HC gp-39 gene is upregulated in glioblastomas

Abstract

Public databases of the Cancer Genome Anatomy Project were used to quantify the relative gene expression levels in glioblastoma multiforme (GBM) and normal brain by Serial Analysis of Gene Expression (SAGE). Analysis revealed HC gp-39 among the genes with the most pronounced changes of expression in tumor cells. Northern hybridization confirmed the results of computer analysis and showed that enhanced expression of the HC gp-39 gene was mainly in GBMs and occasionally in anaplastic astrocytomas. Neither SAGE nor Northern analysis revealed the presence of HC gp-39 mRNA in the glioblastoma cell line, thus the detection of increased quantities of this mRNA in GBMs may be associated with activated macrophages. Since the numbers of infiltrating macrophages and small vessel density are higher in glioblastomas than in anaplastic astrocytomas or astrocytomas, the HC gp-39 gene can be used as a molecular marker in the analysis of malignant progression of astrocytic gliomas. q

YKL-40 Expression is Associated with Poorer Response to Radiation and Shorter Overall Survival in Glioblastoma

“…Positive staining for YKL-40 was found in the cytoplasm of glioblastoma tumor cells (Fig. 2) tumor-associated macrophages (36). YKL-40 staining was scored as strongly positive (2+) in 85 of 147 cases (58%), weakly positive (1+) in 28 cases (19%), and negative in 34 cases (23%).…”

Brain Barriers and a Subpopulation of Astroglial Progenitors of Developing Human Forebrain Are Immunostained for the Glycoprotein YKL-40

“…Following surgery for glioblastoma and anaplastic glioma, plasma levels of YKL-40 are lower in patients with no radiographic evidence of disease as compared with patients with radiographic evidence, and results suggest that increases in YKL-40 plasma concentrations during the follow-up are associated with shorter survival times (Iwamoto et al 2011). Microarray gene analyses have shown that YKL-40 is overexpressed in glioblastoma multiforme, as compared with normal tissue (Lal et al 1999;Markert et al 2001;Tanwar et al 2002;Shostak et al 2003;Nigro et al 2005;Ku et al 2011). Tumor stem cells may be involved in the initiation of gliomas and bear a resemblance to neural stem cells (Schiffer et al 2010), which are present during the early development of the brain.…”

Chitinase 3-like protein 2 (CHI3L2, YKL-39) activates phosphorylation of extracellular signal-regulated kinases ERK1/ERK2 in human embryonic kidney (HEK293) and human glioblastoma (U87 MG) cells

“…It is overex pressed in macrophages during the last stages of differentiation; its expression is increasing signifi cantly under pathological conditions such as inflammation or different tumors notably squa mous cell carcinoma of the head and neck, multi ple myeloma, acute myeloid leukemia, small cell lung cancer, primary breast cancer, ovarian cancer stage III, colorectal carcinoma, and glioblastoma [15]. CHI3L1 is overexpressed in glioblastomas in comparison with low grade gliomas and normal brain [16] and a correlation between high expres sion of CHI3L1 and short survival of patients was observed [17]. It was reported that YKL 40 pro motes the growth of human synovial cells as well as skin and fetal lung fibroblasts [10].…”