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Aberrant p53, mdm2, and Proliferation Differ in Glioblastomas from Long-Term Compared with Typical Survivors1

Eric C. Burton, Kathleen R. Lamborn, Peter Forsyth, James Scott, Jason O’Campo, Jane Uyehara-Lock, Michael Prados, Mitchel Berger, Sandra Passe, Joon Uhm, Brian P. O’Neill, Robert B. Jenkins and Ken D. Aldape
Eric C. Burton
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Kathleen R. Lamborn
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Peter Forsyth
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James Scott
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Jason O’Campo
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Jane Uyehara-Lock
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Michael Prados
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Mitchel Berger
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Sandra Passe
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Joon Uhm
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Brian P. O’Neill
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Robert B. Jenkins
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Ken D. Aldape
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DOI:  Published January 2002
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    Fig. 1.

    Histopathology of glioblastoma from LTSs. Representative photomicrographs of tumor specimens showing features of GBM. A, case 20 shows tumor necrosis (arrowheads). B, case 16 demonstrates marked nuclear atypia and pseudopallisading necrosis (arrows). C, case 14 shows microvascular proliferation characteristic of GBM (arrowheads). D, case 25 displays high cellularity and features of small cell GBM.

Tables

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  • Table 1

    Clinical comparison of LTSs and STSs

    A comparison of the median age (years), KPS, gender (% of cohort that is female), survival (months), and the Ps of both patient groups. Statistical tests performed were Mann-Whitney (for age and KPS) and Fisher’s exact test (for gender).

    LTSSTSP
    Age (yrs)39420.97
    KPS90900.83
    Gender (% F)60%38%0.03
    Survival (mo.)59.011.5
  • Table 2

    p53, EGFR, mdm2, and Ki-67, and status for LTS GBMs

    Individual results are given by case number. Results based on immunohistochemistry are scored as “+” or “−”, except for Ki-67, which is expressed as percentage of positive cells. For the p53 gene, the mutation is represented by showing the mutated codon and amino acid change.

    Casep53 proteinp53 geneEGFRmdm2Ki-67
    1+codon 266 gly→arg++50.1
    2+WTa−+22.9
    3+WT++31.3
    4+codon 152 pro→leu−+35.5
    5+WT++16.4
    6−ND−−5.2
    7−ND−−24.0
    8+ND−−3.4
    9+ND−−11.4
    10+ND−−3.8
    11+ND−−16.8
    12+ND−−16.2
    13+ND−+12.5
    14−ND−−15.0
    15+ND−−6.6
    16−WT−+68.1
    17+codon 273 arg→cys−−6.9
    18+ND−+21.5
    19+WT−−9.5
    20+ND−−12.6
    21+ND−−50.1
    22+WT−−7.8
    23+WT−+85.2
    24+ND−−4.4
    25+WT−+56.0
    26+ND−+4.0
    27+WT−−20.3
    28+WT−+41.4
    29+ND++38.4
    30+codon 280 arg→gly−ND5.9
    31−ND−+12.0
    32+WT−−34.1
    33+WT+−12.5
    34+ND−+10.8
    35+ND−−13.5
    36+WT−+23.0
    37+codon 250 arg→cys−−43.4
    38+ND−−19.0
    39+WT−−ND
    40+ND−+7.9
    41−WT−+15.2
    • a WT, wild type; ND, not determined because of unamplifiable DNA or unavailable slides.

  • Table 3

    p53, EGFR, mdm2, and Ki-67, and status for STS GBMs

    Individual results are given by case number. Results based on immunohistochemistry are scored as “+” or “−”, except for Ki-67, which is expressed as percentage of positive cells. For the p53 gene, the mutation is represented by showing the mutated codon and amino acid change.

    Casep53 proteinp53 geneEGFRmdm2Ki-67
    1−WTc++40.0
    2+ND−−19.6
    3+WT−+7.9
    4+WT−+19.0
    5+ND−−18.6
    6+WT−+62.1
    7−ND−+53.7
    8−WT++15.4
    9−WT−+69.9
    10−WT−+28.3
    11−ND−−16.1
    12+WT−+35.5
    13+WT−+38.2
    14−ND−+23.1
    15−ND−−35.8
    16−ND−+26.6
    17+ND−+50.1
    18−ND+−27.8
    19+codon 273 arg→his−+12.7
    20+codon 132 lys→thr++17.8
    21+ND−−16.1
    22−WT++39.1
    23+ND−+59.4
    24+ND−−29.1
    25−ND−+39.0
    26+ND−+14.7
    27−WT−+33.6
    28+WT++21.4
    29+WT−+20.6
    30+WT++58.0
    31−ND++41.0
    32+WT−+15.4
    33+codon 273 arg→his−−26.6
    34−ND−+55.3
    35+ND−+23.9
    36+ND−+50.2
    37+codon 152 pro→leu−+46.2
    38+codon 175 arg→his−−30.2
    39−codon 237 met→ile−−37.9
    40+WT−+58.1
    41+WT++26.9
    42−ND−+22.5
    43−ND−+6.2
    44+codon 273 arg→cys+−7.3
    45−WT++17.9
    46−ND++51.6
    47−ND−−10.8
    48+G-C splice site intron 4−+44.1
    • a WT, wild type; ND, not determined because of unamplifiable DNA and/or unavailable slides.

  • Table 4

    Comparison of marker status of LTS to STS GBMs

    Results for p53 protein, EGFR, and mdm2 are expressed as the percentage of positive cases within each group. p53 gene is expressed as percentage of mutations in exons 5–8. Except for Ki-67, Ps are from Fisher’s exact test. Ki-67 indices are expressed as medians and are compared using a Mann-Whitney test. The SDs/SEs for the Ki-67 are LTS: 19.0/3.0 and STS 16.5/2.4.

    MarkerLTSSTSP
    p53 protein85% (35/41)56% (27/48)<0.01
    p53 gene25% (5/20)31% (8/26)1.0
    EGFR12% (5/41)25% (12/48)0.12
    mdm245% (18/40)75% (36/48)<0.01
    Ki-6715.7 (range 3.4–85.2)28.1 (range 6.2–69.9)<0.01
  • Table 5

    Multimarker profile comparison of LTS and STS patients

    Since STS patients were more likely to be p53-negative, mdm2-positive, and have a higher Ki-67 labeling index, the number of cases from each group showing each pairwise profile and the combination of all three. Ki-67 scores were dichotomized, where “Ki-67+” indicates a labeling index of >20%.

    ProfileLTSSTSP
    mdm2+/Ki-67+11/41 (27%)27/48 (56%)<0.01
    p53−/Ki-67+2/41 (5%)16/48 (33%)<0.01
    p53−/mdm2+3/41 (7%)16/48 (33%)<0.01
    p53−/mdm2+/Ki-67+1/41 (2%)13/48 (27%)<0.01
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January 2002
Volume 8, Issue 1
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Aberrant p53, mdm2, and Proliferation Differ in Glioblastomas from Long-Term Compared with Typical Survivors1
Eric C. Burton, Kathleen R. Lamborn, Peter Forsyth, James Scott, Jason O’Campo, Jane Uyehara-Lock, Michael Prados, Mitchel Berger, Sandra Passe, Joon Uhm, Brian P. O’Neill, Robert B. Jenkins and Ken D. Aldape
Clin Cancer Res January 1 2002 (8) (1) 180-187;

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Aberrant p53, mdm2, and Proliferation Differ in Glioblastomas from Long-Term Compared with Typical Survivors1
Eric C. Burton, Kathleen R. Lamborn, Peter Forsyth, James Scott, Jason O’Campo, Jane Uyehara-Lock, Michael Prados, Mitchel Berger, Sandra Passe, Joon Uhm, Brian P. O’Neill, Robert B. Jenkins and Ken D. Aldape
Clin Cancer Res January 1 2002 (8) (1) 180-187;
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