{"entity": "journal", "iuid": "78700e2bd5514955982af3fa71ebf101", "timestamp": "2026-07-17T05:36:36.690Z", "links": {"self": {"href": "https://publications.scilifelab.se/journal/Int.%20J.%20Radiat.%20Oncol.%20Biol.%20Phys..json"}, "display": {"href": "https://publications.scilifelab.se/journal/Int.%20J.%20Radiat.%20Oncol.%20Biol.%20Phys."}}, "title": "Int. J. Radiat. Oncol. Biol. Phys.", "issn": "1879-355X", "issn-l": "0360-3016", "publications_count": 2, "publications": [{"entity": "publication", "iuid": "95e3397aa97f499691827ab1770b0047", "links": {"self": {"href": "https://publications.scilifelab.se/publication/95e3397aa97f499691827ab1770b0047.json"}, "display": {"href": "https://publications.scilifelab.se/publication/95e3397aa97f499691827ab1770b0047"}}, "title": "The Critical Role of Dysregulated RhoB Signaling Pathway in Radioresistance of Colorectal Cancer.", "authors": [{"family": "Liu", "given": "Na", "initials": "N"}, {"family": "Cui", "given": "Weiyingqi", "initials": "W"}, {"family": "Jiang", "given": "Xia", "initials": "X"}, {"family": "Zhang", "given": "Zhiyong", "initials": "Z"}, {"family": "Gnosa", "given": "Sebastian", "initials": "S"}, {"family": "Ali", "given": "Zaheer", "initials": "Z"}, {"family": "Jensen", "given": "Lasse", "initials": "L"}, {"family": "J\u00f6nsson", "given": "Jan-Ingvar", "initials": "JI", "orcid": "0000-0003-4814-978X", "researcher": {"href": "https://publications.scilifelab.se/researcher/fcc87190783c48229913c2a35a2782c8.json"}}, {"family": "Blockhuys", "given": "St\u00e9phanie", "initials": "S"}, {"family": "Lam", "given": "Eric W-F", "initials": "EW"}, {"family": "Zhao", "given": "Zengren", "initials": "Z"}, {"family": "Ping", "given": "Jie", "initials": "J"}, {"family": "Xie", "given": "Ning", "initials": "N"}, {"family": "Kopsida", "given": "Maria", "initials": "M"}, {"family": "Wang", "given": "Xin", "initials": "X"}, {"family": "Sun", "given": "Xiao-Feng", "initials": "XF"}], "type": "journal article", "published": "2019-08-01", "journal": {"title": "Int. J. Radiat. Oncol. Biol. Phys.", "issn": "1879-355X", "volume": "104", "issue": "5", "pages": "1153-1164", "issn-l": "0360-3016"}, "abstract": "To explore whether the Rho protein is involved in the radioresistance of colorectal cancer and investigate the underlying mechanisms.\n\nRho GTPase expression was measured after radiation treatment in colon cancer cells. RhoB knockout cell lines were established using the CRISPR/Cas9 system. In vitro assays and zebrafish embryos were used for analyzing radiosensitivity and invasive ability. Mass cytometry was used to detect RhoB downstream signaling factors. RhoB and Forkhead box M1 (FOXM1) expression were detected by immunohistochemistry in rectal cancer patients who participated in a radiation therapy trial.\n\nRhoB expression was related to radiation resistance. Complete depletion of the RhoB protein increased radiosensitivity and impaired radiation-enhanced metastatic potential in vitro and in zebrafish models. Probing signaling using mass cytometry-based single-cell analysis showed that the Akt phosphorylation level was inhibited by RhoB depletion after radiation. FOXM1 was downregulated in RhoB knockout cells, and the inhibition of FOXM1 led to lower survival rates and attenuated migration and invasion abilities of the cells after radiation. In the patients who underwent radiation therapy, RhoB overexpression was related to high FOXM1, late Tumor, Node, Metastasis stage, high distant recurrence, and poor survival independent of other clinical factors.\n\nRhoB plays a critical role in radioresistance of colorectal cancer through Akt and FOXM1 pathways.", "doi": "10.1016/j.ijrobp.2019.04.021", "pmid": "31039421", "labels": {"Cellular Immunomonitoring": "Service"}, "xrefs": [{"db": "pii", "key": "S0360-3016(19)30653-4"}], "notes": [], "created": "2019-12-02T12:43:37.113Z", "modified": "2021-07-08T09:31:31.587Z"}, {"entity": "publication", "iuid": "8ceea6d27ed644f7b3a8459069a59292", "links": {"self": {"href": "https://publications.scilifelab.se/publication/8ceea6d27ed644f7b3a8459069a59292.json"}, "display": {"href": "https://publications.scilifelab.se/publication/8ceea6d27ed644f7b3a8459069a59292"}}, "title": "SNP in TXNRD2 associated with radiation-induced fibrosis: a study of genetic variation in reactive oxygen species metabolism and signaling.", "authors": [{"family": "Edvardsen", "given": "Hege", "initials": "H"}, {"family": "Landmark-H\u00f8yvik", "given": "Hege", "initials": "H"}, {"family": "Reinertsen", "given": "Kristin V", "initials": "KV"}, {"family": "Zhao", "given": "Xi", "initials": "X"}, {"family": "Grenaker-Aln\u00e6s", "given": "Grethe Irene", "initials": "GI"}, {"family": "Nebdal", "given": "Daniel", "initials": "D"}, {"family": "Syv\u00e4nen", "given": "Ann-Christine", "initials": "AC", "orcid": "0000-0002-9681-9146", "researcher": {"href": "https://publications.scilifelab.se/researcher/f7012e35025543379380cb90efd71243.json"}}, {"family": "R\u00f8dningen", "given": "Olaug", "initials": "O"}, {"family": "Alsner", "given": "Jan", "initials": "J"}, {"family": "Overgaard", "given": "Jens", "initials": "J"}, {"family": "Borresen-Dale", "given": "Anne-Lise", "initials": "AL"}, {"family": "Foss\u00e5", "given": "Sophie D", "initials": "SD"}, {"family": "Kristensen", "given": "Vessela N", "initials": "VN"}], "type": "journal article", "published": "2013-07-15", "journal": {"volume": "86", "issn": "1879-355X", "issue": "4", "pages": "791-799", "title": "Int. J. Radiat. Oncol. Biol. Phys.", "issn-l": "0360-3016"}, "abstract": "The aim of the study was to identify noninvasive markers of treatment-induced side effects. Reactive oxygen species (ROS) are generated after irradiation, and genetic variation in genes related to ROS metabolism might influence the level of radiation-induced adverse effects (AEs).\n\n92 breast cancer (BC) survivors previously treated with hypofractionated radiation therapy were assessed for the AEs subcutaneous atrophy and fibrosis, costal fractures, lung fibrosis, pleural thickening, and telangiectasias (median follow-up time 17.1 years). Single-nucleotide polymorphisms (SNPs) in 203 genes were analyzed for association to AE grade. SNPs associated with subcutaneous fibrosis were validated in an independent BC survivor material (n=283). The influence of the studied genetic variation on messenger ribonucleic acid (mRNA) expression level of 18 genes previously associated with fibrosis was assessed in fibroblast cell lines from BC patients.\n\nSubcutaneous fibrosis and atrophy had the highest correlation (r=0.76) of all assessed AEs. The nonsynonymous SNP rs1139793 in TXNRD2 was associated with grade of subcutaneous fibrosis, the reference T-allele being more prevalent in the group experiencing severe levels of fibrosis. This was confirmed in another sample cohort of 283 BC survivors, and rs1139793 was found significantly associated with mRNA expression level of TXNRD2 in blood. Genetic variation in 24 ROS-related genes, including EGFR, CENPE, APEX1, and GSTP1, was associated with mRNA expression of 14 genes previously linked to fibrosis (P\u2264.005).\n\nDevelopment of subcutaneous fibrosis can be associated with genetic variation in the mitochondrial enzyme TXNRD2, critically involved in removal of ROS, and maintenance of the intracellular redox balance.", "doi": "10.1016/j.ijrobp.2013.02.025", "pmid": "23597419", "labels": {"National Genomics Infrastructure": null, "NGI Uppsala (SNP&SEQ Technology Platform)": null}, "xrefs": [{"db": "pii", "key": "S0360-3016(13)00217-4"}], "notes": [], "created": "2017-05-04T15:01:19.734Z", "modified": "2021-07-07T15:11:02.591Z"}], "created": "2017-05-09T09:12:41.233Z", "modified": "2020-11-27T13:14:07.981Z"}