Glioblastoma
J Neurooncol. 2008
Jul;88(3):339-47. Epub
2008 Apr 4. Ananthnarayan S, Bahng J, Roring J, Nghiemphu P, Lai
A, Cloughesy T, Pope
WB. Department of Radiology,
David Geffen School of Medicine, University of California at Los Angeles,
10833 Le Conte Ave., BL-428, CHS, Los Angeles, CA, 90095-1721, USA. Glioblastoma
multiforme (GBM) are morphologically heterogeneous
tumors, with varying amounts of necrosis, and edema. Previous studies have
shown that treatments incorporating the VEGF antibody bevacizumab
can reduce edema and tumor burden in GBM. Additionally it has been
suggested that bevacizumab regimen treatment reduces
the percent of tumoral necrosis. Therefore we
sought to (1) determine the time course of change in necrosis, tumor, and
edema volume in patients who respond to bevacizumab
regimen treatment and (2) determine if GBM that progress following a
response to bevacizumab regimen treatment are
morphologically different from their appearance at prior tumor progression.
Therefore, we retrospectively assessed tumor, necrosis, and edema volumes
on MRI scans from 15 patients with recurrent GBM who responded to bevacizumab regimen treatment, and had extended (>7
month) follow-up. We found that the median time to best tumor response was
158 days (range, 16-261, SD = 63). The median best response was 72.1%
reduction in tumor volume and 72.8% reduction in peritumoral
edema. Most tumors (77.8%) showed resolution of necrotic areas. The
relative reduction of edema and necrosis was sustained, even in patients (n
= 7) who developed tumor progression. Thus the mean ratio of edema-to-tumor
volume at progression on bevacizumab regimen
treatment was 38.4% lower than that for the same tumors seen on progression
scans following prior chemotherapy. The percentage of necrotic tumor also
was diminished following progression on bevacizumab
regimen treatment. These findings illustrate the time course of changes in
edema and tumor volume with prolonged bevacizumab
regimen treatment, and support the conclusion that the morphology of
recurrent GBM following bevacizumab regimen
therapy is distinct from that on other chemotherapy. PMID: 18389177 [PubMed
- in process] Anticancer
Res. 2008 Jan-Feb;28(1A):15-9. Dipartimento
di Biologia Animale, Università di Pavia, Italia. facoetti@unipv.it p53 is
a cell cycle regulator that has been well-recognized as the key molecule
that triggers the induction and the control of cell proliferation and
apoptosis in a wide variety of tumours, including
astrocytoma. Apoptosis and proliferation are two
processes intimately coupled, that occur simultaneously in tumour tissue. Previous studies of the correlations
between proliferation and apoptotic index with p53 expression in astrocytic tumours have
remained inconclusive. The aim of this study was to investigate the
correlation of p53 expression with the apoptotic index (AI) and the cell
proliferation index (PI) in pilocytic astrocytoma (PA) and glioblastoma
multiforme (GBM). A correlation of p53 expression
with AI and PI was found in pilocytic astrocytoma but not in glioblastoma,
probably because of the mutated p53 phenotype in the latter. PMID: 18383819 [PubMed
- indexed for MEDLINE] J Neurooncol. 2008
Jul;88(3):339-47. Epub
2008 Apr 4. Ananthnarayan S, Bahng J, Roring J, Nghiemphu P, Lai
A, Cloughesy T, Pope
WB. Department of Radiology,
David Geffen School of Medicine, University of California at Los Angeles,
10833 Le Conte Ave., BL-428, CHS, Los Angeles, CA, 90095-1721, USA. Glioblastoma
multiforme (GBM) are morphologically heterogeneous
tumors, with varying amounts of necrosis, and edema. Previous studies have
shown that treatments incorporating the VEGF antibody bevacizumab
can reduce edema and tumor burden in GBM. Additionally it has been
suggested that bevacizumab regimen treatment
reduces the percent of tumoral necrosis.
Therefore we sought to (1) determine the time course of change in necrosis,
tumor, and edema volume in patients who respond to bevacizumab
regimen treatment and (2) determine if GBM that progress following a
response to bevacizumab regimen treatment are
morphologically different from their appearance at prior tumor progression.
Therefore, we retrospectively assessed tumor, necrosis, and edema volumes
on MRI scans from 15 patients with recurrent GBM who responded to bevacizumab regimen treatment, and had extended (>7
month) follow-up. We found that the median time to best tumor response was
158 days (range, 16-261, SD = 63). The median best response was 72.1%
reduction in tumor volume and 72.8% reduction in peritumoral
edema. Most tumors (77.8%) showed resolution of necrotic areas. The
relative reduction of edema and necrosis was sustained, even in patients (n
= 7) who developed tumor progression. Thus the mean ratio of edema-to-tumor
volume at progression on bevacizumab regimen
treatment was 38.4% lower than that for the same tumors seen on progression
scans following prior chemotherapy. The percentage of necrotic tumor also
was diminished following progression on bevacizumab
regimen treatment. These findings illustrate the time course of changes in
edema and tumor volume with prolonged bevacizumab
regimen treatment, and support the conclusion that the morphology of
recurrent GBM following bevacizumab regimen
therapy is distinct from that on other chemotherapy. PMID: 18389177 [PubMed
- in process] Neuro Oncol. 2008
Mar 21. [Epub ahead of print] Du R, Petritsch C, Lu
K, Liu
P, Haller
A, Ganss R, Song
H, Vandenberg
S, Bergers G. Department of Neurological, Surgery University of
California San Francisco, San Francisco, CA, USA; Department of
Neurological Surgery, Brigham and Womenâ€
2008/6/21-38
Time course of imaging changes of GBM during
extended bevacizumab treatment.
Proliferation and programmed cell death: role
of p53 protein in high and low grade astrocytoma.
Time course of imaging changes of GBM during
extended bevacizumab treatment.
Matrix metalloproteinase-2 regulates vascular
patterning and growth affecting tumor cell survival and invasion in GBM.