology , Wilhelminen Hospital, Vienna , Austria ;

Published: November 2016

AI Article Synopsis

  • Immune suppression is a key feature of multiple myeloma (MM), and this study investigated the role of the chemokine MIG in understanding immune effects in MM.
  • Elevated MIG levels were found in newly diagnosed MM patients compared to both healthy controls and those with a different condition (MGUS), indicating its potential importance in the disease's progression.
  • High MIG serum levels correlated with worse overall survival and various established prognostic markers, suggesting it could serve as an independent prognostic factor for patient outcomes in MM.

Article Abstract

Immune suppression is a hallmark of multiple myeloma (MM), but data on soluble factors involved in the fate of immune effector cells are limited. The CXCR3-binding chemokine monokine induced by interferon-gamma (MIG/CXCL9) has been associated with tumor progression, immune escape, and angiogenesis in several malignancies. We here aimed to evaluate the prognostic relevance of MIG in MM. MIG serum levels were significantly elevated in newly diagnosed MM patients (n = 105) compared to patients with monoclonal gammopathy of undetermined significance (MGUS; n = 17) and healthy controls (n = 37). MIG expression in stromal compartments but not purified MM cells correlated with serum levels. High MIG serum levels were significantly associated with established prognostic markers (international staging system: R = 0.25, p = 0.001; age: R = 0.47, p < 0.0001; lactate-dehydrogenase: R = 0.34, p = 0.0005) and poor overall survival (OS) (median OS 17.0 months vs. not reached, p < 0.001). A similar association was found for CXCL10 and CXCL11. Multivariate regression analysis indicated MIG as an independent prognostic factor of OS.

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Source
http://dx.doi.org/10.3109/10428194.2016.1151511DOI Listing

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