ArticleWorld journal of gastroenterology2016
Evaluation of therapeutic effectiveness of (131)I-antiEGFR-BSA-PCL in a mouse model of colorectal cancer.
Article in World journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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7 citing papers in PubMed, 14 citations in OpenAlex.
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the biological effects of internal irradiation, and the therapeutic effectiveness was assessed of (131)I-labeled anti-epidermal growth factor receptor (EGFR) liposomes, derived from cetuximab, when used as a tumor-targeting carrier in a colorectal cancer mouse model.
methodsWe described the liposomes and characterized their EGFR-targeted binding and cellular uptake in EGFR-overexpressing LS180 colorectal cancer cells. After intra-tumor injections of 74 MBq (740 MBq/mL) (131)I-antiEGFR-BSA-PCL, we investigated the biological effects of internal irradiation and the therapeutic efficacy of (131)I-antiEGFR-BSA-PCL on colorectal cancer in a male BALB/c mouse model. Tumor size, body weight, histopathology, and SPECT imaging were monitored for 33 d post-therapy.
resultsThe rapid radioiodine uptake of (131)I-antiEGFR-BSA-PCL and (131)I-BSA-PCL reached maximum levels at 4 h after incubation, and the (131)I uptake of (131)I-antiEGFR-BSA-PCL was higher than that of (131)I-BSA-PCL in vitro. The (131)I tissue distribution assay revealed that (131)I-antiEGFR-BSA-PCL was markedly taken up by the tumor. Furthermore, a tissue distribution assay revealed that (131)I-antiEGFR-BSA-PCL was markedly taken up by the tumor and reached its maximal uptake value of 21.0 ± 1.01 %ID/g (%ID/g is the percentage injected dose per gram of tissue) at 72 h following therapy; the drug concentration in the tumor was higher than that in the liver, heart, colon, or spleen. Tumor size measurements showed that tumor development was significantly inhibited by treatments with (131)I-antiEGFR-BSA-PCL and (131)I-BSA-PCL. The volume of tumor increased, and treatment rate with (131)I-antiEGFR-BSA-PCL was 124% ± 7%, lower than that with (131)I-BSA-PCL (127% ± 9%), (131)I (143% ± 7%), and normal saline (146% ± 10%). The percentage losses in original body weights were 39% ± 3%, 41% ± 4%, 49% ± 5%, and 55% ± 13%, respectively. The best survival and cure rates were obtained in the group treated with (131)I-antiEGFR-BSA-PCL. The animals injected with (131)I-antiEGFR-BSA-PCL and (131)I-BSA-PCL showed more uniform focused liposome distribution within the tumor area.
conclusionThis study demonstrated the potential beneficial application of (131)I-antiEGFR-BSA-PCL for treating colorectal cancer. (131)I-antiEGFR-BSA-PCL suppressed the development of xenografted colorectal cancer in nude mice, thereby providing a novel candidate for receptor-mediated targeted radiotherapy.
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