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Relevant bibliographies by topics / Neoplasm DNA

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Academic literature on the topic 'Neoplasm DNA'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Neoplasm DNA"

1

Clemo, F. A. S., D. B. DeNicola, W. W. Carlton, W. B. Morrison, and E. Walker. "Flow Cytometric DNA Ploidy Analysis in Canine Transitional Cell Carcinoma of Urinary Bladders." Veterinary Pathology 31, no. 2 (March 1994): 207–15. http://dx.doi.org/10.1177/030098589403100208.

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Flow cytometric analysis of DNA ploidy was performed on 51 formalin-fixed, paraffin-embedded samples of canine transitional cell carcinoma of the urinary bladder. The DNA ploidy data obtained were compared to several clinicopathologic features. In addition, the DNA ploidy of 15 hyperplastic/inflamed and 8 normal canine urinary bladders was measured. Forty-three of the 51 neoplastic samples had interpretable DNA histograms. DNA aneuploidy was found in 34/43 (79%) of the transitional cell carcinoma samples. Of the 34 aneuploid neoplasms, 16 (47%) were hyperdiploid, 17 (50%) were tetraploid, and 1 (3%) was hypertetra-ploid. No significant correlation was found between the presence of DNA aneuploidy and the growth pattern. histologic grade, clinical stage, or individual morphologic features of this neoplasm. Additionally, the DNA ploidy was not related to the sex, age, or survival time of dogs with transitional cell carcinoma. All of the normal and all but one of the hyperplastic/inflamed urinary bladders were diploid. The results from this study demonstrated that DNA ploidy can be measured from paraffin-embedded canine samples by flow cytometry, a majority of the canine transitional cell carcinomas were aneuploid, and a significant correlation did not exist between the DNA ploidy and specific clinicopathologic features of this neoplasm.

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Van Treeck, Benjamin J., Mira Lotfalla, Thomas W. Czeczok, Taofic Mounajjed, Roger K. Moreira, Daniela S. Allende, Michelle D. Reid, et al. "Molecular and Immunohistochemical Analysis of Mucinous Cystic Neoplasm of the Liver." American Journal of Clinical Pathology 154, no. 6 (September 3, 2020): 837–47. http://dx.doi.org/10.1093/ajcp/aqaa115.

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Abstract Objectives Mucinous cystic neoplasm of the liver is characterized by neoplastic mucinous and/or biliary epithelium surrounded by ovarian-type stroma. Immunohistochemical studies have shown that the ovarian-type stroma expresses estrogen receptor, suggesting potential hormonal responsiveness. The molecular biology of mucinous cystic neoplasm of the liver remains poorly studied. Methods Transcriptome sequencing and immunohistochemistry were performed on a series of mucinous cystic neoplasms. Results Mucinous cystic neoplasm of the liver exhibited significantly increased RNA expression of ovarian stromal markers WT1, PR, and ER2 and sex cord stromal markers SF-1, inhibin-α, and calretinin compared with nonneoplastic liver. Immunohistochemistry confirmed the RNA-level data. Evidence for sex hormone biosynthesis was identified by significant overexpression of multiple estrogen biosynthetic enzymes. Expression of 17β-hydroxysteroid dehydrogenase 1 was confirmed immunohistochemically. Pathway analysis also identified significant upregulation of the hedgehog and Wnt pathways and significant downregulation of T-helper 1 and T-helper 2 pathways. Conclusions Mucinous cystic neoplasm of the liver recapitulates ovarian stroma at the morphologic, DNA, RNA, and protein levels. These data support the concept that this tumor likely arises from ectopic primitive gonadal tissue and/or stromal cells with capacity to transdifferentiate to ovarian cortical cells.

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Chen, Tsai-Yun, Jiann-Shiuh Chen, Wu-Chou Su, Ming-Shiuan Wu, and Chao-Jung Tsao. "Expression of DNA repair gene Ku80 in lymphoid neoplasm." European Journal of Haematology 74, no. 6 (June 2005): 481–88. http://dx.doi.org/10.1111/j.1600-0609.2005.00428.x.

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Curti, P., P. Beltrami, C. Tallarigo, G. Malossini, A. D'Amico, and D. Schiavone. "Flow Cytometry Role of DNA Analysis." Urologia Journal 61, no. 3 (June 1994): 226–28. http://dx.doi.org/10.1177/039156039406100313.

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We analyzed the results obtained by flow cytometry DNA analysis in prostatic cancer. We considered the diagnostic role of this investigation and the prognostic value observed from correlating the DNA analysis with usual diagnostic and prognostic factors such as staging, grading, PSA, size, etc. Results in literature suggest that further studies are necessary to explain both the biological and cytometrical heterogeneous aspects of this neoplasm.

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Pronier, Elodie, Carole Almire, Hayat Mokrani, Aparna Vasanthakumar, Audrey Simon, Barbara da Costa Reis Monte Mor, Aline Massé, et al. "Inhibition of TET2-mediated conversion of 5-methylcytosine to 5-hydroxymethylcytosine disturbs erythroid and granulomonocytic differentiation of human hematopoietic progenitors." Blood 118, no. 9 (September 1, 2011): 2551–55. http://dx.doi.org/10.1182/blood-2010-12-324707.

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Abstract TET2 converts 5-methylcytosine to 5-hydroxymethylcytosine (5-hmC) in DNA and is frequently mutated in myeloid malignancies, including myeloproliferative neoplasms. Here we show that the level of 5-hmC is decreased in granulocyte DNA from myeloproliferative neoplasm patients with TET2 mutations compared with granulocyte DNA from healthy patients. Inhibition of TET2 by RNA interference decreases 5-hmC levels in both human leukemia cell lines and cord blood CD34+ cells. These results confirm the enzymatic function of TET2 in human hematopoietic cells. Knockdown of TET2 in cord blood CD34+ cells skews progenitor differentiation toward the granulomonocytic lineage at the expense of lymphoid and erythroid lineages. In addition, by monitoring in vitro granulomonocytic development we found a decreased granulocytic differentiation and an increase in monocytic cells. Our results indicate that TET2 disruption affects 5-hmC levels in human myeloid cells and participates in the pathogenesis of myeloid malignancies through the disturbance of myeloid differentiation.

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Grady, W. M. "Epigenetic events in the colorectum and in colon cancer." Biochemical Society Transactions 33, no. 4 (August 1, 2005): 684–88. http://dx.doi.org/10.1042/bst0330684.

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Colon cancers arise from benign neoplasms and evolve into adenocarcinomas through a stepwise histological progression sequence, proceeding from either adenomas or hyperplastic polyps/serrated adenomas. Genetic alterations have been associated with specific steps in this polyp–adenocarcinoma sequence and are believed to drive the histological progression of colon cancer. Recently, epigenetic alterations, which include CGI (CpG island) DNA methylation, have been shown to occur in colon polyps and colon cancer. The aberrant methylation of genes appears to co-operate with the genetic alterations to drive the initiation and progression of colon polyps to colon cancer. CGI DNA methylation is an epigenetic mechanism that represses gene transcription in normal cellular processes, but it becomes excessive and aberrant in many neoplasms. The aberrant DNA methylation affects CpG-rich regions, called CGIs, in the 5′ region of genes and results in transcriptional silencing through effects on transcription factor binding and associated changes in chromatin structure. These hypermethylated genes are not only probable pathogenic events affecting colon-cancer formation, but also neoplasm-specific molecular events that may be useful as molecular markers for colon tumours. Furthermore, aberrant DNA methylation of tumour-suppressor genes may occur secondary to a genetic predisposition or to a field-cancerization effect in the colon and may be useful as molecular markers for the risk of developing colon cancer.

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Shepro, David, and Michael Miller. "Gemcitabine in Blastic Plasmacytoid Dendritic Cell Neoplasm (CD4+CD56+ hematodermic neoplasm)." Blood 124, no. 21 (December 6, 2014): 5457. http://dx.doi.org/10.1182/blood.v124.21.5457.5457.

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Abstract Once thought to be a natural killer cell lymphoma, blastic plasmacytoid dendritic cell neoplasm, also termed CD4+CD56+ hematodermic neoplasm, is a rare clinical entity which derives from plasmacytoid dendritic cells. Cutaneous predominant (with better prognosis) and non-cutaneous subtypes (often accompanied by mediastinal involvement and a poorer prognosis) have been described. Many patients are treated with CHOP-like regimens, but the prognosis remains poor. Patients presenting with only skin lesions (median survival 21 months) had a better prognosis than patients presenting with both cutaneous and extra-cutaneous disease. We describe an 86 yo female with a distant history of breast cancer. She noted rapid development of mildly itchy round pink cutaneous nodlues on the arms, buttock, and legs. She was treated with topical steroids without improvement. The CBC, calcium, and LDH were normal. ECOG 0. There was no adenopathy or organomegaly. Skin biopsy demonstrated a dense lymphoid infiltrate involving the upper and mid dermis, as well as adnexal structures, without epidermotropism. The infiltrate was composed predominantly of large to intermediate sized lymphoid cells having moderate amounts of cytoplasm and oval to cleaved nuclei having open chromatin and one or more small nucleoli. Mitotic figures were present. The neoplastic cells expressed CD4, CD56. Ki-67 was expressed by many of the cells. The cells were negative for CD1a, CD3, CD5, CD7, CD8, PAX-5, CD20, CD79a, CD10, CD23, CD30, CD163, bcl-2, bcl-6, myeloperoxidase, kappa/lambda light chains, p63, Tdt, tryptase, chromogranin, MART-1, mammoglobin, CAM 5.2, and AE1/3. The morphology and immunophenotype was consistent with a CD4+/CD56+ hematodermic neoplasm. The patient preferred no additional staging studies or therapy. Based on the available data, cutaneous-only disease was suggested. The disease was observed without intervention for a few weeks, but progressed on her skin. She then requested a gentle therapy that might provide palliative improvement and prevent progression. Gemcitabine (2′,2′-difluorodeoxycytidine) is a well tolerated pyrimidine antimetabolite that impairs DNA synthesis and promotes induction of apoptosis. In patients with relapsed or refractory aggressive non-Hodgkin lymphoma, gemcitabine led to a 20% response rate with median survival of 6 months. Therapy with Gemcitabine was administered at 1000 mg/M2 on days 1, 8, 15 every 28 days. There was rapid and marked improvement of the skin nodules. Treatment was very well tolerated with minimal bilateral leg edema. A 4 week chemotherapy holiday was associated with regrowth. Photographs document the disease progression before therapy and response of disease with ongoing therapy. Gemcitabine may provide palliative benefit in some patients with blastic plasmacytoid dendritic cell neoplasm. Table Pre Therapy May 15 2014 Day 1 Chemotherapy May 23 2014 Day 22 Chemotherapy June 6 2014 Figure 1 Figure 1. Figure 2 Figure 2. Figure 3 Figure 3. Disclosures Off Label Use: Gemcitabine in blastic plasmacytoid dendritic cell neoplasm (CD4+CD56+ hematodermic neoplasm).

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Weinerman, David J., Rashid Z. Syed, Isaac Galandauer, and Shireen A. Pais. "Mo1217 Does Fluid DNA Analysis Change the Management of Pancreatic Cystic Neoplasm?" Gastrointestinal Endoscopy 75, no. 4 (April 2012): AB354. http://dx.doi.org/10.1016/j.gie.2012.03.923.

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Haferlach, Claudia, Constance Baer, Stephan Hutter, Anna Stengel, Niroshan Nadarajah, Wencke Walter, Manja Meggendorfer, Wolfgang Kern, and Torsten Haferlach. "Primary and Secondary Hematological Neoplasms - Are They Related?" Blood 134, Supplement_1 (November 13, 2019): 1702. http://dx.doi.org/10.1182/blood-2019-126585.

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Background: The pathogenesis of secondary hematological neoplasms occurring after a primary hematological neoplasm and the relationship between both is still unclear. We set up this study in order to evaluate whether both diseases share genomic alterations. Patients and Methods: We selected 25 patients who were diagnosed with a first hematological neoplasm (FHN) (CLL: n=14, other mature B cell neoplasm: n=6, AML: n=4, CML: n=1) and in median 48 months later (range: 16-119) with a second hematological neoplasm (SHN) (t-MDS: n= 21; t-AML: n=1, CMML: n=1; t-MPN: n=1, t-MDS/MPN: n=1). In 9 cases bone marrow was available that had been drawn in complete cytomorphological remission (CR) between FHN and SHN. Whole genome sequencing was performed for all 59 samples: 150 bp paired-end sequences where generated on Illumina HiseqX and NovaSeq 6000 machines (Illumina, San Diego, CA, USA) (median coverage 106x). A mixture of genomic DNA from multiple anonymous donors was used as normal controls. The overlap of genomic alterations present at the different points in time was evaluated. For the assessment of mutations as germline the following parameters were considered: a) variant allele frequency (VAF) 0.4-0.6; b) gnomAD frequency <0.005%; c) CLINVAR entry; d) high pathogenicity rating in the HePPy predictor (Hutter et al. ASH 2019) based on the most common in silico predictors included in dbNSFP. Results: 1) Relation of FHN and SHN by germline variants: In 8 cases 10 variants with a high pathogenicity in silico MLL predictor score in cancer predisposition genes were found (TP53,RUNX1, GATA2, BRCA2, MLH1, FAM175A, TMEM127, PALB2, ANKRD26, and PMS2). However, in CLINVAR only variants in GATA2 and PMS2 were scored as pathogenic/likely pathogenic, while for all other variants either no or conflicting data were available. 2) Relation of FHN and SHN by acquired mutations: A NOTCH2 mutation was detected at the time of CLL diagnosis (VAF 0.42) as well as at the time of t-MDS diagnosis (VAF 0.44) 16 months later, which might be either germline or somatic relating both diseases. In none of the remaining 19 pairs of a primary lymphatic neoplasm and a secondary myeloid neoplasm, there was evidence for shared acquired mutations. Regarding primary myeloid neoplasms, in one NPM1 mutated AML case an IDH1 mutation was present at AML and at t-MDS stage (VAF 0.45; 0.14), while it was not detectable in CR (2 months after diagnosis of AML and 43 months prior to diagnosis of t-MDS). In this case one DNMT3A mutation was present at all 3 points in time (VAF: 0.47, 0.44; 0.37), while a second one was gained at MDS stage (figure 1). No shared acquired mutations were identified between primary and secondary myeloid neoplasm in the remaining cases. 3) Independent/parallel development of FHN and SHN: In 5/9 cases with an available CR sample, mutations, structural variants and/or copy number variations present in the secondary malignancy were already detectable in CR. These included mutations in TP53 (n=3), AHR (n=1), CSNK1A1 (n=1), ASXL2 (n=1), t(2;3)(p16;q26) (n=1), del(2q), del(5q) and del(7p) (n=1). In 3/16 cases without remission sample a clone of the later emerging second neoplasm could be identified in the sample drawn at the time point of diagnosis of the primary disease. These clones harbored mutations in SRSF2 (n=2), PTPN11 (n=1), U2AF1 (n=1), WNK1 (n=1), MLH1 (n=1), TET2 (n=1). These secondary neoplasms were diagnosed 24, 24, and 76 months after the primary neoplasm, respectively. Summary: In more than half of the cases no genetic relation between the first and second hematological neoplasm was identified. Remarkably, in several cases a parallel development of FHN and SHN was observed suggesting that therapy for FNH allowed the outgrowth of SHN. Disclosures Haferlach: MLL Munich Leukemia Laboratory: Employment, Equity Ownership. Baer:MLL Munich Leukemia Laboratory: Employment. Hutter:MLL Munich Leukemia Laboratory: Employment. Stengel:MLL Munich Leukemia Laboratory: Employment. Nadarajah:MLL Munich Leukemia Laboratory: Employment. Walter:MLL Munich Leukemia Laboratory: Employment. Meggendorfer:MLL Munich Leukemia Laboratory: Employment. Kern:MLL Munich Leukemia Laboratory: Employment, Equity Ownership. Haferlach:MLL Munich Leukemia Laboratory: Employment, Equity Ownership.

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Gulley, Margaret L., and Weihua Tang. "Using Epstein-Barr Viral Load Assays To Diagnose, Monitor, and Prevent Posttransplant Lymphoproliferative Disorder." Clinical Microbiology Reviews 23, no. 2 (April 2010): 350–66. http://dx.doi.org/10.1128/cmr.00006-09.

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SUMMARYEpstein-Barr virus (EBV) DNA measurement is being incorporated into routine medical practice to help diagnose, monitor, and predict posttransplant lymphoproliferative disorder (PTLD) in immunocompromised graft recipients. PTLD is an aggressive neoplasm that almost always harbors EBV DNA within the neoplastic lymphocytes, and it is often fatal if not recognized and treated promptly. Validated protocols, commercial reagents, and automated instruments facilitate implementation of EBV load assays by real-time PCR. When applied to either whole blood or plasma, EBV DNA levels reflect clinical status with respect to EBV-related neoplasia. While many healthy transplant recipients have low viral loads, high EBV loads are strongly associated with current or impending PTLD. Complementary laboratory assays as well as histopathologic examination of lesional tissue help in interpreting modest elevations in viral load. Circulating EBV levels in serial samples reflect changes in tumor burden and represent an effective, noninvasive tool for monitoring the efficacy of therapy. In high-risk patients, serial testing permits early clinical intervention to prevent progression toward frank PTLD. Restoring T cell immunity against EBV is a major strategy for overcoming PTLD, and novel EBV-directed therapies are being explored to thwart virus-driven neoplasia.

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Dissertations / Theses on the topic "Neoplasm DNA"

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Yakisich, Juan Sebastián. "Regulation of ongoing DNA synthesis in normal and neoplastic brain tissue /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-433-3/.

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Mosolits, Szilvia. "Natural and induced immunity aginst the tumour-associated antigen, Ep-CAM /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-752-5.

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Ma, Shuhua. "O6-methylguanine-DNA-methyltransferase and DNA mismatch repair in relation to drug resistance in malignant melanoma /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-892-0/.

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Lundgren, Caroline. "Endometrial carcinoma : prognostic factors and protein expression profiling /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-002-8/.

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Holgersson, Åsa. "DNA-dependent protein kinase in normal and malignant cells : with special reference to anti-tumour agent sensitivity /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-431-3/.

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Lenander, Claes. "Molecular markers and new techniques in the evaluation of colorectal cancer /." Stockholm : Karolinska institutet, 2002. http://diss.kib.ki.se/2002/91-7349-205-1.

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Campos, Elisabete Aparecida 1961. "Viabilidade do DNA-HPV extraido e coletado no meio UCM de material desnaturado em diferentes tempos de estocagem." [s.n.], 2007. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309934.

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Orientadores: Jose Antonio Simões, Sophie Françoise Mauricette Derchain
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-09T07:56:09Z (GMT). No. of bitstreams: 1 Campos_ElisabeteAparecida_M.pdf: 376476 bytes, checksum: 5cb1313dd5ebc4ab5d963f22dad4830d (MD5) Previous issue date: 2007
Resumo: Objetivo: Avaliar a recuperação e estabilidade do DNA para detecção do papillomavírus humano (HPV) através da Reação em Cadeia da Polimerase (PCR) utilizando amostras estocadas por até 24 meses em Universal Collection Medium (UCM) com reagente desnaturante. Métodos: Sessenta amostras de citologia da cérvix uterina positivas para HPV, - que foram coletadas em UCM com resultado de Papanicolaou NIC 2 e NIC 3 entre os anos de 2003 e 2005 e que foram estocadas - foram utilizadas para este estudo. Todas as amostras haviam sido congeladas a ¿20°C após a adição do reagente desnaturante (0,05% de azida sódica + solução de NaOH) e da retirada da alíquota necessária para a realização do teste de Captura¿Híbrida 2 (CH 2) para identificação do DNA-HPV. O tempo de estocagem das amostras utilizadas foi de 6, 12 e 24 meses (20 amostras para cada tempo de estocagem). A extração do DNA foi realizada de acordo com protocolo específico para este tipo de material. A técnica de PCR foi realizada para confirmação da presença e da integridade do DNA através da detecção da ß-globina humana utilizando-se primers de consenso G73 e G74, e a detecção do DNA-HPV foi realizada utilizando-se os primers de consenso PGMY09 e PGMY11. Resultados: O DNA extraído do material desnaturado foi recuperado em 57 das 60 (95%) amostras estudadas. O DNA-HPV só não pôde ser detectado por PCR em uma destas amostras recuperadas. Conclusão: A recuperação e a estabilidade do DNA-HPV foi excelente após dois anos de estocagem do material cervical colhido em UCM com reagente desnaturan
Abstract: Objective: To evaluate the recovery and stability of DNA for the detection of HPV by Polymerase Chain Reaction (PCR) from clinical specimens stored for up to 24 months in Universal Collection Medium (UCM) with denatured reagent. Materials and methods: Sixty stores HPV-positive cervical smears collected from women with CIN 2 or CIN 3 diagnosis at Pap smear cytology between 2003 and 2005 were utilized to study. All samples were stored at ¿20°C after add of the denaturing reagent (sódica azida 0,05% and solution NaOH) and removing the aliquot required for carrying out the hybrid capture 2 assay for the identification of HPV-DNA, the samples were stored for 6, 12 or 24 months (20 samples for each storage time). DNA-HPV extraction was performed according to a protocol specifically designed for this type of material. The presence and quality of DNA was confirmed by human ß-globin detection using the consensus primers G73 and G74 and HPV was detected using the consensus primers PGMY09 and PGMY11 through the technique of PCR. Results: The DNA extracted from the denatured material was recovered in 57 out of 60 (95%) of the samples studied. DNA-HPV failed to be detected in one of the recovered samples. Conclusions: The recovery and stability of DNA-HPV from cervical samples stored for up to two years in UCM were excellent
Mestrado
Ciencias Biomedicas
Mestre em Tocoginecologia

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Guo, Dongli. "Expression of Wnt signaling targets and their clinico-pathological significance in colorectal neoplasm a tissue microarray study /." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B38610541.

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Ehnfors, Jacob. "On the mechanisms and consequences of cell to cell DNA transfer /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-455-6/.

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Guo, Dongli, and 郭冬麗. "Expression of Wnt signaling targets and their clinico-pathological significance in colorectal neoplasm: a tissuemicroarray study." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B38610541.

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Books on the topic "Neoplasm DNA"

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DNA ploidy and cell cycle analysis in pathology. New York: Igaku-Shoin, 1996.

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IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Some antiviral and antineoplastic drugs, and other pharmaceutical agents. Lyon, France: IARC, 2000.

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Marikki, Laiho, and SpringerLink (Online service), eds. Molecular Determinants of Radiation Response. New York, NY: Springer Science+Business Media, LLC, 2011.

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DNA repair in cancer therapy: Molecular targets and clinical applications. London: Elsevier/Academic Press, 2012.

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Kelley, Mark Richard. DNA repair in cancer therapy: Molecular targets and clinical applications. London: Elsevier/Academic Press, 2012.

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Introduction to cancer biology. Cambridge: Cambridge University Press, 2013.

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Yosef, Shiloh, and SpringerLink (Online service), eds. The DNA Damage Response: Implications on Cancer Formation and Treatment. Dordrecht: Springer Netherlands, 2009.

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Knudsen, Steen. Cancer Diagnostics with DNA Microarrays. New York: John Wiley & Sons, Ltd., 2006.

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International Symposium on DNA Topoisomerases in Chemotherapy (1991 Nagoya-shi, Japan). Molecular biology of DNA topoisomerases and its application to chemotherapy: Proceedings of the International Symposium on DNA Topoisomerases in Chemotherapy, Nagoya, Japan, November 18-20, 1991 (ISTOP 1991). Boca Raton: CRC Press, 1993.

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NATO Advanced Study Institute on Radiation Carcinogenesis and DNA Alterations (1984 Kerkyra, Greece). Radiation carcinogenesis and DNA alterations. New York: Plenum Press, 1986.

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Book chapters on the topic "Neoplasm DNA"

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Beland, Frederick A., and Miriam C. Poirier. "DNA Adducts and Carcinogenesis." In The Pathobiology of Neoplasia, 57–80. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5523-6_4.

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Dresler, Steven L. "DNA Repair Mechanisms and Carcinogenesis." In The Pathobiology of Neoplasia, 173–97. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5523-6_9.

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Dang, Chi V., and Linda A. Lee. "DNA Binding Properties of Myc." In c-Myc Function in Neoplasia, 165–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22681-0_9.

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Kanai, Yae, and Eri Arai. "DNA Methylation Status in Chronic Liver Disease and Hepatocellular Carcinoma." In Molecular Genetics of Liver Neoplasia, 147–59. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6082-5_8.

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Okumura, Yutaka, Makoto Ihara, Tatsuya Shimasaki, Satoshi Takeshita, and Kumio Okaichi. "Heat Inactivation of DNA-Dependent Protein Kinase: Possible Mechanism of Hyperthermic Radiosensitization." In Thermotherapy for Neoplasia, Inflammation, and Pain, 420–23. Tokyo: Springer Japan, 2001. http://dx.doi.org/10.1007/978-4-431-67035-3_46.

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Hnilica, L. S., R. Olinski, Z. M. Banjar, W. N. Schmidt, and R. C. Briggs. "DNA-Protein Crosslinking of Platinum Coordination Complex in Living Cells: Implication to Evaluate the Cytotoxic Effects of Chemotherapeutic Agents." In New Experimental Modalities in the Control of Neoplasia, 223–33. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5242-6_16.

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Kerbel, Robert S., Philip Frost, Douglas A. Carlow, and Bruce E. Elliott. "Tumor specific antigens induced by mutagens and DNA hypomethylating agents: implications for the immunobiology of neoplasia." In Cancer Immunology: Innovative Approaches to Therapy, 29–67. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2629-8_2.

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Economopoulou, Panagiota, Vassiliki Pappa, Sotirios Papageorgiou, John Dervenoulas, and Theofanis Economopoulos. "DNA Repair Deficiency Associated with Hematological Neoplasms." In DNA Repair and Human Health. InTech, 2011. http://dx.doi.org/10.5772/24610.

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Springs, Clark L. "Corneal Complications." In Complications of Glaucoma Surgery. Oxford University Press, 2013. http://dx.doi.org/10.1093/oso/9780195382365.003.0042.

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The desired effects of antifibrotic agents 5-fluorouracil (5-FU) and mitomycin-C (MMC) in glaucoma filtration surgery result from their ability to limit postoperative scarring by inhibiting vascular proliferation and fibroblastic transformation. However, these same mechanisms of action can have deleterious effects on surrounding normal tissues such as the cornea. Knowing how to use these agents is important in preventing antifibrotic-related complications. 5-FU is an inhibitor of DNA synthesis, specifically thymidylate synthetase, and blocks thymidine from being incorporated into DNA. In addition to affecting DNA synthesis, 5-FU also may be incorporated into RNA, interfering with RNA synthesis and therefore protein synthesis. Thus, it is more toxic to actively proliferating cells. In glaucoma filtration surgery, 5-FU is generally administered intraoperatively (50 mg/mL for 5 minutes). 5-FU can also be administered as a subconjunctival injection postoperatively with a dosage of 5.0–7.5 mg in 0.1–0.15 mL solution directly from the 50 mg/mL bottle. A series of injections may be given over several weeks and titrated based on clinical response. In addition to glaucoma filtration surgery, 5-FU has also been used for other ophthalmic applications such as pterygium surgery, lacrimal surgery, and during vitrectomy to prevent proliferative vitreoretinopathy. MMC is an alkylating agent that crosslinks DNA. It requires enzymatic activation via cytochrome p450 prior to exerting its inhibitory effects on DNA synthesis. MMC activity is independent of cell cycle and affects both actively replicating and nonreplicating cells. However, variations in enzymatic activity among individuals may contribute to the diﬀerences in eﬃcacy, as well as toxicity of MMC. In glaucoma ﬁltration surgery, MMC is typically administered as a single intraoperative application. It is applied after dissection of the conjunctival ﬂap and prior to the formation of the scleral ﬂap. Most surgeons use a dose of 0.1–0.5 mg/mL with an exposure time of 1–5 minutes depending upon the clinical indication. MMC use has also been well established for refractive surgery to prevent corneal haze after photorefractive keratectomy in patients at high risk of developing corneal haze, pterygium surgery, and corneal intraepithelial neoplasia. For more information on 5-FU and MMC in glaucoma surgery, see Chapter 3.

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Baylln, Stephen B., James G. Herman, Jeremy R. Graff, Paula M. Vertino, and Jean-Pierre Issa. "Alterations in DNA Methylation: A Fundamental Aspect of Neoplasia." In Advances in Cancer Research, 141–96. Elsevier, 1997. http://dx.doi.org/10.1016/s0065-230x(08)60702-2.

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Conference papers on the topic "Neoplasm DNA"

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Ahlquist, David A. "Abstract IA13: Stool DNA detection of colorectal neoplasia." In Abstracts: AACR Special Conference: Colorectal Cancer: From Initiation to Outcomes; September 17-20, 2016; Tampa, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.crc16-ia13.

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Adams, Gregory, Sharifeh Mehrabi, Tesfamariam Mehreteab, Edward E. Grizzle, and Felix O. Aikhionbare. "Abstract 3806: Mitochondrial DNA (MtDNA) analysis in colorectal neoplasia." 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.am2011-3806.

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FARIA DOMINGUES, LEONARDO, Marilda Mazzali, and Willian Nishiwaki Alves. "Cutaneous Neoplasms in Renal Transplant Recipients." In XXV Congresso de Iniciação Cientifica da Unicamp. Campinas - SP, Brazil: Galoa, 2017. http://dx.doi.org/10.19146/pibic-2017-78838.

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Isquith, Jane, Qingfei Jiang, Raymond Diep, Jessica Pham, Frida Holm, and Catriona Jamieson. "Abstract 3675: Elucidating the role and function of APOBEC3 DNA deaminases in myeloproliferative neoplasms." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3675.

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Isquith, Jane, Qingfei Jiang, Raymond Diep, Jessica Pham, Frida Holm, and Catriona Jamieson. "Abstract 3675: Elucidating the role and function of APOBEC3 DNA deaminases in myeloproliferative neoplasms." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3675.

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Bartak, BK, A. Kalmar, A. Patai, O. Galamb, G. Valcz, B. Wichmann, ZB Nagy, Z. Tulassay, P. Igaz, and B. Molnar. "PO-384 Manual and automated detection of DNA methylation alterations in colorectal neoplasia in circulating cell-free DNA fraction." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.411.

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Wu, Jianchun, and David L. Crowe. "Abstract 1464: Telomere DNA damage links benign prostatic hypertrophy, intraepithelial neoplasia, and prostate cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1464.

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Thuijs, NB, S. Duin, AP van Splunter, DRA Swarts, DAM Heideman, J. Berkhof, M. van Beurden, RDM Steenbergen, and MCG Bleeker. "P189 Host cell DNA methylation markers for cancer risk stratification of vulvar intraepithelial neoplasia." In ESGO Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-esgo.246.

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Ahlquist, David A. "Abstract PL02-01: Stool DNA detection of colorectal neoplasia: A new high bar for noninvasive screening." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-pl02-01.

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Vidal, Adriana C., David Skaar, Zhiquing Huang, Fidel Valea, Rex Bentley, Margaret Gradison, Kimberly S. H. Yarnall, et al. "Abstract B01: PEG3 DNA methylation and cervical intraepithelial neoplasia in African American and European American women." In Abstracts: Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; November 9-12, 2014; San Antonio, TX. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7755.disp14-b01.

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