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Mutation Research 312: 51–60, 1994\nTucker JD, Morgan WF, Awa AA, Bauchinger M, Blakey D, Cornforth MN, Littlefield LG, Natarajan AT, Shasserre C: A proposed system for scoring structural aberrations detected by chromosome painting. Cytogenet Cell Genet 68: 211–221, 1995\nSchrock E, du Manoir S, Veldman T, Schoell B, Wienberg J, Ferguson-Smith MA, Ning Y, Ledbetter DH, Bar-Am I, Soenksen D, Garini Y, Ried T: Multicolor spectral karyotyping of human chromosomes. Science 273: 494–498, 1996\nSpeicher M, Ballard S, Ward D: Karyotyping human chromosomes by combinatorial multi-fluor FISH. Nature Genetics 12: 368–375, 1996\nCornforth MN: Analyzing radiation-induced complex chromosome rearrangements by combinatorial painting. Radiation Research 155: 643–659, 2001\nLoucas BD, Cornforth MN: Complex chromosome exchanges induced by g rays in human lymphocytes: An mFISH study. Radiat Res 155: 660–671, 2001\nGuan Y, Zhang H, Bittner M, Jiang Y, Meltzer P, Trent J: Chromosome arm painting probes. Nature Genetics 12: 10–11, 1996\nNatarajan AT, Boei JJWA, Vermeulen S, Balajee AS: Frequencies of X-ray induced pericentric inversions and centric rings in human blood lymphocytes detected by FISH using chromosome arm specific DNA libraries. Mutation Research 372: 1–7, 1996\nTeixeira MR, Micci F, Dietrich CU, Heim S: Cross-species color banding characterization of chromosomal rearrangements in leukemias with incomplete G-band karyotypes. Genes Chromosomes Cancer 26: 13–19, 1999\nLiehr T, Weise A, Heller A, Starke H, Mrasek K, Kuechler A, Weier HU, Claussen U: Multicolor chromosome banding (MCB) with YAC\u002FBAC-based probes and region-specific microdissection DNA libraries. Cytogenet Genome Res 97: 43–50, 2002\nHande MP, Azizova TV, Geard CR, Burak LE, Mitchell CR, Khokhryakov VF, Vasilenko EK, Brenner DJ: Past exposure to densely ionizing radiation leaves a unique permanent signature in the genome. Am J Hum Genet 72: 1162–1170, 2003\nLansdorp PM, Verwoerd NP, van de Rijke FM, Dragowska V, Little MT, Dirks RW, Raap AK, Tanke HJ: Heterogeneity in telomere length of human chromosomes. Hum Mol Genet 5: 685–689, 1996\nChristian AT, Pattee MS, Attix CM, Reed BE, Sorensen KJ, Tucker JD: Detection of DNA point mutations and mRNA expression levels by rolling circle amplification in individual cells. Proc Nat'l Acad Sci 98: 14,238–214,243, 2001\nJones IM, Galick H, Kato P, Langlois RG, Mendelsohn ML, Murphy GA, Pleshanov P, Ramsey MJ, Thomas CB, Tucker JD, Tureva L, Vorobtsova I, Nelson DO: Three somatic genetic biomarkers and covariates in radiation exposed Russian clean-up workers of the Chernobyl nuclear reactor, 6-13 years after exposure. Radiation Research 158: 424–442, 2002\nMatsumoto K, Ramsey MJ, Nelson DO, Tucker JD: Persistence of radiation-induced translocations in human peripheral blood determined by chromosome painting. Radiation Research 149: 602–613, 1998\nPluth JM, Ramsey MJ, Tucker JD: Role of maternal exposures and newborn genotypes on newborn chromosome aberration frequencies. Mutation Research 465: 101–111, 2000\nAmundson SA, Bittner M, Fornace AJ Jr.: Functional genomics as a window on radiation stress signaling. Oncogene 22: 5828–5833, 2003\nAmundson S, Fornace A Jr.: Monitoring human radiation exposure by gene expression profiling: Possibilities and pitfalls. Health Phys 85: 36–42, 2003\nFalt S, Holmberg K, Lambert B, Wennborg A: Long-term global gene expression patterns in irradiated human lymphocytes. Carcinogenesis 24: 1837–1845, 2003\nChaudhry MA, Chodosh LA, McKenna WG, Muschel RJ: Gene expression profile of human cells irradiated in G1 and G2 phases of cell cycle. Cancer Lett 195: 221–233, 2003\nJen KY, Cheung VG: Transcriptional response of lymphoblastoid cells to ionizing radiation. Genome Res 13: 2092–2100, 2003\nHeller MJ: DNA microarray technology: Devices, systems, and applications. Annu Rev Biomed Eng 4: 129–153, 2002\nNtzani EE, Ioannidis JP: Predictive ability of DNA microarrays for cancer outcomes and correlates: An empirical assessment. Lancet 362: 1439–1444, 2003\nStruski S, Doco-Fenzy M, Cornillet-Lefebvre P: Compilation of published comparative genomic hybridization studies. Cancer Genet Cytogenet 135: 63–90, 2002\nTeixeira MR: Combined classical and molecular cytogenetic analysis of cancer. Eur J Cancer 38: 1580–1584, 2002\nAlbertson DG: Profiling breast cancer by array CGH. Breast Cancer Res Treat 78: 289–298, 2003\nLengauer C, Kinzler KW, Vogelstein B: Genetic instabilities in human cancers. Nature 396: 643–649, 1998\nRied T, Heselmeyer-Haddad K, Blegen H, Schrock E, Auer G: Genomic changes defining the genesis, progression, and malignancy potential in solid human tumors: A phenotype\u002Fgenotype correlation. Genes Chromosomes Cancer 25: 195–204, 1999\nMorgan WF: Non-targeted and delayed effects of exposure to ionizing radiation: II. Radiation-induced genomic instability and bystander effects in vivo, clastogenic factors and transgenerational effects. Radiat Res 159: 581–596, 2003\nCharames GS, Bapat B: Genomic instability and cancer. Curr Mol Med 3: 589–596, 2003\nLengauer C, Kinzler KW, Vogelstein B: Genetic instability in colorectal cancers. Nature 386: 623–627, 1997\nFulop Z, Csernus B, Timar B, Szepesi A, Matolcsy A: Microsatellite instability and hMLH1 promoter hypermethylation in Richter's transformation of chronic lymphocytic leukemia. Leukemia 17: 411–415, 2003\nHo PJ, Campbell LJ, Gibson J, Brown R, Joshua D: The biology and cytogenetics of multiple myeloma. Rev Clin Exp Hematol 6: 276–300, 2002\nHampl J, Hall M, Mufti NA, Yao YM, MacQueen DB, Wright WH, Cooper DE: Upconverting phosphor reporters in immunochromatographic assays. Anal Biochem 288: 176–187, 2001\nCorstjens PL, Zuiderwijk M, Nilsson M, Feindt H, Sam Niedbala R, Tanke HJ: Lateral-flow and up-converting phosphor reporters to detect single-stranded nucleic acids in a sandwich-hybridization assay. Anal Biochem 312: 191–200, 2003\nTucker JD: FISH cytogenetics and the future of radiation biodosimetry. Radiation Protection Dosimetry 97: 55–60, 2001\nRamsey MJ, Moore II DH, Briner JF, Lee DA, Olsen LA, Senft JR, Tucker JD: The effects of age and lifestyle factors on the accumulation of cytogenetic damage as measured by chromosome painting. Mutation Res 338: 95–106, 1995\nMorgan WF: Is there a common mechanism underlying genomic instability, bystander effects and other nontargeted effects of exposure to ionizing radiation? Oncogene 22: 7094–7099, 2003\nPrise KM, Folkard M, Michael BD: A review of the bystander effect and its implications for low-dose exposure. Radiat Prot Dosimetry 104: 347–355, 2003\nElkahloun AG, Gaudet J, Robinson GS, Sgroi DC: In situ gene expression analysis of cancer using laser capture microdissection, microarrays and real time quantitative PCR. Cancer Biol Ther 1: 354–358, 2002\nDe Preter K, Vandesompele J, Heimann P, Kockx MM, Van Gele M, Hoebeeck J, De Smet E, Demarche M, Laureys G, Van Roy N, De Paepe A, Speleman F: Application of laser capture microdissection in genetic analysis of neuroblastoma and neuroblastoma precursor cells. Cancer Lett 197: 53–61, 2003",{"EN":1396},"This paper provides a broad overview of radiation cytogenetics that is divided into four sections. The first section provides a brief history of metaphase-based analyses for detecting and quantifying human exposure to ionizing radiation. The second section describes technologies for detecting cellular responses to radiation exposure other than DNA damage. 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Mutations in the RAS-MAPK, PI(3)K (phosphatidylinositol-3-OH kinase) signaling network correlate with poor survival in a population-based series of colon cancers. International Journal of Cancer, 122(10), 2255–2259.\nRao, B., Gao, Y., Huang, J., Gao, X., Fu, X., Huang, M., Wang, J., et al. (2011). Mutations of p53 and K-ras correlate TF expression in human colorectal carcinomas: TF downregulation as a marker of poor prognosis. International Journal of Colorectal Disease, 26(5), 593.\nChang, Y.-Y., Lin, P.-C., Lin, H.-H., Lin, J.-K., Chen, W.-S., Jiang, J.-K., Chang, S.-C., et al. (2016). Mutation spectra of RAS gene family in colorectal cancer. The American Journal of Surgery, 212, (3), 537–544.e3.\nCorso, G., Pascale, V., Flauti, G., Ferrara, F., Marrelli, D., & Roviello, F. (2013). Oncogenic mutations and microsatellite instability phenotype predict specific anatomical subsite in colorectal cancer patients. European Journal of Human Genetics, 21(12), 1383–1388.\nTortola, S., Marcuello, E., González, I., Reyes, G., Arribas, R., Aiza, G., Capella, G., et al. (1999). p53 and K-ras gene mutations correlate with tumor aggressiveness but are not of routine prognostic value in colorectal cancer. Journal of Clinical Oncology, 17(5), 1375–1375.\nKato, S., Iida, S., Higuchi, T., Ishikawa, T., Takagi, Y., Yasuno, M., Sugihara, K., et al. (2007). PIK3CA mutation is predictive of poor survival in patients with colorectal cancer. International Journal of Cancer, 121(8), 1771–1778.\nPalomba, G., Colombino, M., Contu, A., Massidda, B., Baldino, G., Pazzola, A., Cossu, A., et al. (2012). Prevalence of KRAS, BRAF, and PIK3CA somatic mutations in patients with colorectal carcinoma may vary in the same population: clues from Sardinia. Journal of Translational Medicine, 10, 178.\nPalomba, G., Cossu, A., Paliogiannis, P., Pazzola, A., Baldino, G., Scartozzi, M., Palmieri, G., et al. (2016). Prognostic role of KRAS mutations in Sardinian patients with colorectal carcinoma. Oncology Letters, 12(2), 1415–1421.\nInoue, Y., Saigusa, S., Iwata, T., Okugawa, Y., Toiyama, Y., Tanaka, K., Kusunoki, M., et al. (2012). The prognostic value of KRAS mutations in patients with colorectal cancer. Oncology Reports, 28(5), 1579–1584.\nHasegawa, S., Goto, S., Matsumoto, T., Hida, K., Kawada, K., Matsusue, R., Sakai, Y., et al. (2017). A multicenter phase 2 study on the feasibility and efficacy of neoadjuvant chemotherapy without radiotherapy for locally advanced rectal cancer. Annals of Surgical Oncology, 24(12), 3587–3595.\nThiebault, Q., Defossez, G., Karayan-Tapon, L., Ingrand, P., Silvain, C., & Tougeron, D. (2017). Analysis of factors influencing molecular testing at diagnostic of colorectal cancer. BMC Cancer, 17, 765.\nPang, X.-L., Li, Q.-X., Ma, Z.-P., Shi, Y., Ma, Y.-Q., Li, X.-X., Zhang, W., et al. (2017). 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Overexpression of MutL homolog 1 and MutS homolog 2 proteins have reversed prognostic implications for stage I–II colon cancer patients. Biomedical Journal, 40(1), 39–48.\nJones, R. P., Sutton, P. A., Evans, J. P., Clifford, R., McAvoy, A., Lewis, J., Malik, H. Z., et al. (2017). Specific mutations in KRAS codon 12 are associated with worse overall survival in patients with advanced and recurrent colorectal cancer. British Journal of Cancer, 116(7), bjc201737.\nPeng, J., Huang, D., Poston, G., Ma, X., Wang, R., Sheng, W., Cai, S., et al. (2017). The molecular heterogeneity of sporadic colorectal cancer with different tumor sites in Chinese patients. Oncotarget, 8(30), 49076–49083.\nGodai, T., Suda, T., Sugano, N., Tsuchida, K., Shiozawa, M., Sekiguchi, H., Miyagi, Y., et al. (2009). Identification of colorectal cancer patients with tumors carrying the TP53 mutation on the codon 72 proline allele that benefited most from 5-fluorouracil (5-FU) based postoperative chemotherapy. 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Cancer Genetics and Cytogenetics, 196(2), 133–139.\nNaguib, A., Cooke, J. C., Happerfield, L., Kerr, L., Gay, L. J., Luben, R. N., Arends, M. J., et al. (2011). Alterations in PTEN and PIK3CA in colorectal cancers in the EPIC Norfolk study: associations with clinicopathological and dietary factors. BMC Cancer, 11, 123.\nPhipps, A. I., Makar, K. W., & Newcomb, P. A. (2013). Descriptive profile of PIK3CA-mutated colorectal cancer in postmenopausal women. International Journal of Colorectal Disease, 28(12).\nDay, F. L., Jorissen, R. N., Lipton, L., Mouradov, D., Sakthianandeswaren, A., Christie, M., Sieber, O. M., et al. (2013). PIK3CA and PTEN gene and exon mutation-specific clinicopathologic and molecular associations in colorectal cancer. Clinical Cancer Research, 19(12), 3285–3296.\nIida, S., Kato, S., Ishiguro, M., Matsuyama, T., Ishikawa, T., Kobayashi, H., Sugihara, K., et al. (2012). PIK3CA mutation and methylation influences the outcome of colorectal cancer. Oncology Letters, 3(3), 565–570.\nNosho, K., Kawasaki, T., Ohnishi, M., Suemoto, Y., Kirkner, G. J., Zepf, D., Ogino, S., et al. (2008). PIK3CA mutation in colorectal cancer: relationship with genetic and epigenetic alterations. Neoplasia (New York, N.Y.), 10(6), 534–541.\nHerreros-Villanueva, M., Gomez-Manero, N., Muñiz, P., García-Girón, C., & del Corral, M. J. C. (2011). PIK3CA mutations in KRAS and BRAF wild type colorectal cancer patients. A study of Spanish population. Molecular Biology Reports, 38(2), 1347–1351.\nAndo, T., Sugai, T., Habano, W., Jiao, Y.-F., & Suzuki, K. (2005). Analysis of SMAD4\u002FDPC4 gene alterations in multiploid colorectal carcinomas. Journal of Gastroenterology, 40(7), 708–715.\nMiyaki, M., Iijima, T., Konishi, M., Sakai, K., Ishii, A., Yasuno, M., Hishima, T., Koike, M., Shitara, N., Iwama, T., Utsunomiya, J., et al. (1999). Higher frequency of Smad4 gene mutation in human colorectal cancer with distant metastasis. 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Prognostic value of loss of heterozygosity and sub-cellular localization of SMAD4 varies with tumor stage in colorectal cancer. Oncotarget, 8(12), 20198–20212.\nSui, X., Zhu, J., Tang, H., Wang, C., Zhou, J., Han, W., He, C., et al. (2015). p53 controls colorectal cancer cell invasion by inhibiting the NF-κB-mediated activation of Fascin. Oncotarget, 6(26), 22869–22879.\nNaxerova, K., Reiter, J. G., Brachtel, E., Lennerz, J. K., van de Wetering, M., Rowan, A., Jain, R. K., et al. (2017). Origins of lymphatic and distant metastases in human colorectal cancer. Science, 357(6346), 55–60.\nMao, C., Zhou, J., Yang, Z., Huang, Y., Wu, X., Shen, H., Chen, Q., et al. (2012). KRAS, BRAF and PIK3CA mutations and the loss of PTEN expression in Chinese patients with colorectal cancer. PLoS One, 7(5), e36653.",{"EN":3242},"The association between mutations of key driver genes and colorectal cancer (CRC) metastasis has been investigated by many studies. However, the results of these studies have been contradictory. Here, we perform a comprehensive analysis to screen key driver genes from the TCGA database and validate the roles of these mutations in CRC metastasis. Using bioinformatics analysis, we identified six key driver genes, namely APC, KRAS, BRAF, PIK3CA, SMAD4 and p53. Through a systematic search, 120 articles published by November 30, 2017, were included, which all showed roles for these gene mutations in CRC metastasis. A meta-analysis showed that KRAS mutations (combined OR 1.18, 95% CI 1.05–1.33) and p53 mutations (combined OR 1.49, 95% CI 1.23–1.80) were associated with CRC metastasis, including lymphatic and distant metastases. Moreover, CRC patients with a KRAS mutation (combined OR 1.29, 95% CI 1.13–1.47), p53 mutation (combined OR 1.35, 95% CI 1.06–1.72) or SMAD4 mutation (combined OR 2.04, 95% CI 1.41–2.95) were at a higher risk of distant metastasis. Subgroup analysis stratified by ethnic populations indicated that the BRAF mutation was related to CRC metastasis (combined OR 1.42, 95% CI 1.18–1.71) and distant metastasis (combined OR 1.51, 95% CI 1.20–1.91) in an Asian population. No significant association was found between mutations of APC or PIK3CA and CRC metastasis. In conclusion, mutations of KRAS, p53, SMAD4 and BRAF play significant roles in CRC metastasis and may be both potential biomarkers of CRC metastasis as well as therapeutic targets.",{"EN":3244},"Mutations of key driver genes in colorectal cancer progression and metastasis",{"VOID":3246},"10.1007\u002Fs10555-017-9726-5","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs10555-017-9726-5",[3249,3266,3281,3293,3306,3318,3330,3342,3354,3366,3390],{"id":3250,"sortIndex":1549,"researcher":18,"roles":3251,"affiliations":3252,"properties":3263},"d0d76f8a-9e06-4282-a7d1-18ec5d654c56",[1409],[3253],{"id":18,"sortIndex":19,"affiliation":3254,"properties":18},{"id":3255,"createTime":3256,"updateTime":3257,"relativeEntities":3258,"slug":3259,"properties":3260,"entityType":46,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"97b37ae4-0583-4b4e-af82-9e6e6426b730","2023-12-23T00:25:06.472+00:00","2024-09-02T02:18:09.716+00:00",[],"Department-of-Pathology-Key-Laboratory-of-Disease-Proteomics-of-Zhejiang-Province-School-of-Medicine-Zhejiang-University-Hangzhou-China",{"title":3261},{"VI":3262},"Department of Pathology, Key Laboratory of Disease Proteomics of Zhejiang Province, School of Medicine, Zhejiang University, Hangzhou, China",{"title":3264},{"VI":3265},"Honghe Zhang",{"id":3267,"sortIndex":1548,"researcher":18,"roles":3268,"affiliations":3269,"properties":3278},"5f3d96c0-94e1-4960-ab25-99aa6e136ec0",[1409],[3270],{"id":18,"sortIndex":19,"affiliation":3271,"properties":18},{"id":3272,"createTime":3273,"updateTime":3273,"relativeEntities":3274,"slug":18,"properties":3275,"entityType":46,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"b20bc300-d3ec-4e5e-ae8b-473a82c5b00d","2024-02-09T15:45:49.001+00:00",[],{"title":3276},{"VI":3277},"Department of Toxicology, School of Public Health, Zhejiang University, Hangzhou, China",{"title":3279},{"VI":3280},"Yihua Wu",{"id":3282,"sortIndex":104,"researcher":18,"roles":3283,"affiliations":3284,"properties":3290},"01980b62-8992-4476-9cc2-7c7105791936",[1409],[3285],{"id":18,"sortIndex":19,"affiliation":3286,"properties":18},{"id":3255,"createTime":3256,"updateTime":3257,"relativeEntities":3287,"slug":3259,"properties":3288,"entityType":46,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":3289},{"VI":3262},{"title":3291},{"VI":3292},"Wenjie Sun",{"id":3294,"sortIndex":3295,"researcher":18,"roles":3296,"affiliations":3297,"properties":3303},"f80abcc6-115f-4fd7-a794-672100d9d5af",7,[1409],[3298],{"id":18,"sortIndex":19,"affiliation":3299,"properties":18},{"id":3255,"createTime":3256,"updateTime":3257,"relativeEntities":3300,"slug":3259,"properties":3301,"entityType":46,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":3302},{"VI":3262},{"title":3304},{"VI":3305},"Enping Xu",{"id":3307,"sortIndex":19,"researcher":18,"roles":3308,"affiliations":3309,"properties":3315},"03d0a137-9b9c-495b-9d06-381ac8a79cda",[1409],[3310],{"id":18,"sortIndex":19,"affiliation":3311,"properties":18},{"id":3255,"createTime":3256,"updateTime":3257,"relativeEntities":3312,"slug":3259,"properties":3313,"entityType":46,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":3314},{"VI":3262},{"title":3316},{"VI":3317},"Dongdong 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K., Zhang, Y., & McDannold, N. J. (2016). Growth inhibition in a brain metastasis model by antibody delivery using focused ultrasound-mediated blood-brain barrier disruption. Journal of Controlled Release, 238, 281–288.",{"doi":3860},"10.1016\u002Fj.jconrel.2016.08.001",{"id":3862,"createTime":3863,"updateTime":3864,"relativeEntities":3865,"slug":3866,"properties":3867,"entityType":235,"verifyStatus":1401,"verifyTime":3864,"verifyNote":1403,"syncStatus":17,"languages":3876,"translateLanguages":18,"viewCount":19,"primaryUrl":3877,"fullTextUrl":18,"authors":3878,"publicationType":329,"publisherRelationship":3930,"citationCount":18,"citationInfo":18,"publishDate":3963,"publishYear":3964,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":3965,"isForceReanalyzing":1385},"e3dcbe19-3db6-4646-81a3-9ef62f59cc11","2024-04-16T19:12:57.545+00:00","2024-09-14T23:52:12.534+00:00",[],"Colorectal-carcinoma-in-black-and-white-race",{"keywords":3868,"abstract":3870,"title":3872,"doi":3874},{"EN":3869},"",{"EN":3871},"Worldwide, colorectal carcinoma (CRC) varies by race-ethnicity. The highest incidence occurs in whites of European descent. Rates in blacks of South Africa are much lower, but rise with migration to westernized countries, i.e. African Americans (blacks) in the US. In the US, CRC age-specific incidence rates increased dramatically with biologic aging for black and white men and women. For all ages, rates were slightly higher for black than for whites. Among whites, overall annual rates peaked in the 1980s then declined. Stage- and subsite-specific rate shifts suggested earlier detection of cancers through screening, particularly in the distal colon. Blacks have not experienced the same stage- and subsite temporal shifts, which were observed in whites. CRC racial differences have been attributed to biologic and\u002For non-biologic factors as well as to routine screening patterns. Racial variations demonstrate the need for a more comprehensive understanding of colorectal carcinogenesis, epidemiology, and colorectal screening patterns for low- and high-risk populations.",{"EN":3873},"Colorectal carcinoma in black and white race",{"VOID":3875},"10.1023\u002FA:1022264002228",[237],"https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1023\u002FA:1022264002228",[3879,3897,3917],{"id":3880,"sortIndex":19,"researcher":18,"roles":3881,"affiliations":3882,"properties":3894},"d30675fc-0b28-4e7d-ab44-2c5b1f2e69d8",[],[3883],{"id":3884,"sortIndex":19,"affiliation":3885,"properties":18},"9e008eac-d979-45bf-ac83-fac78f21ea76",{"id":3886,"createTime":3887,"updateTime":3888,"relativeEntities":3889,"slug":3890,"properties":3891,"entityType":46,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"07c86ecf-0b51-4124-a400-1917f5041517","2024-04-16T19:12:57.564+00:00","2025-06-11T20:48:33.323+00:00",[],"National-Cancer-Institute-Division-of-Cancer-Prevention-Gastrointestinal-Cancer-and-Other-Cancers-Research-Group-Bethesda",{"title":3892},{"EN":3893},"National Cancer Institute\u002FDivision of Cancer Prevention\u002FGastrointestinal Cancer and Other Cancers Research Group, Bethesda",{"title":3895},{"EN":3896},"William F. 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Carcinogenesis 21: 1971-1975, 2000",{"id":4255,"createTime":4256,"updateTime":4257,"relativeEntities":4258,"slug":4259,"properties":4260,"entityType":235,"verifyStatus":1401,"verifyTime":4257,"verifyNote":1403,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":4269,"fullTextUrl":18,"authors":4270,"publicationType":329,"publisherRelationship":4301,"citationCount":18,"citationInfo":18,"publishDate":4334,"publishYear":4335,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":18,"isForceReanalyzing":1385},"4c616344-a2d9-4d8a-a0e4-0a1e9dfaaab3","2024-02-12T00:06:15.767+00:00","2025-01-23T23:51:24.659+00:00",[],"Molecular-staging-of-head-and-neck-squamous-carcinoma",{"references":4261,"abstract":4263,"title":4265,"doi":4267},{"VOID":4262},"Beahrs OH, Henson DE, Hutter RVP, Myers MH (eds): Manual for staging of cancer. 3rd ed. Philadelphia: J.B. 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Am J Surg 168: 429–432, 1994\nKoch WM, Boule JO, Mao L, Hakim J, Hruban RH, Sidransky D: p53 gene mutations as markers of tumor spread in synchronous oral cancers. Arch Otolaryngol Head Neck Surg 120: 943–947, 1994",{"EN":4264},"The staging system of head and neck cancer is a Tumor-Node-Metastases system that was developed by the American Joint Committee on Cancer. The stage of the head and neck cancer defines the extent of the lesion and is determined by physical examination, radiologic studies, and pathologic examination. Accurate staging of head and neck cancer is critical since it will determine the treatment modalities used to cure the disease. Recent advances in the field of molecular genetics have allowed clinicians to detect occult cancer cells previously missed by physical examination and standard histopathologic techniques. Molecular assays are 500 times more sensitive in identifying cancer cells than standard techniques and provide more objective analyses with fewer sampling errors. Consequently, these techniques are currently being used to perform molecular staging of head and neck cancer patients. 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Faseb J, 3: 3, 2003",{"EN":4419},"In both the pre- and post-human genome sequencing eras, there has been an increase in the understanding of the molecular mechanisms influencing cellular sensitivity to DNA damaging agents such as ionizing radiation. Out of this work have arisen many cellular factors that could be specifically targeted, at the molecular level, to alter the functionality of a single protein or pathway involved in the response to radiation damage as a means to increase cell killing following radiation treatment. As such, there are many promising new combination radio-gene therapy approaches being developed and assessed in pre-clinical and clinical studies for several different malignancies. Combination of such modalities aims to increase the therapeutic index, giving rise to increased tumor cell killing with a simultaneous reduction in normal cell toxicity. Restricted delivery and\u002For targeting modalities combined with conformal radiotherapy regimes could provide significant local control of tumors, impeding their development into metastatic disease, which poses a greater challenge for palliative and curative treatments. This review will summarize current and novel gene therapy strategies that are being developed aimed at enhancing the effects of radiotherapy through the use of directed molecular targeting approaches.",{"EN":4421},"Enhanced radiation response through directed molecular targeting approaches",{"VOID":4423},"10.1023\u002FB:CANC.0000031767.30730.d1","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1023\u002FB:CANC.0000031767.30730.d1",[4426,4441],{"id":4427,"sortIndex":104,"researcher":18,"roles":4428,"affiliations":4429,"properties":4438},"faaa7974-c64a-459b-9763-d2720d16a655",[1409],[4430],{"id":18,"sortIndex":19,"affiliation":4431,"properties":18},{"id":4432,"createTime":4433,"updateTime":4433,"relativeEntities":4434,"slug":18,"properties":4435,"entityType":46,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"8f550ecd-7e9d-4df0-ad5b-93f923189ef6","2024-01-19T01:42:14.237+00:00",[],{"title":4436},{"VI":4437},"Department of Radiation Oncology and Molecular Radiation Sciences, The Johns Hopkins Oncology Center, Johns Hopkins University School of Medicine, Baltimore",{"title":4439},{"VI":4440},"Theodore L. 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