Relevant bibliographies by topics / Adenocarcinoma Aneuploidy

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Academic literature on the topic 'Adenocarcinoma Aneuploidy'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

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Journal articles on the topic "Adenocarcinoma Aneuploidy"

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Wu, Chuanxin, Jing Zhang, Hua Bao, Ao Wang, Zhuang Luo, Yi Shen, Shuyu Wu, Xue Wu, Yang Shao, and Jianfeng Huang. "Distinct genomic instability landscape of lung adenocarcinoma associated with treatment and metastasis." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): 9534. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.9534.

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9534 Background: Lung adenocarcinoma (LUAD) is the most common subtype of non-small cell lung cancer (NSCLC). Genomic instability, defined as genome-wide copy number alterations, is a key pathogenic signature which occurs at the early stage of most cancers and is associated with an increased risk of recurrence or death. We examined the pattern of genomic instability in primary and metastatic LUAD. Methods: We performed deep targeted sequencing (425 genes) of 3395 tissue samples and whole exome sequencing (WES) of 60 tissue samples from LUAD patients. Whole-genome doubling (WGD) and arm level aneuploidy were analyzed to uncover correlation with clinical phenotypes and other genomic alterations including driver mutations, tumor mutation burden (TMB), and microsatellite instability (MSI). Results: Overall, targeted sequencing revealed that WGD occurred in 64.33% LUAD samples, which was comparable with WES results. Compared to primary site, metastasis exhibited higher proportion of WGD (1.14 fold). Specifically, liver metastasis has the highest WGD percentage among metastasis sites (~87.5%; 1.40 fold increase compared to primary). Interestingly, patients who received tyrosine kinase inhibitors (TKI) had higher frequency of WGD than patients without TKI treatment. In addition, TMB was higher in WGD+ patients but MSI status was not significantly different between groups. Arm-level aneuploidy was prevalent in this cohort. The most common amplification events were 7p gain (62%), 5p gain (54%), and 8q gain (53%); top deletion events were 19p loss (47%), 15q loss (42%), and 10 q loss (41%). Patients with EGFR or TP53 mutation were more likely to have aneuploidy compared to wildtypes. Subgroup analysis showed distinct patterns of aneuploidy among metastasis sites, suggesting organ-specific alterations. Evolution analysis showed 7p gain was an early event common in primary tumor whereas metastatic tumor had multiple distinct evolutionary trajectories following 7p gain. Several copy number signatures were associated with specific TKI and chemotherapies. For example, TKI-naïve tumors lacked 7p gain but had 19p loss as the most common alteration. Conclusions: The genomic landscape of LUAD was characterized by widespread large-scale copy number alterations including WGD and chromosomal aneuploidy. Metastasis had elevated level of aneuploidy compared to primary tumors which were specific to metastatic site. Copy number signature associated with different treatments may contribute to distinct long-term survival and side effects among patients.
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Lin, Jen-Kou, Shih-Ching Chang, Ya-Chien Yang, and Anna Fen-Yau Li. "Loss of Heterozygosity and DNA Aneuploidy in Colorectal Adenocarcinoma." Annals of Surgical Oncology 10, no. 9 (January 2003): 1086–94. http://dx.doi.org/10.1245/aso.2003.12.014.

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Williams, L. J., D. L. Guernsey, and A. G. Casson. "Biomarkers in the Molecular Pathogenesis of Esophageal (Barrett) Adenocarcinoma." Current Oncology 13, no. 1 (February 1, 2006): 33–43. http://dx.doi.org/10.3747/co.v13i1.76.

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Since the early 1970s, a dramatic change has occurred in the epidemiology of esophageal malignancy in both North America and Europe: the incidence of adenocarcinomas of the lower esophagus and esophagogastric junction is increasing. Several lifestyle factors are implicated in this change, including gastroesophageal reflux disease (gerd). Primary esophageal adenocarcinomas are thought to arise from Barrett esophagus, an acquired condition in which the normal esophageal squamous epithelium is replaced by a specialized metaplastic columnar-cell-lined epithelium. Today, gerd is recognized as an important risk factor in Barrett esophagus. Progression of Barrett esophagus to invasive adenocarcinoma is reflected histologically by the metaplasia–dysplasia–carcinoma sequence. Although several molecular alterations associated with progression of Barrett esophagus to invasive adenocarcinoma have been identified, relatively few will ultimately have clinical application. Currently, the histologic finding of high-grade dysplasia remains the most reliable predictor of progression to invasive esophageal adenocarcinoma. However other promising molecular biomarkers include aneuploidy; 17p loss of heterozygosity, which implicates the TP53 tumour suppressor gene; cyclin D1 protein overexpression; and p16 alterations. It is anticipated that models incorporating combinations of objective scores of sociodemographic and lifestyle risk factors (that is, age, sex, body mass index), severity of gerd, endoscopic and histologic findings, and a panel of biomarkers will be developed to better identify patients with Barrett esophagus at increased risk for malignant progression, leading to more rational endoscopic surveillance and screening programs.
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Gao, Beili, Fujun Yang, Ming Han, Hua Bao, Yi Shen, Ran Cao, Xue Wu, Yang Shao, Changhong Liu, and Zhe Zhang. "Genomic landscape and evolution of arm aneuploidy in lung adenocarcinoma." Neoplasia 23, no. 9 (September 2021): 870–78. http://dx.doi.org/10.1016/j.neo.2021.06.003.

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Davison, Jon M., J. Michael Krill-Burger, Melissa K. Yee, Tyler J. Foxwell, Maureen A. Lyons-Weiler, James D. Luketich, Katie S. Nason, George K. Michalopoulos, and William A. LaFramboise. "The degree of segmental aneuploidy measured by total copy number abnormalities to predict survival and recurrence in superficial gastroesophageal adenocarcinoma." Journal of Clinical Oncology 32, no. 3_suppl (January 20, 2014): 62. http://dx.doi.org/10.1200/jco.2014.32.3_suppl.62.

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62 Background: Prognostic biomarkers are needed for superficial gastroesophageal adenocarcinoma (EAC) to predict clinical outcomes and select therapy. Although recurrent mutations have been characterized in EAC, little is known about their clinical and prognostic significance. Aneuploidy is predictive of clinical outcome in many malignancies but has not been evaluated in superficial EAC. SNP arrays offer the opportunity to evaluate segmental aneuploidy at high resolution throughout the genome. Methods: We quantified copy number changes in 41 superficial EAC using Affymetrix SNP 6.0 arrays. We identified recurrent chromosomal gains and losses and calculated the total copy number abnormality (CNA) count for each tumor as a measure of aneuploidy. We correlated CNA count with overall survival and time to first recurrence in univariate and multivariate analyses. Results: Recurrent segmental gains and losses involved multiple genes, including: HER2, EGFR, MET, CDK6 , KRAS (recurrent gains); and FHIT, WWOX, CDKN2A/B, SMAD4, RUNX1 (recurrent losses). There was a 40-fold variation in CNA count across all cases. Tumors with the lowest and highest quartile CNA count had significantly better overall survival (p=0.032, log rank test) and time to first recurrence (p=0.010, log rank test) compared to those with intermediate CNA counts. In multivariate Cox analysis, there was a 3.4-fold (95% CI, 1.1–10.4) increased hazard of death among cases with intermediate CNA counts after adjusting for other predictors of survival (N stage, angiolymphatic invasion and tumor size). Similarly, there was a 7.3-fold (95% CI, 1.5-34) increased risk of recurrence for these patients. Conclusions: SNP arrays facilitate the assessment of recurrent chromosomal gain and loss and allow high resolution, quantitative assessment of segmental aneuploidy (total CNA count).The non-monotonic association of segmental aneuploidy with survival has been described in other tumors such as breast and ovarian carcinoma. The degree of segmental aneuploidy is a promising prognostic biomarker in a potentially curable form of EAC.
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Viganó, Cristina, Conrad von Schubert, Erik Ahrné, Alexander Schmidt, Thomas Lorber, Lukas Bubendorf, Judith R. F. De Vetter, Guido J. R. Zaman, Zuzana Storchova, and Erich A. Nigg. "Quantitative proteomic and phosphoproteomic comparison of human colon cancer DLD-1 cells differing in ploidy and chromosome stability." Molecular Biology of the Cell 29, no. 9 (May 2018): 1031–47. http://dx.doi.org/10.1091/mbc.e17-10-0577.

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Although aneuploidy is poorly tolerated during embryogenesis, aneuploidy and whole chromosomal instability (CIN) are common hallmarks of cancer, raising the question of how cancer cells can thrive in spite of chromosome aberrations. Here we present a comprehensive and quantitative proteomics analysis of isogenic DLD-1 colorectal adenocarcinoma cells lines, aimed at identifying cellular responses to changes in ploidy and/or CIN. Specifically, we compared diploid (2N) and tetraploid (4N) cells with posttetraploid aneuploid (PTA) clones and engineered trisomic clones. Our study provides a comparative data set on the proteomes and phosphoproteomes of the above cell lines, comprising several thousand proteins and phosphopeptides. In comparison to the parental 2N line, we observed changes in proteins associated with stress responses and with interferon signaling. Although we did not detect a conspicuous protein signature associated with CIN, we observed many changes in phosphopeptides that relate to fundamental cellular processes, including mitotic progression and spindle function. Most importantly, we found that most changes detectable in PTA cells were already present in the 4N progenitor line. This suggests that activation of mitotic pathways through hyper-phosphorylation likely constitutes an important response to chromosomal burden. In line with this conclusion, cells with extensive chromosome gains showed differential sensitivity toward a number of inhibitors targeting cell cycle kinases, suggesting that the efficacy of anti-mitotic drugs may depend on the karyotype of cancer cells.
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Tsiambas, E., D. Alexopoulou, S. Lambropoulou, K. Gerontopoulos, P. Karakitsos, and A. Karameris. "Targeting topoisomerase IIa in endometrial adenocarcinoma." International Journal of Gynecologic Cancer 16, no. 3 (2006): 1424–31. http://dx.doi.org/10.1136/ijgc-00009577-200605000-00073.

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Topoisomerase IIa is a nucleic enzyme that affects the topological structure of DNA and also is a target for chemotherapy (ie, anthracyclines). In this study, we coevaluated its protein expression with chromosome 17 and gene status. Using tissue microarrays, 40 cases of sporadic, primary endometrial adenocarcinomas, 5 cases of atypical hyperplasia, and 5 cases of benign hyperplasia were obtained and reembedded into two paraffin blocks with a core diameter of 1 mm. Immunohistochemistry combined with chromogenic in situ hybridization was performed in 2 and 5 μm sections, respectively. Finally using a semiautomated Image Analysis System, we evaluated the levels of Nuclear labeling index of topoisomerase IIa expression. Statistical analysis was performed by SPSS version 11.0 software. The results indicate that chromosome 17 instability (aneuploidy in 7/40 cases) and Topo IIa gene deregulation (amplification in 3/40 and deletion in 1/40 cases) are significant genetic events correlated with biologic behavior in endometrial adenocarcinoma. Because protein overexpression was observed in a significant proportion of the tumors (18/40), detection of the specific gene deregulation mechanism is a crucial process for application of targeted chemotherapies, which are characterized by different levels of cardiotoxicity and other serious effects.
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Nanus, D. M., D. P. Kelsen, D. Niedzwiecki, D. Chapman, M. Brennan, E. Cheng, and M. Melamed. "Flow cytometry as a predictive indicator in patients with operable gastric cancer." Journal of Clinical Oncology 7, no. 8 (August 1989): 1105–12. http://dx.doi.org/10.1200/jco.1989.7.8.1105.

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Adenocarcinoma of the proximal portion of the stomach (gastroesophageal [GE] junction and cardia) is increasing in incidence. The inferior survival of patients with GE-cardia lesions as compared with patients with tumors located in the body and antrum has been attributed to anatomic features. To determine if a biological difference could explain the varying prognosis, flow cytometric studies were performed prospectively in 50 patients with operable gastric cancer and analyzed for association with site, histology, gender, age, stage, and disease-free survival. DNA aneuploidy significantly correlated with tumor location: 96% of GE-cardia carcinomas were aneuploid as compared with 48% of body-antrum tumors (P = .0008). Nodal involvement was more common in aneuploid tumors (P = .0548), and women were more likely to have diploid tumors than were men (P = .0233). The median disease-free survival for patients with diploid tumors was 18.5 months as compared with 5.4 months for patients with aneuploid carcinomas (P = .076). Furthermore, within the body-antrum of the stomach, patients with diploid tumors had a significantly better disease-free survival than did those with aneuploid tumors from the same site (18.4 v 4.7 months, P = .0185). These results indicate there is a difference in the DNA content of gastric tumors located in different sites within the stomach and that DNA content correlates with prognosis.
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Makiyama, Kazuya, Masaki Tokunaga, Minoru Itsuno, Walter Zea-Iriarte, Kohei Hara, and Tohru Nakagoe. "DNA aneuploidy in a case of rectosigmoid adenocarcinoma complicated by ulcerative colitis." Journal of Gastroenterology 30, no. 2 (April 1995): 258–63. http://dx.doi.org/10.1007/bf02348675.

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Maley, Carlo C., and Anil K. Rustgi. "Barrett's Esophagus and Its Progression to Adenocarcinoma." Journal of the National Comprehensive Cancer Network 4, no. 4 (April 2006): 367–74. http://dx.doi.org/10.6004/jnccn.2006.0031.

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Barrett's esophagus (BE) is the only known precursor for esophageal adenocarcinoma (EA). Therefore, the presence of BE identifies a high-risk group of patients who may be followed-up for early detection of EA and treated to reduce the risk for its progression. The initiating event for BE is unknown, although it is associated with chronic gastric reflux. Many of the genetic lesions involved in BE neoplastic progression are known, including loss of CDKN2A (p16) and TP53 (p53) and the development of tetraploidy and aneuploidy. Intensive endoscopic surveillance has been shown to improve survival although it can be difficult to implement in practice. Several exposures may be altered to reduce the risk for progression, including weight, diet, and the use of nonsteroidal anti-inflammatory drugs. However, most of these results should be confirmed in additional cohorts before they are used to change clinical practice.
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Dissertations / Theses on the topic "Adenocarcinoma Aneuploidy"

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Kronenwett, Ulrike. "Genomic instability, gene expression and prognosis in breast cancer /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-214-4/.

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Siahpush, Seyed Hossein. "Longitudinal study of insulin-like growth factor-I, binding protein-3, and their polymorphisms : risk of neoplastic progression in Barrett's esophagus /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/10870.

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Conference papers on the topic "Adenocarcinoma Aneuploidy"

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Bao, Hua, Ming Han, Yi Shen, Xue Wu, and Yang Shao. "Abstract 2210: Chromosome arm aneuploidy landscape in lung adenocarcinoma." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2210.

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Barrett, Michael T., Elizabeth Lenkiewicz, Lisa Evers, Tara Holley, Emily Leproust, Moraima Guadalupe, Scott Happe, et al. "Abstract LB-266: Clonal analysis of aneuploid pancreatic ductal adenocarcinoma genomes in patient biopsies using Agilent oligonucleotide technologies and Pacific Biosciences SMRT™ sequencing system." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-266.

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