ArticleMedical oncology (Northwood, London, England)2012
Unexpected effect of the monoclonal antibody Panitumumab on human cancer cells with different KRAS status.
Article in Medical oncology (Northwood, London, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Panitumumab is the first fully human monoclonal antibody targeting the epidermal growth factor receptor whose clinical use is limited to patients with a non-mutated KRAS status. The aim of this in vitro study was to evaluate whether the KRAS status might influence the cytotoxic and radiosensitizing efficacy of Panitumumab. Exponentially growing cancer cells (HT-29: KRAS wild-type, A549: KRAS mutant) were either treated with the monoclonal antibody alone in growth and proliferation assays or in combination with radiation in metabolic and colony-forming assays. For the assessment of ionizing radiation-induced DNA damage and to evaluate Panitumumab's influence on DNA damage repair, the γH2AX foci assay was performed. Treatment with Panitumumab resulted in a concentration-independent growth inhibition as well as a cytotoxic effect only in the KRAS-mutated cell line A549. BrdU assay confirmed an antiproliferative influence of Panitumumab. When combined with irradiation, incubation with the antibody was found to result in an enhanced radiosensitivity. Contrary to expectations, Panitumumab had no influence on the cell growth, LDH release or clonogenic survival of KRAS wild-type cells HT-29. Our results suggest that response to Panitumumab treatment is not only controlled by the KRAS status but may also be essentially influenced by other regulating factors.
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