ArticleCancer gene therapy2006
Expression of the coxsackievirus- and adenovirus receptor in gastrointestinal cancer correlates with tumor differentiation.
Article in Cancer gene therapy, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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
34 citing papers in PubMed, 67 citations in OpenAlex.
- Virotherapy for Spinal and Spinal Cord Tumors: Current Evidence and Future Perspectives.Microorganisms · 2026Review
- Oncolytic adenovirus serotype 35 mediated tumor growth suppressionJournal for immunotherapy of cancer · 2025Article
- Receptors and Host Factors for Enterovirus Infection: Implications for Cancer Therapy.Cancers · 2024Review
- Construction and application of adenoviral vectors.Molecular therapy. Nucleic acids · 2023Review
- Article
- A Renaissance for Oncolytic Adenoviruses?Viruses · 2023Review
- Development of a low-seroprevalence, αvβ6 integrin-selective virotherapy based on human adenovirus type 10.Molecular therapy oncolytics · 2022Article
- Article
- Coxsackievirus and Adenovirus Receptor (CXADR): Recent Findings and Its Role and Regulation in Spermatogenesis.Advances in experimental medicine and biology · 2021Review
- Hitting the Target but Missing the Point: Recent Progress towards Adenovirus-Based Precision Virotherapies.Cancers · 2020Review
- Bone and Soft-Tissue Sarcoma: A New Target for Telomerase-Specific Oncolytic Virotherapy.Cancers · 2020Review
- Coxsackievirus Type B3 Is a Potent Oncolytic Virus againstMolecular therapy oncolytics · 2019Article
- Oncolytic viruses: adenoviruses.Virus genes · 2017Review
- Loss of coxsackie and adenovirus receptor expression in human colorectal cancer: A potential impact on the efficacy of adenovirus-mediated gene therapy in Chinese Han population.Molecular medicine reports · 2016Article
- JAM-related proteins in mucosal homeostasis and inflammation.Seminars in immunopathology · 2014Review
- Species D human adenovirus type 9 exhibits better virus-spread ability for antitumor efficacy among alternative serotypes.PloS one · 2014Article
- CAR regulates epithelial cell junction stability through control of E-cadherin trafficking.Scientific reports · 2013Article
- Presence of the coxsackievirus and adenovirus receptor (CAR) in human neoplasms: a multitumour array analysis.British journal of cancer · 2013Article
- A simple detection system for adenovirus receptor expression using a telomerase-specific replication-competent adenovirus.Gene therapy · 2013Article
- Enhanced delivery of mda-7/IL-24 using a serotype chimeric adenovirus (Ad.5/3) in combination with the Apogossypol derivative BI-97C1 (Sabutoclax) improves therapeutic efficacy in low CAR colorectal cancer cells.Journal of cellular physiology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Modified adenoviruses represent a new approach to treatment of gastrointestinal cancer. However, their uptake by cells in many cases requires the major receptor for adenoviruses, the coxsackievirus and adenovirus receptor (CAR). Thus, lack of CAR expression is a potential cause of intrinsic resistance of tumor cells to this type of treatment. To evaluate this, we studied the localization of CAR protein in normal and malignant gastrointestinal tissues. In normal tissues, CAR was concentrated at sites of cell-cell interaction, in particular at the apico-lateral cellular surface. Expression was particularly strong around bile and pancreatic ducts, which is in agreement with CAR's physiological function as a tight-junction protein. In GI malignancies (esophageal, pancreatic, colorectal and liver cancer), expression of the receptor varied substantially. Loss of CAR expression at cell-cell junction was evident in many samples. A significant correlation between CAR expression and histological grade was found, with moderately to poorly differentiated tumors most frequently demonstrating loss or reduction of CAR expression. These data indicate that CAR expression is frequently altered in gastrointestinal malignancy, potentially reducing the efficacy of adenovirus-based therapies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.