In the article on oncolytic and gene therapy using HYPR-Ad-IL4 in the July 15, 2007 issue of Cancer Research (1), there was an error in the size of the printing of Fig. 4 The corrected full page figure appears on the previous page. This correction does not change the content or conclusions of the figure.

Figure 4.
Figure 4. Histology and immunohistochemistry of HYPR-Ad-mIL4–treated tumors. LN229 tumors were intratumorally treated with PBS (A), HYPR-Ad-mIL4 (B),or dl309-Ad (C) as described in the legend of Fig. 3. Fifteen days from the start of treatment, animals were injected with pimonidazole hydrochloride (a 2-nitroimidazolehypoxia marker) and sacrificed, and the tumors were harvested. Deparaffinized tumor sections were stained with H&E for tumor histology and detection of infiltratingPMN leukocytes and with Masson's trichrome to detect collagen (blue). Immunostaining was done for Ad hexon protein, pimonidazole (hypoxia) adduct, andCD45 leukocyte common antigen, a pan-lymphocyte marker. Magnifications: A, C, and D, 50×; B, 100×; and E, 400×. Representative sections are shown.
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Histology and immunohistochemistry of HYPR-Ad-mIL4–treated tumors. LN229 tumors were intratumorally treated with PBS (A), HYPR-Ad-mIL4 (B),or dl309-Ad (C) as described in the legend of Fig. 3. Fifteen days from the start of treatment, animals were injected with pimonidazole hydrochloride (a 2-nitroimidazolehypoxia marker) and sacrificed, and the tumors were harvested. Deparaffinized tumor sections were stained with H&E for tumor histology and detection of infiltratingPMN leukocytes and with Masson's trichrome to detect collagen (blue). Immunostaining was done for Ad hexon protein, pimonidazole (hypoxia) adduct, andCD45 leukocyte common antigen, a pan-lymphocyte marker. Magnifications: A, C, and D, 50×; B, 100×; and E, 400×. Representative sections are shown.

Figure 4.
Figure 4. Histology and immunohistochemistry of HYPR-Ad-mIL4–treated tumors. LN229 tumors were intratumorally treated with PBS (A), HYPR-Ad-mIL4 (B),or dl309-Ad (C) as described in the legend of Fig. 3. Fifteen days from the start of treatment, animals were injected with pimonidazole hydrochloride (a 2-nitroimidazolehypoxia marker) and sacrificed, and the tumors were harvested. Deparaffinized tumor sections were stained with H&E for tumor histology and detection of infiltratingPMN leukocytes and with Masson's trichrome to detect collagen (blue). Immunostaining was done for Ad hexon protein, pimonidazole (hypoxia) adduct, andCD45 leukocyte common antigen, a pan-lymphocyte marker. Magnifications: A, C, and D, 50×; B, 100×; and E, 400×. Representative sections are shown.
View largeDownload slide

Histology and immunohistochemistry of HYPR-Ad-mIL4–treated tumors. LN229 tumors were intratumorally treated with PBS (A), HYPR-Ad-mIL4 (B),or dl309-Ad (C) as described in the legend of Fig. 3. Fifteen days from the start of treatment, animals were injected with pimonidazole hydrochloride (a 2-nitroimidazolehypoxia marker) and sacrificed, and the tumors were harvested. Deparaffinized tumor sections were stained with H&E for tumor histology and detection of infiltratingPMN leukocytes and with Masson's trichrome to detect collagen (blue). Immunostaining was done for Ad hexon protein, pimonidazole (hypoxia) adduct, andCD45 leukocyte common antigen, a pan-lymphocyte marker. Magnifications: A, C, and D, 50×; B, 100×; and E, 400×. Representative sections are shown.

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1
Post DE, Sandberg EM, Kyle MM, Devi NS, Brat DJ, Xu Z, Tighiouart M, Van Meir EG. Targeted cancer gene therapy using a hypoxia inducible factor-dependent oncolytic adenovirus armed with interleukin-4.
Cancer Res
 
2007
;
67
:
6872
–81.
View Original Article
©2007 American Association for Cancer Research.
2007