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  • American Association for Cancer Research (AACR)  (3)
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  • American Association for Cancer Research (AACR)  (3)
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  • 1
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Prevention Research Vol. 5, No. 11_Supplement ( 2012-11-01), p. A13-A13
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 5, No. 11_Supplement ( 2012-11-01), p. A13-A13
    Abstract: Introduction: Current study found that about one-third of the incidence of colorectal cancer have genetic related. Hereditary nonpolyposis colorectal cancer (HNPCC) and familial adenomatous polyposis (FAP) is the most common hereditary colorectal cancer type, each account 5% of the total colorectal cancers and about 1%. But addition to the two and several other more rare hereditary colorectal cancer, 20-25% of colorectal cancer have a clear cancer family history. The causal relationship of this genetic susceptibility population is not yet clear, but the diagnostic and intervention of this genetic susceptibility population is very important. High risk of genetic susceptibility screening, early detection, and early intervention, blocking susceptibility factor in colorectal cancer especially in colorectal adenoma, is an important way to improve the overall level of diagnosis and treatment. By comparing the proteomic difference of the patients with family history colorectal adenomas and no family history sporadic colorectal adenomas, we aim to find new markers to screen high-risk genetic susceptible populations, as a complement to the clinical diagnostic criteria of dependence on family history. Materials and Methods: A total of 90 serum samples were analyzed in this study, including 30 patients with family history colorectal adenomas, 30 no family history sporadic colorectal adenomas, and 30 healthy individuals. All samples were sex and age matched. Weak Cation Exchange magnetic beads kits were used to fractionate serum samples according to the manufacture's protocols. After binding and washing, the bound proteins and peptides were eluted from the magnetic beads and mixed with matrix and spotted on to targets. Protein profiles were generated using microflex MALDI-TOF MS (Bruker Daltonics). The protein profiles were then analyzed using bioinformatics tool Zhejiang University - ProteinChip Data Analysis System software to analyze the proteomic fingerprints and find the biomarkers. Results: The pattern to separate the patients with family history colorectal adenomas and sporadic colorectal adenomas by bioinformatics was constructed, which had a specificity of 93.3% and sensitivity of 100%, respectively. The model was comprised of 6 potential biomarkers with m/z of 4644, 2218, 2082, 2071, 4615 and 2210Da, respectively. The peak, 2218, 2082, 2071 and 2210Da, was Significantly (p & lt;0.01) highly expressed in family history colorectal adenomas compared to which in no family history patients; and the other 2 peaks were weakly expressed in family history colorectal adenomas. In order to confirm the correlation of these protein markers and the family history colorectal adenomas, the family history colorectal adenomas group is also compared to the healthy individuals. Significantly highly expressed in family history colorectal adenomas also was found in The peak, 2218, 2082, 2071 and 2210Da compared to which in healthy individuals, and the other 2 biomarkers 4644, 4615 also appeared to be expressed in an opposite way. Conclusions: Applying the proteomics approach, we found 6 peaks which differently express in patients with family history colorectal adenomas compare to sporadic colorectal adenomas and healthy individuals. In addition to the gene level detection, these proteins maybe are new colorectal cancer genetic susceptibility biomarkers, which can help to apply to screen high-risk genetic susceptible populations. Citation Format: Yu Jiekai, Huang Yanqin, Lin Chen, Yuan Ying, Zheng Shu. Applied the proteomics characteristics to detect the inherited colorectal adenomas. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr A13.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2422346-3
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  • 2
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 27, No. 9 ( 2021-05-01), p. 2663-2663
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 3
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 26, No. 2 ( 2020-01-15), p. 465-476
    Abstract: Pancreatic cancer remains one of the most lethal cancers, and late detection renders most tumors refractory to conventional therapies. Development of cancer prophylaxis may be the most realistic option for improving mortality associated with this disease. Here, we develop a novel individualized prophylactic and therapeutic vaccination regimen using induced pluripotent stem cells (iPSC), gene editing, and tumor-targeted replicating oncolytic viruses. Experimental Design: We created a Virus-Infected, Reprogrammed Somatic cell-derived Tumor cell (VIReST) regime. iPSCs from healthy cells were induced to pancreatic tumor cells using in situ gene editing via stable provision of KRasG12D and p53R172H tumor driver mutations. These cells were preinfected with oncolytic Adenovirus (AdV) as prime or Vaccinia virus (VV) as boost, to improve vaccine immunogenicity, prior to delivery of vaccines in a sequential regime to young KPC transgenic mice, genetically programmed to develop pancreatic cancer, to prevent and delay disease development. Results: Tumor cells preinfected with oncolytic AdV as prime or VV as boost were the best regime to induce tumor-specific immunity. iPSC-derived tumor cells were highly related in antigen repertoire to pancreatic cancer cells of KPC transgenic mice, suggesting that an individual's stem cells can provide an antigenically matched whole tumor cell vaccine. The VIReST vaccination primed tumor-specific T-cell responses, resulting in delayed disease emergence and progression and significantly prolonged survival of KPC transgenic mice. Importantly, this regime was well-tolerated and nontoxic. Conclusions: These results provide both proof of concept and a robust technology platform for the development of personalized prophylactic cancer vaccines to prevent pancreatic malignancies in at-risk individuals.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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