The following figures and table appeared incorrectly in the article by Antonella Calogero et al., which appeared in the September 2001, issue of Clinical Cancer Research (pp. 2788–2796). The corrected figures and table appear below.

In the article by P. F. Bross, et al., which appeared in the June 2001, issue of Clinical Cancer Research (pp. 1490–1496), the currently approved labeled indication is for patients “sixty years of age or older who are not candidates for other cytotoxic chemotherapy.” The original label was revised to clarify that Gemtuzumab ozogamicin is in itself highly cytotoxic. The intent was to limit the use of this product to patients who might otherwise not be able to receive treatment for their relapsed leukemia, until further studies can be completed confirming clinical benefit in other clinical situations.

Due to manufacturing constraints, approximately 50% of the antibody is unconjugated. The average molar loading ratio is 2–3 molecules of calechiamicin/antibody, not 4–6 molecules/antibody as reported in the article. However of the conjugated molecules, the molar loading is closer to 4–6 molecules/antibody. The clinical effect of the unconjugated antibodies is unknown.

The infusion time is two hours, not four hours as reported in the article. In the abstract, the correct units to report platelet count are 30,000/μl not 30,000 per ml. On page 1492, “Pharmacokinetics,” the corrected units for AUC are mg-hr/liter. On page 1493, first column, 61 was the median age, not the mean age.

In the article by Wen G. Jiang et al., which appeared in the August 2001, issue of Clinical Cancer Research (pp. 2555–2562), the name of author Roger Abounder was misspelled. The correct spelling is Roger Abounader.

Fig. 4.

EGR-1 expression correlates with p53 in mutated gliomas. Immunohistochemical evaluation of the percentage of EGR-1-positive cells in tissues from tumors carrying wild-type p53 (•) or mutated copies of the gene (○). Staining of the p53 protein was demonstrated in all sections from the mutated tumors but not in sections from wild-type-p53 tumors. The percentage of EGR-1-positive cells significantly overlapped the percentage of cells showing p53 protein accumulation in all of the three p53-mutated tumors investigated (correlaton coefficient rPearson = 0.86; P = 0.0067).

Fig. 4.

EGR-1 expression correlates with p53 in mutated gliomas. Immunohistochemical evaluation of the percentage of EGR-1-positive cells in tissues from tumors carrying wild-type p53 (•) or mutated copies of the gene (○). Staining of the p53 protein was demonstrated in all sections from the mutated tumors but not in sections from wild-type-p53 tumors. The percentage of EGR-1-positive cells significantly overlapped the percentage of cells showing p53 protein accumulation in all of the three p53-mutated tumors investigated (correlaton coefficient rPearson = 0.86; P = 0.0067).

Close modal
Fig. 5.

Allele dosage for Mdm2 and p16INK4a genes as determined by Southern analysis in representative tumor samples. A, 3 tumors (T45, T31, and T27) show amplified copies of the Mdm2 gene. B, 5 tumors (T36, T24, T11, T3, and T1) show absence of both alleles of p16/MTS1. Tumor T16 shows single-allele deletion. C, the same filter as in A and B hybridized with a probe from the HTSHR gene (HTSHR), for signal normalization.

Fig. 5.

Allele dosage for Mdm2 and p16INK4a genes as determined by Southern analysis in representative tumor samples. A, 3 tumors (T45, T31, and T27) show amplified copies of the Mdm2 gene. B, 5 tumors (T36, T24, T11, T3, and T1) show absence of both alleles of p16/MTS1. Tumor T16 shows single-allele deletion. C, the same filter as in A and B hybridized with a probe from the HTSHR gene (HTSHR), for signal normalization.

Close modal
Table 1

Summary of mutations found in a series of 31 astrocytic tumors.

CaseDiagnosisExonCodonMutationSubstitutionMdm2 DNAEgr-1 RNA (% Normal)P16 Genotype
T26 Ga 213 C→G Arg→Gly  200 +/+ 
T21 152 C→T Pro→Leu  100 +/+ 
T28 241 C→T Ser→Phe Ib 90 +/+ 
T46 241 C→T Ser→Phe 75 +/+ 
 T2 216 G→A Val→Met  12 +/+ 
 T7 237 G→A Met→Ile 30 +/+ 
T15 175 G→A Arg→His 20 +/+ 
T33 278 C→T Pro→Leu 36 +/+ 
T40 193 A→T His→Leu 24 +/+ 
T48 266 G→C Gly→Arg  35 +/+ 
        Av: <66>  
T27 No Change     Amplified 30 +/+ 
T31 No Change     Amplified 15 +/+ 
T45 No Change     Amplified 13 +/+ 
        Av: <19>  
 T1 No Change     del/del 
 T3 No Change     del/del 
T11 No Change     del/del 
T16 No Change     10 +/del 
T36 No Change     del/del 
        Av: <3>  
T13 No Change     25 +/+ 
T14 No Change     +/+ 
T18 No Change     30 +/+ 
T19 No Change     10 +/+ 
T25 No Change     +/+ 
T32 No Change     12 +/+ 
T42 No Change     +/+ 
T44 No Change     45 +/+ 
 T5 No Change     +/+ 
 T6 No Change     +/+ 
 T9 No Change     30 +/+ 
T10 No Change     +/+ 
T12 No Change     15 +/+ 
        Av: <13>  
CaseDiagnosisExonCodonMutationSubstitutionMdm2 DNAEgr-1 RNA (% Normal)P16 Genotype
T26 Ga 213 C→G Arg→Gly  200 +/+ 
T21 152 C→T Pro→Leu  100 +/+ 
T28 241 C→T Ser→Phe Ib 90 +/+ 
T46 241 C→T Ser→Phe 75 +/+ 
 T2 216 G→A Val→Met  12 +/+ 
 T7 237 G→A Met→Ile 30 +/+ 
T15 175 G→A Arg→His 20 +/+ 
T33 278 C→T Pro→Leu 36 +/+ 
T40 193 A→T His→Leu 24 +/+ 
T48 266 G→C Gly→Arg  35 +/+ 
        Av: <66>  
T27 No Change     Amplified 30 +/+ 
T31 No Change     Amplified 15 +/+ 
T45 No Change     Amplified 13 +/+ 
        Av: <19>  
 T1 No Change     del/del 
 T3 No Change     del/del 
T11 No Change     del/del 
T16 No Change     10 +/del 
T36 No Change     del/del 
        Av: <3>  
T13 No Change     25 +/+ 
T14 No Change     +/+ 
T18 No Change     30 +/+ 
T19 No Change     10 +/+ 
T25 No Change     +/+ 
T32 No Change     12 +/+ 
T42 No Change     +/+ 
T44 No Change     45 +/+ 
 T5 No Change     +/+ 
 T6 No Change     +/+ 
 T9 No Change     30 +/+ 
T10 No Change     +/+ 
T12 No Change     15 +/+ 
        Av: <13>  
a

G, glioblastoma multiforme; A, astrocytoma; N, normal genotype; del, deleted allele; Av, mean percentage.

b

I, mutation with probable inactivating function. These mutations fall into highly conserved structural motifs.