Genes and pathways driving glioblastomas in humans and murine disease models

Merlo, Adrian

doi:10.1007/s10143-003-0267-8

Cited by 62 publications

(47 citation statements)

References 98 publications

(116 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Because chromosome instability is associated with tumor progression, these findings indicate that loss of BCCIP may be associated with tumor aggression. The human BCCIP gene is located at 10q26 (Liu et al, 2001), which has been implicated in many forms of human tumors, including astrocytic brain tumors (Rasheed et al, 1992;Maier et al, 1998;Merlo, 2003;Ohgaki et al, 2004). We have previously shown that BCCIP expression is downregulated in kidney cancer (Meng et al, 2003), BCCIPa expression was not detectable in astrocytic brain cancer cell line A172 (Liu et al, 2001), and BCCIP deletion has been suggested in a brain tumor cell line (Roversi et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Roles of BCCIP in chromosome stability and cytokinesis

Meng

Fan²,

Shen

2007

Oncogene

View full text Add to dashboard Cite

The BRCA2 gene is involved in recombinational DNA repair and cytokinesis. BRCA2 defects are associated with chromosomal abnormalities, which is a hallmark of genomic instability that contributes to tumorigenesis. Here, we show that downregulation of a BRCA2 interacting protein (BCCIP) in HT1080 cells leads to chromosomal polyploidization, centrosome amplification and abnormal mitotic spindle formation. The BCCIP knockdown cells can enter mitosis and retain spindle checkpoint, but fail to complete cytokinesis. Our data suggest an essential role of BCCIP in the maintenance of genomic integrity.

show abstract

Section: Discussionmentioning

confidence: 99%

Roles of BCCIP in chromosome stability and cytokinesis

Meng

Fan²,

Shen

2007

Oncogene

View full text Add to dashboard Cite

show abstract

“…Survivin has emerged as an attractive therapeutic target and potentially important prognostic marker in many tumor types, including human gliomas (Ambrosini et al, 1997;Adida et al, 1998Adida et al, , 2000Kawasaki et al, 1998;Lu et al, 1998;Monzo et al, 1999;Asanuma et al, 2000;Islam et al, 2000;Olie et al, 2000;Tanaka et al, 2000;Grossman et al, 2001;Smith et al, 2001;Merlo, 2003). There have been four recent studies demonstrating that Survivin expression is associated with glioma progression from low-to high grade (Tan et al, 1993;Chakravarti et al, 2002;Sasaki et al, 2002;Kajiwara et al, 2003;Katoh et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Survivin enhances radiation resistance in primary human glioblastoma cells via caspase-independent mechanisms

et al. 2004

View full text Add to dashboard Cite

The observed radioresistance of human glioblastoma multiforme (GBM) poses a major challenge, which, if overcome, may lead to significant advances in the management of this patient population. There is accumulating evidence from correlative studies that Survivin expression is associated with increased malignant potential of human gliomas. The purpose of this study was to investigate whether Survivin plays a direct role in mediating radiation resistance in primary human glioma cell lines, and, if so, investigating the underlying mechanisms. Our panel of GBM cell lines included two that were relatively radiation resistant (GM20 and GM21) and two that were more radiation sensitive (GM22 and GM23), which demonstrated differential levels of Survivin expression between the two groups. Through the use of adenoviral vectors containing either dominant-negative (pAd-S(T34A)) or wild-type Suvrivin (pAd-S(WT)), we were able to inactivate or overexpress Survivin, respectively. Our findings suggest that Survivin plays a critical role in mediating radiation resistance in primary GBM cells, in part through suppression of apoptotic cell death via a caspase-independent manner. We have identified novel mechanisms by which Survivin may enhance tumor cell survival upon radiation exposure such as regulation of double-strand DNA break repair and tumor cell metabolism, which were most evident in the radiation-resistant cell lines. These differences in Survivin function both in radiation-resistant vs radiation-sensitive cell lines and in the presence vs absence of radiation exposure warrant further investigation and highlight potentially important mechanisms of radiation resistance in these tumors.

show abstract

“…GBM has a complex tumor structure consisting of accumulating tumors cells, abnormal vessel and necrotic debris. The increasing tumor mass leads to increased capillary and venous collapse (Merlo, 2003). The new formed vessels are structurally and functionally abnormal, and leaky, leading to edema, and low oxygen tension (Bani-Yaghoub et al, 2006).…”

Section: Midkine and Glioblastomamentioning

confidence: 99%