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1
Yang, Shiguang, Kui Zhao, Xiaodong Yang, and Chungen Xing. "Downregulation of Circ-PITHD1 Suppressed Colorectal Cancer via Glycolysis Inhibition through miR-590-5p/HK2 Axis." Evidence-Based Complementary and Alternative Medicine 2022 (October 14, 2022): 1–10. http://dx.doi.org/10.1155/2022/7696841.
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Colorectal cancer (CRC) is a frequent malignancy around the globe. Circular RNAs (circRNAs) are implicated in CRC development. Nevertheless, the regulatory mechanisms and biological functions regarding circRNAs in CRC progression are largely unclear. The present investigation employed next-generation sequencing (NGS) to study the abnormal circRNA expression in CRC tissues. The regulatory mechanism and targets were then analyzed by bioinformatics, luciferase reporter analysis, CCK8, colony formation, and Transwell migration. In vivo metastasis and tumorigenesis assays were conducted to elucidate circ-PITHD1 roles regarding CRC. The data showed that circ-PITHD1 expression increased in a CRC cell line and tissues, which indicated that circ-PITHD1 functioned in CRC progression. circ-PITHD1 downregulation inhibited CRC invasion and proliferation in the experiments. Luciferase reporter results confirmed that both miR-590-5p and hexokinase 2 (HK2) were circ-PITHD1 downstream targets. HK2 overexpression or miR-590-5p suppression reversed CRC cell proliferation and invasion after silencing of circ-PITHD1 by regulation of glycolysis. Taken together, this investigation discovered that circ-PITHD1 downregulation suppressed CRC progression by inhibiting glycolysis via the miR-590-5p/HK2 axis.
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Li, Minghao, Jianbin Zhuang, Di Kang, Yuzhuo Chen, and Weiliang Song. "Identification of circRNA circ-CSPP1 as a potent driver of colorectal cancer by directly targeting the miR-431/LASP1 axis." Open Life Sciences 16, no. 1 (January 1, 2021): 523–36. http://dx.doi.org/10.1515/biol-2021-0053.
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Abstract Colorectal cancer (CRC) is the third most common malignancy worldwide. Circular RNAs (circRNAs) have been implicated in cancer biology. The purpose of the current work is to investigate the precise parts of circRNA centrosome and spindle pole-associated protein 1 (circ-CSPP1) in the progression of CRC. Our data showed that circ-CSPP1 was significantly overexpressed in CRC tissues and cells. The knockdown of circ-CSPP1 attenuated cell proliferation, migration, invasion and promoted apoptosis in vitro and weakened tumor growth in vivo. circ-CSPP1 directly targeted miR-431, and circ-CSPP1 knockdown modulated CRC cell progression in vitro via upregulating miR-431. Moreover, LIM and SH3 protein 1 (LASP1) was a functional target of miR-431 in modulating CRC cell malignant progression. Furthermore, circ-CSPP1 in CRC cells functioned as a posttranscriptional regulator on LASP1 expression by targeting miR-431. Our present study identified the oncogenic role of circ-CSPP1 in CRC partially by the modulation of the miR-431/LASP1 axis, providing evidence for circ-CSPP1 as a promising biomarker for CRC management.
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Wang, Xiangjie, Shuang Liu, Bin Xu, Yabin Liu, Peng Kong, Changlin Li, and Binghui Li. "circ-SIRT1 Promotes Colorectal Cancer Proliferation and EMT by Recruiting and Binding to eIF4A3." Analytical Cellular Pathology 2021 (October 8, 2021): 1–11. http://dx.doi.org/10.1155/2021/5739769.
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Circular RNA (circRNA), a recently identified type of endogenous noncoding RNA, has been implicated in the occurrence and development of a variety of tumors; however, whether circ-SIRT1, derived from pre-mRNA of the parental SIRT1 gene, is involved in colorectal cancer (CRC) remains unknown, as do the potential underlying mechanisms. The expression of circ-SIRT1 in CRC cells and tissue was detected by RT-qPCR. Colony formation and Cell Counting Kit-8 assays were used to evaluate the effect of circ-SIRT1 knockdown on the proliferative ability of CRC cells. Wound healing and Transwell assays were used to assess the effect of circ-SIRT1 knockdown on the migratory and invasive capacity of CRC cells. RNA immunoprecipitation and RNA pull-down assays were employed to validate the binding of circ-SIRT1 to EIF4A3. Western blot was used to identify the changes in the expression of EIF4A3 and EMT-related proteins. The RT-qPCR results showed that circ-SIRT1 was highly expressed in CRC cells and tissue and was positively correlated with the depth of tumor invasion. Knocking down circ-SIRT1 inhibited the proliferation and invasion of CRC cells and EMT. We further found that EIF4A3 could bind to circ-SIRT1, and that overexpressing circ-SIRT1 decreased the abundance of EIF4A3 at the mRNAs of the EMT marker proteins N-cadherin and vimentin. Combined, our findings suggested that circ-SIRT1 regulates the expression of EMT-related proteins by preventing EIF4A3 recruitment to the respective mRNAs. Our results further indicate that circ-SIRT1 functions as an oncogene in CRC by promoting the proliferation, invasion, and EMT of CRC cells through the circ-SIRT1/EIF4A3/N-cadherin/vimentin pathway.
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Uchino, M., H. Ikeuchi, T. Noiguchi, K. Okabayashi, K. Futami, S. Tanaka, H. Ohge, et al. "P234 Differentiation of histopathological features between sporadic and colitis-associated colorectal cancer in a nationwide large cohort." Journal of Crohn's and Colitis 17, Supplement_1 (January 30, 2023): i387—i388. http://dx.doi.org/10.1093/ecco-jcc/jjac190.0364.
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Abstract Background Colitis-associated colorectal cancer (CAC) can develop in patients with inflammatory bowel disease, and histological features differ between CAC and sporadic colorectal cancer (CRC). Moreover, advanced CAC has a poorer prognosis than sporadic CRC. Therefore, we compared histopathological findings distinct from cancer stage between CAC and sporadic CRC to evaluate the features of CAC. Methods We reviewed the clinical and histopathological data collected from 43 institutions, including surgery and gastroenterology departments, in the Japanese Society for Cancer of the Colon and Rectum between 1983 and 2020. Patient characteristics were compared between ulcerative colitis (UC), Crohn’s disease (CD), and sporadic CRC. Comparisons were performed by using all collected data or propensity score-matched data. Results A total of 1,077 patients with UC-CAC, 297 with CD-CAC, and 136,927 with sporadic CRC were included in all collected data. Although the prevalence of well or moderately differentiated adenocarcinoma (G1:well differentiated and G2:moderately differentiated) decreased according to tumor progression in all diseases (p<0.01, figure1), the prevalence of G3,G4, including signet ring cell carcinoma, mucinous carcinoma, poorly differentiated adenocarcinoma, neuroendocrine carcinoma and squamous cell carcinoma, was significantly higher in CAC than in sporadic CRC. Based on propensity score-matched data for 982 patients with UC and 268 with CD, the prevalence of histopathological findings other than G1 and G2 was also significantly higher in CAC (figure2,3). At pT4, mucinous carcinoma occurred at a significantly higher rate in patients with CD (45/86 (52.3%)) than in those with sporadic CRC (13/88 (14.8%)) (p<0.01). Conclusion Malignant potential is higher in CAC than in sporadic CRC according to tumor progression, which may lead to the poor prognosis of CAC.
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Paszat, Lawrence, Rinku Sutradhar, Jill Tinmouth, Nancy Baxter, and Linda Rabeneck. "Interval Colorectal Cancers following Guaiac Fecal Occult Blood Testing in the Ontario ColonCancerCheck Program." Canadian Journal of Gastroenterology and Hepatology 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/4768728.
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Background.This work examines the occurrence of interval colorectal cancers (CRCs) in the Ontario ColonCancerCheck (CCC) program. We define interval CRC as CRC diagnosed within 2 years following normal guaiac fecal occult blood testing (gFOBT).Methods.Persons aged 50–74 who completed a baseline CCC gFOBT kit in 2008 and 2009, without a prior history of CRC, or recent colonoscopy, flexible sigmoidoscopy, or gFOBT, were identified. Rates of CRC following positive and normal results at baseline and subsequent gFOBT screens were computed and overall survival was compared between those following positive and normal results.Results.Interval CRC was diagnosed within 24 months following the baseline screen among 0.16% of normals and following the subsequent screen among 0.18% of normals. Interval cancers comprised 38.70% of CRC following the baseline screen and 50.86% following the subsequent screen. Adjusting for age and sex, the hazard ratio (HR) for death following interval cancer compared to CRC following positive result was 1.65 (1.32, 2.05) following the first screen and 1.71 (1.00, 2.91) following the second screen.Conclusion.Interval CRCs following gFOBT screening comprise a significant proportion of CRC diagnosed within 2 years after gFOBT testing and are associated with a higher risk of death.
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Cui, Xiaomin, Jiying Feng, Jian Wu, Xiaobao Zhang, and Mengyao Ding. "Propofol postpones colorectal cancer development through circ_0026344/miR-645/Akt/mTOR signal pathway." Open Medicine 16, no. 1 (January 1, 2021): 570–80. http://dx.doi.org/10.1515/med-2021-0254.
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Abstract Colorectal cancer (CRC) is responsible for thousands of slow and painful annual deaths. Propofol, an anesthetic, is commonly used in CRC surgery. The role of circularRNA0026344 (circ_0026344) in propofol-treated CRC remains unclear, which was further explored in this study. Real-time polymerase chain reaction (qPCR) was used to detect the expression of circ_0026344 and microRNA645 (miR-645) in CRC cells and normal cells. Western blot was devoted to testing the protein expression of phospho-protein kinase B (p-AKT), AKT, phospho-mammalian target of rapamycin (p-mTOR), and mTOR in CRC cells. Moreover, cell counting kit-8 (CCK8), colony formation, flow cytometry, and transwell assays were employed to assess the proliferation, apoptosis, and metastasis in CRC cells. Circinteractome online tool was applied to predict the combination between circ_0026344 and miR-645, which was further verified by dual-luciferase reporter system. circ_0026344 was lowly expressed and miR-645 was abundantly expressed in CRC cells. The relative protein expression of p-AKT/AKT and p-mTOR/mTOR was strikingly elevated by si-circ#1, which could be reversed by anti-miR-645 in propofol-treated CRC cells. circ_0026344 overexpression inhibited the proliferation and metastasis and promoted apoptosis in CRC cells. Propofol treatment induced the restraint in proliferation and metastasis and stimulation in apoptosis, which were allayed by si-circ#1; meanwhile, this alleviation could further be abolished by anti-miR-645 in CRC cells. Furthermore, circ_0026344 sponged miR-645 to inhibited Akt/mTOR signal pathway in propofol-treated CRC cells. Propofol postponed CRC process by circ_0026344/miR-645/Akt/mTOR axis. This finding might provide a possibility to improve the therapy of CRC with propofol.
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Itatani, Yoshiro, Takamasa Yamamoto, Cuiling Zhong, Alfredo A. Molinolo, Jane Ruppel, Priti Hegde, M. Mark Taketo, and Napoleone Ferrara. "Suppressing neutrophil-dependent angiogenesis abrogates resistance to anti-VEGF antibody in a genetic model of colorectal cancer." Proceedings of the National Academy of Sciences 117, no. 35 (August 19, 2020): 21598–608. http://dx.doi.org/10.1073/pnas.2008112117.
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We testedcis-ApcΔ716/Smad4+/−andcis-ApcΔ716/Smad4+/−KrasG12Dmice, which recapitulate key genetic abnormalities accumulating during colorectal cancer (CRC) tumorigenesis in humans, for responsiveness to anti-VEGF therapy. We found that even tumors incis-ApcΔ716/Smad4+/−KrasG12Dmice, although highly aggressive, were suppressed by anti-VEGF treatment. We tested the hypothesis that inflammation, a major risk factor and trigger for CRC, may affect responsiveness to anti-VEGF. Chemically induced colitis (CIC) incis-ApcΔ716/Smad4+/−andcis-ApcΔ716/Smad4+/−KrasG12Dmice promoted development of colon tumors that were largely resistant to anti-VEGF treatment. The myeloid growth factor G-CSF was markedly increased in the serum after induction of colitis. Antibodies blocking G-CSF, or its target Bv8/PROK2, suppressed tumor progression and myeloid cell infiltration when combined with anti-VEGF in CIC-associated CRC and in anti-VEGF-resistant CRC liver metastasis models. In a series of CRC specimens, tumor-infiltrating neutrophils strongly expressed Bv8/PROK2. CRC patients had significantly higher plasma Bv8/PROK2 levels than healthy volunteers and high plasma Bv8/PROK2 levels were inversely correlated with overall survival. Our findings establish Bv8/PROK2 as a translational target in CRC, in combination with anti-VEGF agents.
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Chatila, Walid Khaled, Henry S. Walch, Jamal Benhamida, Jaclyn Frances Hechtman, Francisco M. Barriga, Ritika Kundra, Dorina Ismalgeci, et al. "Genomic alterations in colitis-associated cancers in comparison to those found in sporadic colorectal cancer and present in precancerous dysplasia." Journal of Clinical Oncology 38, no. 4_suppl (February 1, 2020): 191. http://dx.doi.org/10.1200/jco.2020.38.4_suppl.191.
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191 Background: Patients with inflammatory bowel disease (IBD) [Crohn’s disease (CD) and ulcerative colitis (UC)] are at increased risk for small bowel or colorectal cancers (Colitis Associated Cancers, CAC). Currently CAC is treated the same as sporadic colorectal cancer (CRC) with significantly shorter overall survival for advanced CAC compared to matched patients with CRC. In a pilot series, we found that tumors developing in IBD have distinct genomic alterations (GA) with potential implications for early detection and treatment. We now extend this analysis and characterize the relationship of GA in synchronous dysplasia and cancer. Methods: 104 CAC (54 UC-associated and 50 CD-associated) were sequenced with targeted-exome sequencing of > 300 cancer-related genes. GA in CAC were compared to those reported for sporadic CRC. Whole exome sequencing was performed on paired mucosa, dysplasia and carcinoma samples obtained from 15 colectomy specimens; in these cases, expert pathology review confirmed normal appearing mucosa intervening between areas of dysplasia and CAC. Results: TP53 mutations (89%), MYC amplifications (24%), and cell cycle copy number alterations (20%) were significantly enriched in CAC compared to sporadic CRC, while APC alterations (21%) were significantly less common in CAC compared to sporadic CRC. Distinct GA in CAC consisted of IDH1 R132 mutations (7%) and FGFR pathway alterations (7%). While IDH1 R132 mutations and PI3K pathway alterations were more common in CD-associated CAC, MAPK ( BRAF/ MEK1) alterations were more common in UC-associated CAC. GA in CACs did not significantly vary by duration of preceding IBD. GA were often shared in dysplasia and carcinoma, despite normal-appearing intervening mucosa. GA involving TP53, APC, KRAS, and IDH1 mutations were identified in dysplasia and shared between CAC and dysplasia. Conclusions: CAC exhibit distinct GA compared to sporadic CRC with near universal TP53 mutation, increased copy number alterations involving transcription factors and cell cycle genes, and unique drivers. A field effect can be seen for GA between distant dysplasia and carcinoma, but many GA remain private to CAC.
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Yu, Hongbin, Chuang Dai, Wei Zhu, Yude Jin, and Chunhui Wang. "PFKFB3 Increases IL-1β and TNF-α in Intestinal Epithelial Cells to Promote Tumorigenesis in Colitis-Associated Colorectal Cancer." Journal of Oncology 2022 (August 16, 2022): 1–8. http://dx.doi.org/10.1155/2022/6367437.
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Colorectal cancer (CRC) is significantly correlated with inflammatory bowel disease, which usually manifests as chronic relapsing-remitting colitis. Phosphofructo-2-kinase/fructose-2,6-biophosphatase 3 (PFKFB3) can catalyze to produce fructose-2,6-bisphosphate and function as an oncogene. In this study, we revealed the function of PFKFB3 in colitis-associated CRC (CAC) and the potential mechanism. RT-qPCR and Western blot were utilized to detect the level of PFKFB3 expression. Increased PFKFB3 expression was observed in the mouse CAC model and CAC patient samples. We identified that overexpression of PFKFB3 in intestinal epithelial cells (IECs) could increase the proliferation, migration, and invasion of CRC cells by the coculture system. Mechanistically, overexpression of PFKFB3 induced phospho-p65 and promoted the expression of IL-1β and tumor necrosis factor alpha (TNF-α) in the development of colitis and CAC. In addition, PFK158, the PFKFB3 inhibitor, could reduce the CRC cell viability, migration, and invasion caused by PFKFB3 overexpression. In conclusion, overexpression of PFKFB3 promoted tumorigenesis in CAC by inducing phospho-p65 and expression of IL-1β and TNF-α. Our study suggested that PFKFB3 acted as a potential treatment target for CAC.
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Alsalman, Alhasan, Mohammad A. Al-Mterin, Ala Abu-Dayeh, Ferial Alloush, Khaled Murshed, and Eyad Elkord. "Associations of Complete Blood Count Parameters with Disease-Free Survival in Right- and Left-Sided Colorectal Cancer Patients." Journal of Personalized Medicine 12, no. 5 (May 18, 2022): 816. http://dx.doi.org/10.3390/jpm12050816.
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Colorectal cancer (CRC) is a leading cause of cancer-related deaths worldwide. Some complete blood count (CBC) parameters are found to be associated with CRC prognosis. In this study, ninety-seven pretreated CRC patients were included, and the patients were divided into two groups: left-sided and right-sided, depending on the anatomical location of the tumor. Based on clinicopathologic features including tumor budding, disease stages, and tumor anatomical location, levels of CBC parameters were compared, and disease-free survivals (DFS) were determined. There were differences between patients with different tumor budding scores for only three parameters, including red cell distribution width (RDW), numbers of platelets, and mean platelet volume (MPV). Furthermore, numbers of WBCs, monocytes, and MPV in CRC patients with early disease stages were higher than those with advanced stages. However, levels of eosinophil in CRC patients with advanced stages were higher than those with early stages. Depending on the tumor anatomical location, we observed that numbers of red blood cells (RBCs), hemoglobin (Hgb), and hematocrit (Hct) in CRC patients with left-sided tumors were higher than those with right-sided tumors. We found that low levels of MPV were associated with shorter DFS. However, high levels of eosinophils were associated with shorter DFS in all CRC patients. When patients were divided based on the tumor anatomical location, higher levels of MPV, MCHC, and Hgb were associated with better DFS in the left-sided but not right-sided CRC patients. However, left-sided, but not right-sided, CRC patients with high levels of eosinophil and RDW had shorter DFS. Furthermore, right-sided, but not left-sided, CRC patients with high levels of platelets tended to have a shorter DFS. Our data show that MPV and eosinophils could serve as potential prognostic biomarkers in pre-treatment CRC patients, regardless of the tumor anatomical location. Additionally, lower levels of MPV, MCHC, and Hgb, and high levels of eosinophils and RDW could be negative predictive biomarkers in left-sided CRC patients.
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Bocchetti, Marco, Maria Grazia Ferraro, Filippo Ricciardiello, Alessandro Ottaiano, Amalia Luce, Alessia Maria Cossu, Marianna Scrima, et al. "The Role of microRNAs in Development of Colitis-Associated Colorectal Cancer." International Journal of Molecular Sciences 22, no. 8 (April 12, 2021): 3967. http://dx.doi.org/10.3390/ijms22083967.
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Colorectal cancer (CRC) is the third most deadly cancer worldwide, and inflammatory bowel disease (IBD) is one of the critical factors in CRC carcinogenesis. IBD is responsible for an unphysiological and sustained chronic inflammation environment favoring the transformation. MicroRNAs (miRNAs) belong to a class of highly conserved short single-stranded segments (18–25 nucleotides) non-coding RNA and have been extensively discussed in both CRC and IBD. However, the role of miRNAs in the development of colitis-associated CRC (CAC) is less clear. The aim of this review is to summarize the major upregulated (miR-18a, miR-19a, miR-21, miR-31, miR-155 and miR-214) and downregulated (miR-124, miR-193a-3p and miR-139-5p) miRNAs in CAC, and their roles in genes’ expression modulation in chronic colonic-inflammation-induced carcinogenesis, including programmed cell-death pathways. These miRNAs dysregulation could be applied for early CAC diagnosis, to predict therapy efficacy and for precision treatment.
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Yu, Mi Ra, Hye Jung Kim, and Hae Ryoun Park. "Fusobacterium nucleatum Accelerates the Progression of Colitis-Associated Colorectal Cancer by Promoting EMT." Cancers 12, no. 10 (September 23, 2020): 2728. http://dx.doi.org/10.3390/cancers12102728.
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Recently, it has been reported that Fusobacterium nucleatum, a major pathogen involved in chronic periodontitis, may play an important role in colorectal cancer (CRC) progression. In addition, inflammatory bowel diseases such as ulcerative colitis and Crohn’s disease represent major predisposing conditions for the development of CRC, and this subtype of cancer is called colitis-associated cancer (CAC). Although the importance of F. nucleatum in CRC has attracted attention, its exact role and related mechanism in CAC progression remain unclear. In this study, we investigated the effects of F. nucleatum in experimental colitis induced with dextran sodium sulfate (DSS), which is a well-known colitis-inducing chemical, on the aggressiveness of CAC and its related mechanism in both in vitro and in vivo models. F. nucleatum synergistically increased the aggressiveness and epithelial–mesenchymal transition (EMT) characteristics of CRC cells that were treated with DSS compared to those in non-treated CRC cells. The role of F. nucleatum in CAC progression was further confirmed in mouse models, as F. nucleatum was found to significantly increase the malignancy of azoxymethane (AOM)/DSS-induced colon cancer. This promoting effect of F. nucleatum was based on activation of the EGFR signaling pathways, including protein kinase B (AKT) and extracellular signal-regulated kinase (ERK), and epidermal growth factor receptor (EGFR) inhibition significantly reduced the F. nucleatum-induced EMT alteration. In conclusion, F. nucleatum accelerates the progression of CAC by promoting EMT through the EGFR signaling pathway.
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Ozemir, Ibrahim Ali, Muhammed Ali Aydemir, Aman Gapbarov, Ozgur Ekinci, and Orhan Alimoglu. "The Effect of the Mucinous Component Presence on the Clinical Outcomes of Colorectal Cancer." Galician Medical Journal 29, no. 4 (December 1, 2022): E202246. http://dx.doi.org/10.21802/gmj.2022.4.6.
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Background. The effect of colorectal cancer (CRC) histological subtypes on the prognosis is still a controversial issue. We aimed to compare clinical findings, histopathologic data, and survival outcomes in CRC patients with classical and mucinous subtypes.
Methods. Patients who were operated on for CRC between 2010 and 2017 were included in the study. Patients were classified into two groups according to the presence of a mucinous component: mucinous adenocarcinoma (MAC) - mucinous component > 50% and classical adenocarcinoma (CAC). Clinical and histopathologic findings, recurrence, metastasis, and survival rates were compared.
Results. Data of the 484 CRC patients were documented. Sixty-nine patients (14.3%) were in the MAC group and 415 (85.7%) patients were in the CAC group. The mean age of patients with MAC and CAC was 63.4 ± 13.5 and 68.5 ± 12.7 years, respectively (p = 0.002). Proximal colon localization was found in 30 (43.5%) MAC patients and 123 (29.6%) CAC patients (p = 0.029). The number of patients with metastatic lymph nodes was higher in the MAC group (58% vs. 41.2%, p = 0.03). Nevertheless, there was no significant difference between the CAC and MAC groups in terms of disease-free survival (63.1% vs. 69.6%, p = 0.37) and disease-related mortality (23.6% vs. 23.2%, p = 0.94) over the follow-up period. Multivariate analysis showed that the presence of perineural invasion, patient’s age, and disease stage were associated with mortality in CRC patients.
Conclusions. MACs occurred at a younger age than CACs and were more likely localized in the proximal colon as compared to CACs. Despite increased lymph node metastasis in MAC patients, no statistical significance was detected in overall survival or disease-free survival. Multivariate analysis revealed that age, perineural invasion, and disease stage were relevant to mortality in CRC patients.
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Patterson, Jeanne Boland. "Canon 10 - CRC Credential—Certified Rehabilitation Counselors (CRC)." Journal of Applied Rehabilitation Counseling 18, no. 4 (December 1, 1987): 45–47. http://dx.doi.org/10.1891/0047-2220.18.4.45.
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Canon 10 of the Code of Professional Ethics contains rules which specifically address the conduct of counselors who hold the CRC designation. This article discusses the meaning of certification and the relationship between the certifying body and the professional associations. It also provides an overview of the implications of Canon 10 to certified rehabilitation counselors.
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Karousi, Paraskevi, Pinelopi I. Artemaki, Christina D. Sotiropoulou, Spyridon Christodoulou, Andreas Scorilas, and Christos K. Kontos. "Identification of Two Novel Circular RNAs Deriving from BCL2L12 and Investigation of Their Potential Value as a Molecular Signature in Colorectal Cancer." International Journal of Molecular Sciences 21, no. 22 (November 23, 2020): 8867. http://dx.doi.org/10.3390/ijms21228867.
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The utility of circular RNAs (circRNAs) as molecular biomarkers has recently emerged. However, only a handful of them have already been studied in colorectal cancer (CRC). The purpose of this study was to identify new circRNAs deriving from BCL2L12, a member of the BCL2 apoptosis-related family, and investigate their potential as biomarkers in CRC. Total RNA extracts from CRC cell lines and tissue samples were reversely transcribed. By combining PCR with divergent primers and nested PCR followed by Sanger sequencing, we were able to discover two BCL2L12 circRNAs. Subsequently, bioinformatical tools were used to predict the interactions of these circRNAs with microRNAs (miRNAs) and RNA-binding proteins (RBPs). Following a PCR-based pre-amplification, real-time qPCR was carried out for the quantification of each circRNA in CRC samples and cell lines. Biostatistical analysis was used to assess their potential prognostic value in CRC. Both novel BCL2L12 circRNAs likely interact with particular miRNAs and RBPs. Interestingly, circ-BCL2L12-2 expression is inversely associated with TNM stage, while circ-BCL2L12-1 overexpression is associated with shorter overall survival in CRC, particularly among TNM stage II patients. Overall, we identified two novel BCL2L12 circRNAs, one of which can further stratify TNM stage II patients into two subgroups with substantially distinct prognosis.
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Kelsen, David Paul, Vincent A. Miller, Laura H. Tang, Marinela Capanu, Sohail Balasubramanian, Jeffrey S. Ross, Philip J. Stephens, and Rona Yaeger. "Clinical and genomic alterations features of patients with advanced colitis associated cancers (CAC)." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): e15010-e15010. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e15010.
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e15010 Background: CAC are a catastrophic complication of inflammatory bowel disease. The spectrum of genomic alterations (GA) in CAC is different than that of sporadic colorectal cancer (CRC) (Yaeger et al PMID 27063727). While the prognosis for CAC patients (pts) may be worse than that of sporadic CRC pts, there is little data regarding outcome for metastatic CAC pts treated with standard chemotherapy regimens. We reviewed demographic features and clinical outcome for pts with metastatic CAC in the context of somatic tumor GA. Methods: We identified small and large bowel CAC cases seen at Memorial Sloan Kettering between 2003 and 2015 with tissue available for study. Hybrid capture based next-generation sequencing analysis of over 300 cancer-related genes was used to comprehensively characterize GA. The electronic medical record of each patient was reviewed. Demographic and clinical data was extracted and outcome reviewed in the context of somatic tumor GA. Results: Clinical features for 17 pts with metastatic CAC are shown below. All pts with initial stage III CAC received FOLFOX adjuvant therapy. First-line treatment for metastatic disease included FOLFOX/FOLFIRINOX/FU-LV in 10 previously untreated pts and FOLFIRI after adjuvant therapy. Median duration of survival from time of metastatic disease was 14.8 months, (95% CI 5.7-24.3;range 2-68+ months), substantially less than that expected for pts with Stage IV CRC. Only 4 patients survived for > 24 months. GA were identified in TP53 (87%) and KRAS (33%); potentially targetable alterations were found in 8 pts ( IDH1 (1), EML4-ALK(1), ERBB2 (1); FGFR1/2 (3); BRAF (1); PIK3CA(1). 2 pts received a targeted agent based on GA; 1 partial response to a FGFR inhibitor is ongoing. No patient had a hyper-mutated tumor. Conclusions: Metastatic CAC pts have an exceedingly poor prognosis, with survival well below that expected for sporadic CRC. BRAF mutations associated with poor outcome in sporadic CRC are rare in CAC. 47% of CAC pts had potentially targetable GA. [Table: see text]
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Friedland, Shai, Drew Watson, Zhen Zhang, Jennifer Y. Pan, Yu Chen, Ashish Nimgaonkar, Zulfiqar Gulzar, et al. "Evaluation of differential contribution of a circulating epithelial cell signal component in a multimodal colorectal neoplasia assay." Journal of Clinical Oncology 40, no. 16_suppl (June 1, 2022): e15527-e15527. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.e15527.
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e15527 Background: Multimodal diagnostic classifiers survey signals from multiple biological compartments and provide iterative, independent and interactive information. Detection of both CRC and AA is critical for noninvasive colorectal screening to improve overall survival and prevent the 2.5-5% annual transition of AA to CRC. FirstSight integrates clinically validated somatic variants from cfDNA and circulating epithelial cells (CECs) adjusting for age and sex. CECs provide information from both intrinsic factors of the adenoma and extrinsic factors such as adenoma microenvironment which facilitates early systemic entry. We sought to assess differential information from CEC signals for the detection of colorectal cancer and/or advanced adenoma (AA). Methods: Blood samples and colonoscopy pathology results were obtained from 438 asymptomatic screening subjects enriched for CRC/AA obtained from 15 US medical centers. The cohort included 18 CRCs and 64 AAs. Somatic variants from cfDNA were identified using NGS and qPCR. CECs were captured by the CellMax biomimetic platform (CMx) using high-avidity EpCAM antibody embedded in the CMx biochip and confirmed with immunostaining (DAPI: nucleus, CK20: epithelial cell and CD45: WBC). CMx platform’s AI/ML analyses of CEC images quantify stain intensities and cellular features. CEC derived signal GM1was evaluated for its predictive capability beyond somatic variants from cfDNA. Results: Genetic or epigenetic variants were not detected in 52% (33/64) of AA cases, limiting the sensitivity of these markers for early disease. However, distinct CEC signals have been identified that aid in the detection of subjects with CRC or AA, or conversely subjects with negative colonoscopies or non-advanced adenomas (nAA). Among them, a novel feature (referred to as GM1) derived from CEC signals was able to differentiate with statistical significance AA from negative/non-neoplastic findings or nAAs in study subjects with negative results in corresponding somatic variants from cfDNA (p < 0.0001). While targeted somatic variants from cfDNA performed well on CRC (17/18), they provided no predictive information for detection of AA for the 353 subjects which were negative for variants, GM1 provided 100.0% (33/33) sensitivity at 35.1% (112/319) specificity, showing its ability to rule out AA with high negative predictive value. Conclusions: Somatic variant detection modes of the First Sight multi-modal assay have high sensitivity for CRC and modest sensitivity for AA. We demonstrate that CEC signal GM1 of FirstSight provides significant independent information for the detection of CRC and AA beyond somatic variants from cfDNA. Additional CEC signals may further improve the sensitivity and specificity for detection of early-stage colorectal neoplasia. The GM1 CEC signal marker will need to be validated further in future studies.
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Tangka, Florence K. L., Sujha Subramanian, Sonja Hoover, Amy DeGroff, Djenaba Joseph, Faye L. Wong, and Lisa C. Richardson. "Economic Evaluation of Interventions to Increase Colorectal Cancer Screening at Federally Qualified Health Centers." Health Promotion Practice 21, no. 6 (September 29, 2020): 877–83. http://dx.doi.org/10.1177/1524839920954168.
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The Centers for Disease Control and Prevention (CDC) has a long-standing commitment to increase colorectal cancer (CRC) screening for vulnerable populations. In 2005, the CDC began a demonstration in five states and, with lessons learned, launched a national program, the Colorectal Cancer Control Program (CRCCP), in 2009. The CRCCP continues today and its current emphasis is the implementation of evidence-based interventions to promote CRC screening. The purpose of this article is to provide an overview of four CRCCP awardees and their federally qualified health center partners as an introduction to the accompanying series of research briefs where we present individual findings on impacts of evidence-based interventions on CRC screening uptake for each awardee. We also include in this article the conceptual framework used to guide our research. Our findings contribute to the evidence base and guide future program implementation to improve sustainability, increase CRC screening, and address disparities in screening uptake.
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Wang, Jue, Kang Ding, Yuhang Wang, Tingdong Yan, Yun Xu, Zirong Deng, Weiling Lin, et al. "Wumei Pill Ameliorates AOM/DSS-Induced Colitis-Associated Colon Cancer through Inhibition of Inflammation and Oxidative Stress by Regulating S-Adenosylhomocysteine Hydrolase- (AHCY-) Mediated Hedgehog Signaling in Mice." Oxidative Medicine and Cellular Longevity 2022 (July 26, 2022): 1–28. http://dx.doi.org/10.1155/2022/4061713.
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Wumei Pill (WMP) is a traditional Chinese herbal formulation and widely used to treat digestive system diseases in clinical. S-Adenosylhomocysteine hydrolase (AHCY) can catalyze the hydrolysis of S-adenosylhomocysteine to adenosine and homocysteine in living organisms, and its abnormal expression is linked to the pathogenesis of many diseases including colorectal cancer (CRC). A previous study reported that WMP could prevent CRC in mice; however, the underlying mechanisms especially the roles of AHCY in WMP-induced anti-CRC remain largely unknown. Here, we investigated the regulatory roles and potential mechanisms of AHCY in WMP-induced anti-CRC. WMP notably alleviated the azoxymethane/dextran sulfate sodium- (AOM/DSS-) induced colitis-associated colon cancer (CAC) in mice. Besides, WMP inhibited the inflammation and oxidative stress in AOM/DSS-induced CAC mice. AHCY was high expression in clinical samples of colon cancer compared to the adjacent tissues. WMP inhibited the AHCY expression in AOM/DSS-induced CAC mice. An in vitro study found that AHCY overexpression induced cell proliferation, colony formation, invasion, and tumor angiogenesis, whereas its knockdown impaired its oncogenic function. AHCY overexpression enhanced, while its knockdown weakened the inflammation and oxidative stress in colon cancer cells. Interestingly, WMP potently suppressed the hedgehog (Hh) signaling in AOM/DSS-induced CAC mice. A further study showed that AHCY overexpression activated the Hh signaling while AHCY knockdown inactivated the Hh signaling. Moreover, activation of the Hh signaling reversed the effect of AHCY silencing on inflammation and oxidative stress in vitro. In conclusion, WMP alleviated the AOM/DSS-induced CAC through inhibition of inflammation and oxidative stress by regulating AHCY-mediated hedgehog signaling in mice. These findings uncovered a potential molecular mechanism underlying the anti-CAC effect of WMP and suggested WMP as a promising therapeutic candidate for CRC.
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Kaviani, R., F. Y. Chou, C. B. He, and V. Marquez. "A95 ASSESSMENT OF BIRTH COHORT SCREENING OF CHRONIC HEPATITIS C IN COLORECTAL CANCER SCREENING PATIENTS IN BRITISH COLUMBIA." Journal of the Canadian Association of Gastroenterology 6, Supplement_1 (March 1, 2023): 51–52. http://dx.doi.org/10.1093/jcag/gwac036.095.
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Abstract Background Birth cohort screening of chronic hepatitis C (CHC) is recommended in British Columbia since 2018 for baby boomers born between 1945 to 1964, with an estimated provincial prevalence of 2.31%. Though there remained a gap in care following anti-hepatitis C positivity, resulting in reflexive ribonucleic acid (RNA) testing provincially. Dual screening of CHC in patients referred to colorectal (CRC) screening programs can provide an opportunity to link patients with healthcare professionals to ensure appropriate follow-up. Purpose We aimed to assess the uptake of CHC screening amongst CRC screening patients after the release of British Columbia’s birth cohort guidelines, both pre and post-COVID-19 pandemic. Method A retrospective review of patients referred to a CRC screening program in Vancouver from October 1st to December 31st, 2019, and December 1st – 31st, 2021, was performed. Collected data included demographics, liver disease history, and co-infection rates with hepatitis B (HBV) or human immunodeficiency virus (HIV). Dates of first-time hepatitis C antibody, RNA and viral load testing were gathered. Descriptive statistics were used to identify the proportion of screening and prevalence of CHC. Result(s) A total of 553 patients were referred for colonoscopy to the CRC screening program, of whom 458 (82.8%) patients were born between 1945 to 1964, and 273 (n=49%) were female. Among the 250 (45.2%) patients screened for CHC, 4 (0.72%) had positive anti-hepatitis C, all of whom were baby boomers. In 2019, 44% (n=183) of patients were screened for CHC; 78.7% (n=144) were screened before colonoscopy referral. In 2020, 48.6% (n=67) of patients were screened for CHC; 100% of cases were screened before colonoscopy referral. Conclusion(s) Birth cohort screening of CHC is underutilized in British Columbia. Dual screening of CHC at the time of referral to CRC screening provides a practical approach to linking patients to healthcare. Please acknowledge all funding agencies by checking the applicable boxes below None Disclosure of Interest None Declared
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Borisov, Alexey V., Olga A. Zakharova, Alisa A. Samarinova, Natalia V. Yunusova, Olga V. Cheremisina, and Yury V. Kistenev. "A Criterion of Colorectal Cancer Diagnosis Using Exosome Fluorescence-Lifetime Imaging." Diagnostics 12, no. 8 (July 24, 2022): 1792. http://dx.doi.org/10.3390/diagnostics12081792.
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This study was aimed to investigate the applicability of the exosome fluorescence-lifetime imaging microscopy (FLIM) for colorectal cancer (CRC) diagnosis. Differential ultra-centrifugation was used to extract exosomes from the blood plasma of 11 patients with colon polyps (CPs) and 13 patients with CRC at the T2-4, N0-3, and M0-1 stages. Analysis was performed using a two-photon FLIM device. In total, 165 and 195 FLIM images were recorded for the CP and CCR patient groups, respectively. Two classes of exosomes differentiated by autofluorescence average lifetime tm were discovered in the samples. The first class of exosomes with tm = (0.21 ± 0.06) ns was mostly found in samples from CRC patients. The second class with tm = (0.43 ± 0.19) ns was mostly found in samples from CP patients. The relative number of “CRC-associated” exosomes Nch in the FLIM dataset was shown to be very small for the CP patient group and large for the CRC patient group. This difference was statistically significant. Therefore, the suggested CRS diagnostics criterion can be as follows. If Nch > 0.5, the probability of CRC is high. If Nch < 0.3, the probability of CRC is low.
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Dénes, Márton István, Valentin Nădășan, Călin Molnar, Șerban Bancu, Cristian Oliviu Borz, and Zoltán Ábrám. "Is awareness enough to bring patients to colorectal screening?" Open Medicine 13, no. 1 (November 25, 2018): 528–33. http://dx.doi.org/10.1515/med-2018-0077.
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AbstractBackgroundThe aim of the study was to assess the awareness of colorectal cancer (CRC) patients about CRC screening methods and to investigate the relationship between awareness, socio-demographic characteristics and the stage in which patients with CRC are diagnosed.MethodsThe observational cross-sectional study included 275 CRC patients admitted between 2014 and 2016 to two surgical clinics from Tîrgu Mureş, Romania. Study variables were collected via face-to-face interview and from patients’ observation sheets.ResultsOnly 41.5% of the patients heard about cancer screening and 6.5% about specific CRC screening methods. Mass-media was the major source of information (85.1%) followed to a much lesser extent (14.9%) by family, friends, and colleagues. Health professionals did not contribute at all to informing patients about screening methods. Awareness about screening methods was statistically associated with the patients’ residence, age, and educational achievement, but not with the stage of CRC.ConclusionThe level of awareness of CRC screening methods was very low among the CRC patients included in the study but it could not predict the stage in which malignancy was diagnosed, suggesting that awareness alone is not enough to bring patients to undergo early CDC screening procedures.
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Hases, Linnea, Madeleine Birgersson, Rajitha Indukuri, Amena Archer, and Cecilia Williams. "Colitis Induces Sex-Specific Intestinal Transcriptomic Responses in Mice." International Journal of Molecular Sciences 23, no. 18 (September 8, 2022): 10408. http://dx.doi.org/10.3390/ijms231810408.
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There are significant sex differences in colorectal cancer (CRC), including in incidence, onset, and molecular characteristics. Further, while inflammatory bowel disease (IBD) is a risk factor for CRC in both sexes, men with IBD have a 60% higher risk of developing CRC compared to women. In this study, we investigated sex differences during colitis-associated CRC (CAC) using a chemically induced CAC mouse model. The mice were treated with azoxymethane (AOM) and dextran sodium sulfate (DSS) and followed for 9 and 15 weeks. We performed RNA-sequencing of colon samples from males (n = 15) and females (n = 15) to study different stages of inflammation and identify corresponding transcriptomic sex differences in non-tumor colon tissue. We found a significant transcriptome response to AOM/DSS treatment in both sexes, including in pathways related to inflammation and cell proliferation. Notably, we found a stronger response in males and that male-specific differentially expressed genes were involved in NFκB signaling and circadian rhythm. Further, an overrepresented proportion of male-specific gene regulations were predicted to be targets of Stat3, whereas for females, targets of the glucocorticoid receptor (Gr/Nr3c1) were overrepresented. At 15 weeks, the most apparent sex difference involved genes with functions in T cell proliferation, followed by the regulation of demethylases. The majority of sex differences were thus related to inflammation and the immune system. Our novel data, profiling the transcriptomic response to chemically induced colitis and CAC, indicate clear sex differences in CRC initiation and progression.
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Lung, M. S., A. Trainer, and I. Campbell. "Identification of novel CRC pathway genes in familial CRC." Annals of Oncology 27 (October 2016): vi2. http://dx.doi.org/10.1093/annonc/mdw362.07.
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S Mackenzie, John, and Lisa Adams. "Australian Biosecurity CRC for Emerging Infectious Diseases (AB-CRC)." Microbiology Australia 24, no. 2 (2003): 38. http://dx.doi.org/10.1071/ma03238.
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The Australian Biosecurity Cooperative Research Centre for Emerging Infectious Disease (AB-CRC) was a successful applicant under the Federal Government?s 2002 CRC programme, and will be formally established from July 2003. The aim of the AB-CRC is to protect Australia?s health, livestock, wildlife and economic resources by developing new capabilities to monitor, assess, predict and respond to emerging and exotic disease threats which impact on national and regional biosecurity. Emerging diseases are defined as those which are novel, previously unrecognised diseases, or those which are increasing in incidence or geographic range. The threats may be natural, accidental (such as an infected traveller) or deliberate (as in bioterrorism).
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Zhao, Lan, and Yi Pan. "SSCS: A Stage Supervised Subtyping System for Colorectal Cancer." Biomedicines 9, no. 12 (December 2, 2021): 1815. http://dx.doi.org/10.3390/biomedicines9121815.
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Colorectal cancer (CRC) is heterogeneous and deadly, and the exact cause of the disease is unknown. Recent progress indicated that CRC is not a single disease, but a group of diseases with significant heterogeneity. Three previous CRC subtyping systems: microsatellite instability (MSI), consensus molecular subtypes (CMS), and tumor-node-metastases (TNM) stage were evaluated for their molecular and clinical implications. Results suggested that the MSI and CMS systems are prognostic and predictive mostly in early-stage CRC. As the stage remains an influential factor for CRC subtype analysis, we developed a new subtyping system named stage supervised CRC subtypes (SSCS), in order to better stratify CRC biologically and clinically. Our subtyping system can be used to classify CRC patients into five subtypes (SSCS1-5). SSCS1 was found to have the highest frequency of MSI-H cases compared to the remaining four subtypes. SSCS2 had the most favorable prognosis, whereas the worst prognosis was seen in SSCS4. SSCS3 had cell cycle and metabolism-related gene sets upregulation, and SSCS5 subtype was enriched with amplicon-associated gene sets. Moreover, tumor-infiltrating fibroblast was found to be predictive for poor disease-free survival (DFS) only within the SSCS4 subtype. Conventional dendritic cells (cDC), on the contrary, were associated with favorable DFS in the SSCS3 subtype. Our study provides a new subtyping system SSCS, which can be used for better stratify CRC patients compared to current standards. Further exploration of the subtype-specific cell types has the potential to be novel therapies for CRC.
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Liu, Jinlin, and Honglin Wang. "Tumor-associated macrophages recruit CCR6+ regulatory T cells and promote the development of colorectal cancer via enhancing CCL20 production in mice (66.33)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 66.33. http://dx.doi.org/10.4049/jimmunol.186.supp.66.33.
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Abstract Background: Tumor-associated macrophages (TAMs) remodel the colorectal cancer (CRC) microenvironment. Yet, findings on the role of TAMs in CRC seem to be contradictory compared with other cancers. Regulatory T (Treg)-cells dominantly infiltrate CRC. However, the underlying molecular mechanism in which TAMs may contribute to the trafficking of Treg-cells to the tumor mass remains unknown. Methodology/Principal Findings: CRC was either induced by MNU and H. pylori or established by subcutaneous injection of mouse colorectal tumor cell line (CMT93) in mice. Recruitment of FoxP3GFP+ Treg-cells was assessed using the IVIS Imaging System. A role for macrophages in trafficking of Treg-cells and in the development of CRC was investigated in CD11b diphtheria toxin receptor (CD11b-DTR) transgenic mice in which macrophages can be selectively depleted. Treg-cells remarkably infiltrated solid tumor, and predominantly expressed the homing chemokine receptor (CCR) 6 in the induced CRC model. Macrophages produced a large amount of CCL20, the sole ligand of CCR6 when co-cultured with CRC cells. Injection of recombinant CCL20 into tumor sites promoted its development with a marked recruitment of Treg-cells. Conditional macrophage ablation decreased CCL20 levels, blocked Treg-cell recruitment and inhibited tumor growth in CD11b-DTR mice. Conclusions/Significance: TAMs recruit CCR6+ Treg-cells to tumor mass and promote its development via enhancing the production of CCL20 in a CRC mouse model.
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Sinaga, Sony Bahagia, Satria Yudha Prayogi, and Frans Ikorasaki. "Implementasi Cyclic Redudancy Check dalam Mendeteksi Bit Error pada Transmisi Data." Blend Sains Jurnal Teknik 1, no. 1 (June 14, 2022): 1–7. http://dx.doi.org/10.56211/blendsains.v1i1.32.
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Pengiriman informasi di dalam dunia telekomunikasi sering kali terjadi kesalahan terhadap data yang dikirim. Kesalahan tersebut disebabkan adanya gangguan pada level fisik, yaitu gangguan pada media saluran transmisi, seperti gangguan radiasi elektromagnetik, cakap silang, petir atau adanya gangguan akibat noise. Gangguan ini menyebabkan informasi yang diterima tidak sesuai dengan informasi yang dikirimkan. CRC adalah salah satu metode yang dapat digunakan untuk mendeteksi kesalahan pada sistem tersebut. Pada dasarnya CRC menggunakan perhitungan matematika terhadap sebuah bilangan yang disebut checksum (disebut juga nilai CRC), yang dibuat berdasarkan total bit yang akan ditransmisikan. Untuk mempermudah proses perhitungan nilai CEC maka dibuatlah suatu langkah atau algoritma yang dapat dimplementasikan kedalam bentuk software (bahasa pemrograman). Dalam penelitian ini dibuat suatu algoritma yang menggunakan CRC, dan mengimplementasikannya ke dalam bahasa pemrograman Visual Basic.
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Frigerio, S., J. Saris, R. Franco Fernandez, P. Koelink, M. van Roest, M. Wildenberg, G. D'Haens, and J. Grootjans. "P096 Characterization of suppressive immune cell subsets in mouse models of colitis-associated colorectal cancer." Journal of Crohn's and Colitis 17, Supplement_1 (January 30, 2023): i260. http://dx.doi.org/10.1093/ecco-jcc/jjac190.0226.
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Abstract Background Chronic colonic inflammation in inflammatory bowel disease (IBD) patients increases the risk of colitis-associated cancer (CAC). Cancer development in CAC is different from that observed in sporadic colorectal cancer (CRC). Most studies have focused on the role of pro-inflammatory immune cell subsets in CAC, yet it is becoming increasingly clear that immunosuppression may also drive cancer progression. We hypothesize that emergence of immunosuppressive cell subsets as a result of chronic intestinal inflammation, dampens anti-tumor immune responses and accelerates the development of CAC. Methods To simulate cancer formation in the background of chronic inflammation, mice were treated with azoxymethane (AOM) followed by three cycles of dextran sodium sulphate (DSS). Apc Min/+ mice treated with AOM were used to model sporadic CRC. After 10 weeks, immune cells from the proximal and distal colonic lamina propria, mesenteric lymph nodes (MLNs) and tumors were obtained for microscopy analyses and processed to obtain single cell suspensions for flow cytometry. Immune cell populations were studied by conventional flow cytometry and immunofluorescence. Results We observed a significant increase in absolute numbers of PD1+CTLA4+TIM3+ ‘exhausted’ CD4+ T cells in the lamina propria from proximal colons in CAC mice as compared to sporadic CRC mice. Interestingly, these numbers showed a positive correlation with the inflammation score in AOM/DSS, demonstrating that chronic inflammation is associated with the emergence of ‘exhausted’ T cells. In addition, we observed a trend to higher numbers of M2-like (MHCII-CD206+) suppressive macrophages and CD4+FoxP3+ regulatory T cells (Tregs) in tumors from CAC mice compared to sporadic CRC. When analysing T cell immune responses in the MLNs, we found a significant decrease in the ratio IFNγ/IL10-producing CD8+ T cells in CAC mice as compared to CRC mice, suggesting a shift towards an anti-inflammatory T cell response in CAC. Conclusion In summary, suppressive immune cell subsets were increased in colonic mucosa and tumors from CAC mice as a result of chronic inflammation, which may be associated with the development of dysplasia. Further functional studies are necessary to prove the role of suppressive immune subsets in IBD-associated dysplasia- and carcinoma progression.
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Tupling, R., and H. Green. "Silver ions induce Ca2+ release from the SR in vitro by acting on the Ca2+ release channel and the Ca2+ pump." Journal of Applied Physiology 92, no. 4 (April 1, 2002): 1603–10. http://dx.doi.org/10.1152/japplphysiol.00756.2001.
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Silver nitrate (AgNO3) is a sulfhydryl oxidizing agent that induces a biphasic Ca2+ release from isolated sarcoplasmic reticulum (SR) vesicles by presumably oxidizing critical sulfhydryl groups in the Ca2+ release channel (CRC), causing the channel to open. To further examine the effects of AgNO3 on the CRC and the Ca2+-ATPase, Ca2+ release was measured in muscle homogenates prepared from rat hindlimb muscle using indo 1. Cyclopiazonic acid (CPA) and ruthenium red (RR) were used to inhibit the Ca2+-ATPase and block the CRC, respectively, before inducing Ca2+ release with both AgNO3 and 4-chloro- m-cresol (4-CMC), a releasing agent specific for the CRC. With AgNO3 and CPA, the early rapid rate of release (phase 1) was increased ( P < 0.05) by 42% (314 ± 5 vs. 446 ± 39 μmol · g protein−1 · min−1), whereas the slower, more prolonged rate of release (phase 2) was decreased ( P < 0.05) by 72% (267 ± 39 vs. 74 ± 7.7 μmol · g protein−1 · min−1). RR, in combination with AgNO3, had no effect on phase 1 ( P > 0.05) (314 ± 51 vs. 334 ± 43 μmol · g protein−1 · min−1) and decreased phase 2 ( P < 0.05) by 65% (245 ± 34 vs. 105 ± 8.2 μmol · g protein−1 · min−1). With 4-CMC, CPA had no effect ( P > 0.05) on either phase 1 or 2. With addition of RR, phase 1 was reduced ( P < 0.05) by 59% (2,468 ± 279 vs. 1,004 ± 87 μmol · g protein−1 · min−1), and RR completely blocked phase 2. Both AgNO3 and 4-CMC fully inhibited Ca2+-ATPase activity measured in homogenates. These findings indicate that AgNO3, but not 4-CMC, induces Ca2+ release by acting on both the CRC and the Ca2+-ATPase.
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Li, Junshu, Xiaolan Su, Lei Dai, Na Chen, Chao Fang, Zhexu Dong, Jiamei Fu, et al. "Temporal DNA methylation pattern and targeted therapy in colitis-associated cancer." Carcinogenesis 41, no. 2 (December 5, 2019): 235–44. http://dx.doi.org/10.1093/carcin/bgz199.
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Abstract DNA methylation plays a crucial role in the pathogenesis of various diseases, including colorectal cancer (CRC). However, the global and temporal DNA methylation pattern during initiation and progression of colitis-associated cancer (CAC) are still unknown, including the potential therapeutic strategy of targeting methylation for CAC. In the present study, the global DNA methylation pattern was determined at different time points during CAC using DNA methylation sequencing, followed by the Starburst plot integrating alterations and potential functional prediction analysis. After demonstrating the regulatory role of DNA methyltransferases (DNMTs) on the expression of hub-genes in CRC cells, DNMT inhibitors were administered to treat CAC mice. Our results indicated that 811 genes were hypermethylated at different time points during initiation and progression of CAC. Genes that were downregulated and hypermethylated during CAC, including hub-genes BAD and inositol polyphosphate phosphatase-like 1 (INPPL1), were involved in MAPK signaling pathways, kit receptor signaling pathways, apoptosis and EGF/EGFR signaling pathways. Upregulated DNMTs (DNMT1, DNMT3A and DNMT3B) mediated downregulation and hypermethylation of BAD and INPPL1 in CAC and CRC cells. Low doses of DNMT inhibitors (decitabine (DAC) and azacitidine (AZA)) exerted efficient antitumor effects in CAC, accompanied with upregulation of BAD and INPPL1 expression, and apoptosis induction. In summary, the present study demonstrates the temporal DNA methylation pattern during CAC and provides a novel therapeutic strategy for treating this disease.
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Krome, Susanne. "Magenkarzinom und CRC." Onkologische Welt 12, no. 04 (September 2021): 256. http://dx.doi.org/10.1055/a-1350-5249.
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Kolorektale Karzinome (CRC) stellen mit 1–4 % die häufigsten konkomitanten Tumoren von Magenkarzinomen dar. Deshalb empfehlen Leitlinien bei Erstdiagnosen eines Magenkarzinoms den präoperativen Ausschluss von CRC. Nach der Gastrektomie kamen in der retrospektiven Fall-Kontroll-Studie CRC-Vorläuferläsionen häufiger vor. Gweon et al. schlagen deshalb die Koloskopie als festen Bestandteil auch im Nachsorgeprogramm vor.
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Ather, Hafiz Mughees, Muhammad Sarfraz, and Touseef Anwaar. "COLORECTAL CANCER (CRC)." Professional Medical Journal 23, no. 04 (April 10, 2016): 364–69. http://dx.doi.org/10.29309/tpmj/2016.23.04.1490.
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Colorectal cancer (CRC) is a common cancer. It has got significant morbidity andmortality. It is a common malignancy. Obesity is defined as BMI equal or above 25.1 kg/m2.Obesity is associated with an increased risk of developing CRC and poor prognosis in patientswith colorectal cancer. We conducted a study on 414 patients to look for correlation of obesitywith T, N, M and DUKES stage and frequency of obesity in CRC patients. Period: It involvedall CRC cases presented between 2004 to 2009. Methods: It was a single center retrospectivechart review. Total patient were 414. Data was collected on Performa and analyzed on SPSSversion 19. Results: Out of 414 patients males were 243 (58.7%) and females were 171 (41.3%).Mean age was 56 years. It was 57.7 years for males and 54.6 years for females. 221 patientswere obese. 123 patients presented in advanced DUKES stage. Mean BMI was 26 and meanCEA level was 76.60. 134 patients presented in advanced T stage (T3 and T4). 20% patientswith positive polyp history were obese while 80% patients with positive polyp history were nonobese. Majority of patients with family history of CRC, previous history of IBD, smoking andprevious colonoscopy were non obese. Abdominal pain, abdominal distension, constipation,bleeding per rectum and fever were more common in obese patients but this difference was notstatistically significant. About 56% of patients with abdominal pain and abdominal distensionwere obese and about 59% of patients with constipation and bleeding per-rectum were obese.About 65% of diabetic and hypertensive patients were obese (P value 0.01, 0.01) while 70%patients with coronary artery disease were obese. Conclusion: CRC affects more males andadvanced age group. Obese CRC patients are more than non-obese patients but obesity is notassociated with advanced stage of disease. Co-morbidities like diabetes mellitus, hypertensionare more common in obese CRC patients.
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Albertengo, G., and R. Sisto. "Parallel CRC generation." IEEE Micro 10, no. 5 (October 1990): 63–71. http://dx.doi.org/10.1109/40.60527.
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Campobello, G., G. Patane, and M. Russo. "Parallel crc realization." IEEE Transactions on Computers 52, no. 10 (October 2003): 1312–19. http://dx.doi.org/10.1109/tc.2003.1234528.
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Thomas, Hugh. "CRC endothelial regulation." Nature Reviews Gastroenterology & Hepatology 13, no. 12 (October 26, 2016): 682. http://dx.doi.org/10.1038/nrgastro.2016.180.
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Rees, D. A. "Booth leaves CRC." BMJ 297, no. 6643 (July 23, 1988): 291. http://dx.doi.org/10.1136/bmj.297.6643.291.
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Peckham, M. "Booth leaves CRC." BMJ 297, no. 6647 (August 20, 1988): 554. http://dx.doi.org/10.1136/bmj.297.6647.554.
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Papamichael, Demetris. "SIOG CRC GUIDELINES." Journal of Geriatric Oncology 5 (July 2014): S7. http://dx.doi.org/10.1016/j.jgo.2014.06.047.
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Thomas, Tim. "CRC malignancy continuum." Nature Cancer 3, no. 12 (December 20, 2022): 1439. http://dx.doi.org/10.1038/s43018-022-00451-5.
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Cremer, A., P. Demetter, M. De Vos, J. F. Rahier, F. Baert, T. Moreels, E. Macken, E. Louis, S. Vermeire, and D. Franchimont. "DOP37 Neoplastic lesions outside diseased area in inflammatory bowel disease patients: A national cohort study." Journal of Crohn's and Colitis 14, Supplement_1 (January 2020): S074—S075. http://dx.doi.org/10.1093/ecco-jcc/jjz203.076.
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Abstract Background Patients with inflammatory bowel diseases (IBD) are at increased risk of dysplasia and colitis-associated cancer (CAC). The presentation of (pre)neoplastic lesions (low-grade dysplasia (LGD), high-grade dysplasia (HGD) or colorectal cancer (CRC) is reported to vary depending if the lesions are located inside disease area (IDA) or outside diseased area (ODA). The primary aim was to analyse the characteristics and prognostic of IDA compared with ODA neoplastic lesions in a large cohort of IBD patients. Methods We performed a multicentre retrospective pathological data collection from 7 tertiary referral regional or academic IBD centres in Belgium. Clinical, endoscopic and pathological data were retrieved through retrospective electronic chart review. From the IBD pathology databases, 1183 colorectal lesions were identified in 541 IBD patients: 415 developed dysplasia (77%) and 126 CRC (23%) during their follow-up. Biopsies and surgical specimen were centrally reviewed by an expert IBD pathologist to confirm the diagnosis of dysplasia and/or CRC. Results Demographic and clinical variables of the study population are summarised in Table 1. More patients with IDA lesions had HGD (9%) or CAC (27%) during their follow-up compared with the group of patients with ODA lesions (3% of HGD and 11% of CRC) (p < 0,0001). Mortality was higher in patients with IDA than in those with ODA lesions (p < 0.05). When comparing IBD patients with IDA lesions and CAC (=111) to those with ODA lesions and sporadic CRC (n = 15), median age at IBD diagnosis was lower (29 (IQR:22–49) vs. 41(IQR:28–54) years; p = 0.0001). Characteristics of the 1183 neoplastic lesions are summarised in Table 2. IDA lesions were more frequently non-visible, non-polypoid and ≥ 1 cm than ODA lesions (p < 0.0001). ODA sporadic CRC was more frequently located in the right colon compared with IDA CAC (5/16 (31%) vs. 21/133 (16%), p < 0.01). Conclusion Neoplastic lesions outside the diseased area were more likely to be visible, polypoid, < 1cm, in the right colon and diagnosed at endoscopy than inside disease area lesions. A lower prevalence of HGD and Cancer were reported with neoplastic lesions outside the diseased area.
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Stolfi, Carmine, Eleonora Franzè, Ivan Monteleone, Roberta Caruso, Luana Franceschilli, Pierpaolo Sileri, Giuseppe S. Sica, et al. "2-Methoxy-5-amino-N-hydroxybenzamide, a derivative of mesalamine, inhibits colon cancer cell growth through cyclo-oxygenase-2-dependent and -independent mechanisms." Clinical Science 123, no. 5 (May 16, 2012): 295–306. http://dx.doi.org/10.1042/cs20110556.
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COX-2 (cyclo-oxygenase-2) and PGE2 (prostaglandin E2) play a key role in sustaining CRC (colorectal cancer) cell growth and survival. Indeed, the use of agents targeting the COX-2/PGE2 axis has been associated with a reduction in the development of CRC in both humans and murine models of colon carcinogenesis. In the present study, we investigated whether 2-methoxy-5-amino-N-hydroxybenzamide (herein termed 2-14), a derivative of mesalamine that inhibits CRC cell growth both in vitro and in vivo, negatively regulates COX-2/PGE2 expression in CRC cells and assessed whether the 2-14-mediated anti-neoplastic effect is strictly dependent on the inhibition of this pathway. Our results show that 2-14 blocks the growth and enhances the death of HT-115, a CRC cell line overexpressing COX-2, and that these effects associate with inhibition of COX-2 but not COX-1. 2-14 also down-regulates TNFα (tumour necrosis factor α)-induced COX-2 in HT-29 cells as well as COX-2/PGE2 expression in ex vivo cultures of human CRC explants. Similarly, 2-14 reduces COX-2, but not COX-1, in tumoural areas developing in a mouse model of CAC (colitis-associated colon cancer). Finally, we show that 2-14 exhibits in vitro and in vivo anti-mitogenic effects in DLD-1, a COX-deficient CRC cell line. Taken together, these results suggest that 2-14 inhibits CRC cell growth through COX-2-dependent and -independent mechanisms.
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Lin, Anqi, Hongman Zhang, Peng Luo, and Jian Zhang. "Age, sex, and specific gene mutations affect the effects of immune checkpoint inhibitors in colorectal cancer." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e16103-e16103. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e16103.
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e16103 Background: The effect of age and sex on the prognosis of colorectal cancer (CRC) patients treated with immune checkpoint inhibitors (ICIs) has been controversial, and the effect of specific gene mutations on the prognosis of patients treated with ICIs remains to be explored. Based on detailed clinical and genetic data, this study analyzed the influence of the above factors on the overall survival (OS) of CRC patients after ICI treatment and explored the influencing mechanism of various prognostic factors. Methods: We performed survival prognostic correlation analysis and bioinformatics analysis on the clinical CRC cohort receiving ICIs published by Samstein et al. and the clinical and genetic data from The Cancer Genome Atlas (TCGA)-CRC dataset, including immunogenicity and immunosignature analysis, DNA damage response and repair (DDR) pathway analysis, and gene set enrichment analysis (GSEA). Results: Both clinical characteristics and specific gene mutations may be prognostic factors for ICI treatment in CRC patients. Mutation count > 11 (tumor mutation burden (TMB)-high), age > 65, male, RNF43, CREBBP, NOTCH3, PTCH1, CIC, DNT1, and SPEN mutant (MT) were associated with longer OS, while APC-mMT and TP53-MT were significantly correlated with shorter OS. The reason why protective prognostic markers provide better survival benefits to CRC patients may be related to factors such as higher immunogenicity, highly infiltrated immunoactive cells and active immunoactive pathways. Conclusions: Our study is the first to elucidate comprehensive prognostic factors for the treatment of ICIs in CRC patients, from clinical characteristics such as age and sex to specific gene mutations, providing new ideas for immunotherapy in CRC.
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Liu, Chao, Ruiqi Liu, Bojun Wang, Jie Lian, Yang Yao, Haoxiu Sun, Chunhui Zhang, et al. "Blocking IL-17A enhances tumor response to anti-PD-1 immunotherapy in microsatellite stable colorectal cancer." Journal for ImmunoTherapy of Cancer 9, no. 1 (January 2021): e001895. http://dx.doi.org/10.1136/jitc-2020-001895.
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BackgroundImmune checkpoint inhibitors (ICIs), including anti-PD-1 therapy, have limited efficacy in patients with microsatellite stable (MSS) colorectal cancer (CRC). Interleukin 17A (IL-17A) activity leads to a protumor microenvironment, dependent on its ability to induce the production of inflammatory mediators, mobilize myeloid cells and reshape the tumor environment. In the present study, we aimed to investigate the role of IL-17A in resistance to antitumor immunity and to explore the feasibility of anti-IL-17A combined with anti-PD-1 therapy in MSS CRC murine models.MethodsThe expression of programmed cell death-ligand 1 (PD-L1) and its regulation by miR-15b-5p were investigated in MSS CRC cell lines and tissues. The effects of miR-15b-5p on tumorigenesis and anti-PD-1 treatment sensitivity were verified both in vitro and in colitis-associated cancer (CAC) and APCmin/+murine models. In vivo efficacy and mechanistic studies were conducted using antibodies targeting IL-17A and PD-1 in mice bearing subcutaneous CT26 and MC38 tumors.ResultsEvaluation of clinical pathological specimens confirmed thatPD-L1mRNA levels are associated with CD8+ T cell infiltration and better prognosis. miR-15b-5p was found to downregulate the expression of PD-L1 at the protein level, inhibit tumorigenesis and enhance anti-PD-1 sensitivity in CAC and APCmin/+CRC models. IL-17A led to high PD-L1 expression in CRC cells through regulating the P65/NRF1/miR-15b-5p axis. Combined IL-17A and PD-1 blockade had efficacy in CT26 and MC38 tumors, with more cytotoxic T lymphocytes cells and fewer myeloid-derived suppressor cells in tumors.ConclusionsIL-17A increases PD-L1 expression through the p65/NRF1/miR-15b-5p axis and promotes resistance to anti-PD-1 therapy. Blocking IL-17A improved the efficacy of anti-PD-1 therapy in MSS CRC murine models. IL-17A might serve as a therapeutic target to sensitize patients with MSS CRC to ICI therapy.
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Lai, Chi-Yu, Kun-Yun Yeh, Bi-Feng Liu, Tzu-Ming Chang, Chuan-Hsun Chang, Yung-Feng Liao, Yi-Wen Liu, and Guor Mour Her. "MicroRNA-21 Plays Multiple Oncometabolic Roles in Colitis-Associated Carcinoma and Colorectal Cancer via the PI3K/AKT, STAT3, and PDCD4/TNF-α Signaling Pathways in Zebrafish." Cancers 13, no. 21 (November 6, 2021): 5565. http://dx.doi.org/10.3390/cancers13215565.
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Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide. Patients with inflammatory bowel disease (IBD) have a high risk of developing CRC. Inflammatory cytokines are regulated by complex gene networks and regulatory RNAs, especially microRNAs. MicroRNA-21 (miR-21) is amongst the most frequently upregulated microRNAs in inflammatory responses and cancer development. miR-21 has become a target for genetic and pharmacological regulation in various diseases. However, the association between inflammation and tumorigenesis in the gut is largely unknown. Hence, in this study, we generated a zebrafish model (ImiR-21) with inducible overexpression of miR-21 in the intestine. The results demonstrate that miR-21 can induce CRC or colitis-associated cancer (CAC) in ImiR-21 through the PI3K/AKT, PDCD4/TNF-α, and IL-6/STAT3 signaling network. miR-21 activated the PI3K/AKT and NF-κB signaling pathways, leading to initial inflammation; thereafter, miR-21 and TNF-α repressed PDCD4 and its tumor suppression activity. Eventually, active STAT3 stimulated a strong inflammatory response and activated the invasion/metastasis process of tumor cells. Hence, our findings indicate that miR-21 is critical for the development of CRC/CAC via the PI3K/AKT, STAT3, and PDCD4/TNF-α signaling networks.
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Verna, Giulio, Marina Liso, Elisabetta Cavalcanti, Raffaele Armentano, Alessandro Miraglia, Vladia Monsurrò, Marcello Chieppa, and Stefania De Santis. "Deletion of TNF in Winnie-APCMin/+ Mice Reveals Its Dual Role in the Onset and Progression of Colitis-Associated Colorectal Cancer." International Journal of Molecular Sciences 23, no. 23 (December 2, 2022): 15145. http://dx.doi.org/10.3390/ijms232315145.
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Colorectal cancer (CRC) is among the best examples for depicting the relationship between inflammation and cancer. The introduction of new therapeutics targeting inflammatory mediators showed a marked decrease in the overall risk of CRC, although their chemopreventive potential is still debated. Specifically, a monoclonal antibody that blocks tumor necrosis factor (TNF), infliximab, increases CRC risk in inflammatory bowel disease patients. To address the axis between TNF and CRC development and progression, we depleted the Tnf from our previously established murine model of colitis-associated cancer (CAC), the Winnie-ApcMin/+ line. We characterized the new Winnie-APCMin/+-TNF-KO line through macroscopical and microscopical analyses. Surprisingly, the latter demonstrated that the deletion of Tnf in Winnie-ApcMin/+ mice resulted in an initial reduction in dysplastic lesion incidence in 5-week-old mice followed by a faster disease progression at 8 weeks. Histological data were confirmed by the molecular profiling obtained from both the real-time PCR analysis of the whole tissue and the RNA sequencing of the macrodissected tumoral lesions from Winnie-APCMin/+-TNF-KO distal colon at 8 weeks. Our results highlight that TNF could exert a dual role in CAC, supporting the promotion of neoplastic lesions onset in the early stage of the disease while inducing their reduction during disease progression.
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O’Keefe, Louise C., Margaret M. Sullivan, Amber McPhail, Kristen Van Buren, and Nathan Dewberry. "Screening for Colorectal Cancer at the Worksite." Workplace Health & Safety 66, no. 4 (October 11, 2017): 183–90. http://dx.doi.org/10.1177/2165079917733483.
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Colorectal cancer (CRC) is the second leading cause of cancer-related deaths among men and women in the United States. To increase statewide CRC screening rates, the Alabama Department of Public Health (through a Centers for Disease Control and Prevention [CDC] Colorectal Cancer Control Program grant) partnered with The University of Alabama in Huntsville (UAH) and The University of South Alabama (USA) to provide free CRC screening opportunities to eligible University employees and dependents. Resources were invested at both universities to ensure participant education, tracking, and monitoring. In total, 86 fecal immunochemical tests (FITs) were distributed at the UAH campus and 62 were returned for testing; 146 FITs were distributed on the USA campus with 111 returned. Fecal immunochemical test return rates were over 70% at each site. Most notably, 21 positive FITs were identified among UAH participants and 25 at USA. Findings from both efforts suggest that employer-based screening initiatives are a systematic and replicable means of improving CRC screening.
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Singh, Roshni, Carla Parraga, Rachel Lin, Leonardo Tamariz, and Ana Palacio. "COLORECTAL CANCER SCREENING (CRC) DISPARITIES: A ZIP CODE–LEVEL ANALYSIS." Innovation in Aging 6, Supplement_1 (November 1, 2022): 481–82. http://dx.doi.org/10.1093/geroni/igac059.1859.
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Abstract CRC is the third leading cause of cancer-related deaths among older adults in the US. CRC screening can prevent disease by early identification, yet there are disparities in CRC screening. This study aimed to determine the impact of race, social determinants, and geographic location at zip-codes level on CRC screening.We conducted a retrospective cross-sectional study of CRC screening among different races, evaluating the relationship with the social deprivation index (SDI) and annual income as health determinant factors using the public available data of 2016-2019 CDC 500 cities project and PLACES project 2020 database combined with 2019 American Community Survey for zip code-based analysis. We conducted a multivariate analysis and a confirmatory factor analysis among race, income, lack of health insurance, access to check-up visits and SDI.Increasing SDI tertile increased the likelihood of being Black and Hispanic and having lower median household income (p< 0.01). Lack of health insurance and lower regular checkup visits were less common in the third tertile of SDI (p< 0.01). The multivariate analysis showed that being black, Hispanic, having a lower income, not having health insurance, not having regular check-ups and SDI were related to decreased screening. In the confirmatory factor analysis, the variables most associated with decreased screening are SDI and access to health insurance.Race, SDI, insurance status, socioeconomic status, all impact CRC screenings, but the two most important factors are SDI and access to healthcare. These data may help implement interventions that specifically target these barriers to promote CRC screenings within disadvantaged communities.
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Kim, Ellen J., LIn Zhu, Wenyue Lu, Safa Ibrahim, Steven Zhu, Nathaly Rubio-Torio, Evelyn González, et al. "Abstract B056: Increasing knowledge of colorectal cancer (CRC) risk factors and screening through a community-based education initiative." Cancer Epidemiology, Biomarkers & Prevention 32, no. 1_Supplement (January 1, 2023): B056. http://dx.doi.org/10.1158/1538-7755.disp22-b056.
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Abstract Background: Colorectal cancer (CRC) screening such as colonoscopy and stool test has been shown to be effective in reducing CRC burden, especially in the underprivileged communities. However, CRC awareness and screening uptake remained suboptimal, especially in racial/ethnic minority populations and non-Hispanic whites. Both CRC incidence and mortality rates are highest in non-Hispanic blacks (approximately 20% and 40%, respectively), and CRC screening uptake rates are lower in racial/ethnic minorities relative to non-Hispanic whites (NHWs). The cause for the disparities in incidence and mortality is multifactorial. One important aspect is the suboptimal knowledge and awareness of risk factors. Methods: To increase awareness of CRC prevention and screening, we collaborated with community-based organizations (CBOs) to develop culturally tailored educational materials targeting African/Black Americans (BAs), Asian Americans (AAs), and Hispanic Americans (HAs). The topics included essential CRC and screening knowledge, a healthy diet (Mediterranean diet), and at-home workout routines. Eligible participants from the Greater Philadelphia area and New York City participated in one-time education. Pre- and post-intervention surveys were designed based on the Colorectal Cancer Quiz provided by the Centers for Disease Control and Prevention (CDC) and were administered to assess the immediate impact of the educational sessions. Results: The analysis sample included 413 participants, among which 388 completed the post-survey. One in ten (10.3%) reported a family history of CRC, and a half (50.6%) had never had a colonoscopy. The baseline CRC knowledge score was 9.5 out of 16, indicating a moderately low level of knowledge. Participants scored particularly low on the age of CRC screening initiation, needs for screening even without symptoms, and the impact of physical activity on CRC risk. The knowledge score significantly increased to 10.9 (p < .001) at post-survey, indicating a significant impact of the educational workshops. Conclusion: The findings of our project confirm that the CRC screening rates are low in racial/ethnic minorities compared to the U.S. national rate of 71.6%. Meanwhile, it also confirmed that culturally tailored, community-based educational initiatives can effectively raise knowledge of CRC in medically underserved populations. Citation Format: Ellen J. Kim, LIn Zhu, Wenyue Lu, Safa Ibrahim, Steven Zhu, Nathaly Rubio-Torio, Evelyn González, Marilyn A. Fraser, Ming-Chin Yeh, Grace X. Ma, Olorunseun O. Ogunwobi, Yin Tan. Increasing knowledge of colorectal cancer (CRC) risk factors and screening through a community-based education initiative [abstract]. In: Proceedings of the 15th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2022 Sep 16-19; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2022;31(1 Suppl):Abstract nr B056.
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Zhang, Xue, Yang Yang, Yalan Wang, and Qi Fan. "Detection of the BRAF V600E Mutation in Colorectal Cancer by NIR Spectroscopy in Conjunction with Counter Propagation Artificial Neural Network." Molecules 24, no. 12 (June 15, 2019): 2238. http://dx.doi.org/10.3390/molecules24122238.
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This paper proposes a sensitive, sample preparation-free, rapid, and low-cost method for the detection of the B-rapidly accelerated fibrosarcoma (BRAF) gene mutation involving a substitution of valine to glutamic acid at codon 600 (V600E) in colorectal cancer (CRC) by near-infrared (NIR) spectroscopy in conjunction with counter propagation artificial neural network (CP-ANN). The NIR spectral data from 104 paraffin-embedded CRC tissue samples consisting of an equal number of the BRAF V600E mutant and wild-type ones calibrated and validated the CP-ANN model. As a result, the CP-ANN model had the classification accuracy of calibration (CAC) 98.0%, cross-validation (CACV) 95.0% and validation (CAV) 94.4%. When used to detect the BRAF V600E mutation in CRC, the model showed a diagnostic sensitivity of 100.0%, a diagnostic specificity of 87.5%, and a diagnostic accuracy of 93.8%. Moreover, this method was proven to distinguish the BRAF V600E mutant from the wild type based on intrinsic differences by using a total of 312 CRC tissue samples paraffin-embedded, deparaffinized, and stained. The novel method can be used for the auxiliary diagnosis of the BRAF V600E mutation in CRC. This work can expand the application of NIR spectroscopy in the auxiliary diagnosis of gene mutation in human cancer.