Relevant bibliographies by topics / Neoplasm RNA

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Neoplasm RNA'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Neoplasm RNA"

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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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Jan, Max, Daniel E. Grinshpun, Julian A. Villalba, Paola Dal Cin, David B. Sykes, A. John Iafrate, Benjamin L. Ebert, Gabriela S. Hobbs, and Valentina Nardi. "A cryptic imatinib-sensitive G3BP1-PDGFRB rearrangement in a myeloid neoplasm with eosinophilia." Blood Advances 4, no. 3 (January 30, 2020): 445–48. http://dx.doi.org/10.1182/bloodadvances.2019001182.

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Key Points Targeted RNA sequencing detected a cryptic G3BP1-PDGFRB rearrangement in a myeloid neoplasm with eosinophilia and normal FISH studies. Consistent with the patient’s response to imatinib, we demonstrate this rearrangement is oncogenic and sensitive to TKI in cell culture.
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Jamieson, Catriona, Qingfei Jiang, Frida Holm, Jane Isquith, Adam Mark, Cayla Mason, Wenxue Ma, et al. "Inflammatory Cytokine Responsive Enzymatic Mutagenesis Fuels Myeloproliferative Neoplasm Pre-Leukemia Stem Cell Evolution." Blood 134, Supplement_1 (November 13, 2019): 3780. http://dx.doi.org/10.1182/blood-2019-131510.

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Innate immune anti-viral adenosine to inosine (A-to-I) base editing enzymes (editases) promote hematopoietic stem cell (HSC) self-renewal and protect the human genome from retroviral integration in response to inflammatory cytokine signaling. However, hyper-editing has been linked to therapeutic resistance and cancer progression. Because myeloproliferative neoplasm (MPN) progression is typified by increased JAK2/STAT-mediated cytokine signaling, we investigated the cell type and context specific role of adenosine deaminase acting on RNA1 (ADAR1) editaseactivity in MPN pre-leukemia stem cell (pre-LSC) evolution into acute myeloid leukemia stem cells (LSCs). Here we show by whole transcriptome sequencing (RNA-seq) of 113 FACS-purified hematopoietic stem cells and progenitors from 78 individuals, including 54 MPN and AML patients and 24healthy young and aged individuals, that anti-viral signaling pathway activation and splice isoform switching from ADAR1p110 to JAK2/STAT-inducible ADAR1p150 RNA editase activation contributes to MPN progression. Pre-LSC evolution to LSC was characterized by ADAR1p150 upregulation, distinctive RNA editome patterns, STAT3 hyper-editing, increased replating as a measure of self-renewal. Moreover, LSC generation was typified by beta-catenin self-renewal pathway upregulation, which was recapitulated by lentiviral ADAR1p150 overexpression and reversed by lentiviral ADAR1p150 shRNA knockdown. Our studyunderscores the importance of inflammatory-cytokine fueled enzymatic mutagenesis in human MPN pre-LSC evolution to LSC. Thus, this study sets the stage for developing predictive RNA editome biomarkers of LSC generation to guidetherapeutic strategies aimed at preventing progression of hematopoietic malignancies. Disclosures Crews: Ionis Pharmaceuticals: Research Funding.
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Wang, Sam C., Ibrahim Nassour, Shu Xiao, Shuyuan Zhang, Xin Luo, Jeon Lee, Lin Li, et al. "SWI/SNF component ARID1A restrains pancreatic neoplasia formation." Gut 68, no. 7 (October 12, 2018): 1259–70. http://dx.doi.org/10.1136/gutjnl-2017-315490.

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ObjectiveARID1A is commonly mutated in pancreatic ductal adenocarcinoma (PDAC), but the functional effects of ARID1A mutations in the pancreas are unclear. Understanding the molecular mechanisms that drive PDAC formation may lead to novel therapies.DesignConcurrent conditional Arid1a deletion and Kras activation mutations were modelled in mice. Small-interfering RNA (siRNA) and CRISPR/Cas9 were used to abrogate ARID1A in human pancreatic ductal epithelial cells.ResultsWe found that pancreas-specific Arid1a loss in mice was sufficient to induce inflammation, pancreatic intraepithelial neoplasia (PanIN) and mucinous cysts. Concurrent Kras activation accelerated the development of cysts that resembled intraductal papillary mucinous neoplasm. Lineage-specific Arid1a deletion confirmed compartment-specific tumour-suppressive effects. Duct-specific Arid1a loss promoted dilated ducts with occasional cyst and PDAC formation. Heterozygous acinar-specific Arid1a loss resulted in accelerated PanIN and PDAC formation with worse survival. RNA-seq showed that Arid1a loss induced gene networks associated with Myc activity and protein translation. ARID1A knockdown in human pancreatic ductal epithelial cells induced increased MYC expression and protein synthesis that was abrogated with MYC knockdown. ChIP-seq against H3K27ac demonstrated an increase in activated enhancers/promoters.ConclusionsArid1a suppresses pancreatic neoplasia in a compartment-specific manner. In duct cells, this process appears to be associated with MYC-facilitated protein synthesis.
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Seibel, NL, and IR Kirsch. "Tumor detection through the use of immunoglobulin gene rearrangements combined with tissue in situ hybridization." Blood 74, no. 5 (October 1, 1989): 1791–95. http://dx.doi.org/10.1182/blood.v74.5.1791.1791.

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Abstract Leukemias and lymphomas can now be classified according to the particular immunoglobulin, T-cell receptor, or growth-affecting genes they are expressing. Recognition of the structural alterations of lymphoid DNA has been used to identify neoplasms of previously uncertain lineage, to aid in diagnosis, and to define the state of differentiation of the neoplasm. We have developed a procedurally simple, rapid turnaround technique for using tumor-specific gene alterations as tumor-specific markers. Probes can be constructed that will recognize only the gene expressed in the tumor and not those in any of the normal cells when used with tissue in situ hybridization. We demonstrate the application of direct sequencing of a specific gene of interest from total RNA from a patient with multiple myeloma. A probe is then generated from this sequence and applied directly to patient material.
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Seibel, NL, and IR Kirsch. "Tumor detection through the use of immunoglobulin gene rearrangements combined with tissue in situ hybridization." Blood 74, no. 5 (October 1, 1989): 1791–95. http://dx.doi.org/10.1182/blood.v74.5.1791.bloodjournal7451791.

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Leukemias and lymphomas can now be classified according to the particular immunoglobulin, T-cell receptor, or growth-affecting genes they are expressing. Recognition of the structural alterations of lymphoid DNA has been used to identify neoplasms of previously uncertain lineage, to aid in diagnosis, and to define the state of differentiation of the neoplasm. We have developed a procedurally simple, rapid turnaround technique for using tumor-specific gene alterations as tumor-specific markers. Probes can be constructed that will recognize only the gene expressed in the tumor and not those in any of the normal cells when used with tissue in situ hybridization. We demonstrate the application of direct sequencing of a specific gene of interest from total RNA from a patient with multiple myeloma. A probe is then generated from this sequence and applied directly to patient material.
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Nambiar, P. R., S. R. Boutin, R. Raja, and D. W. Rosenberg. "Global Gene Expression Profiling: A Complement to Conventional Histopathologic Analysis of Neoplasia." Veterinary Pathology 42, no. 6 (November 2005): 735–52. http://dx.doi.org/10.1354/vp.42-6-735.

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Transcriptional profiling of entire tumors has yielded considerable insight into the molecular mechanisms of heterogeneous cell populations within different types of neoplasms. The data thus acquired can be further refined by microdissection methods that enable the analyses of subpopulations of neoplastic cells. Separation of the various components of a neoplasm (i.e., stromal cells, inflammatory infiltrates, and blood vessels) has been problematic, primarily because of a paucity of tools for accurate microdissection. The advent of laser capture microdissection combined with powerful tools of linear amplification of RNA and high-throughput microarray-based assays have allowed the transcriptional mapping of intricate and highly complex networks within pure populations of neoplastic cells. With this approach, specific “molecular signatures” can be assigned to tumors of distinct or even similar histomorphology, thereby aiding the desired objective of pattern recognition, tumor classification, and prognostication. This review highlights the potential benefits of global gene expression profiling of tumor cells as a complement to conventional histopathologic analyses.
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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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Gupta, Sanjeev Kumar, Nitin Jain, Guilin Tang, Andrew Futreal, Sa A. Wang, Joseph D. Khoury, Richard K. Yang, et al. "A Cryptic BCR-PDGFRB Fusion Resulting in a Chronic Myeloid Neoplasm With Monocytosis and Eosinophilia: A Novel Finding With Treatment Implications." Journal of the National Comprehensive Cancer Network 18, no. 10 (October 2020): 1300–1304. http://dx.doi.org/10.6004/jnccn.2020.7573.

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RNA-seq was used to identify the partner gene and confirm the presence of a BCR-PDGFRB fusion. Identification of this fusion product resulted in successful treatment and long-term remission of this myeloid neoplasm. Based on our results, we suggest that despite current WHO recommendations, screening for PDGFRB rearrangement in cases of leukocytosis with eosinophilia and no other etiologic explanation is necessary, even if the karyotype is normal.
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Lim, Ha Jin, Jun Hyung Lee, Ju-Hyeon Shin, Seung Yeob Lee, Hyun-Woo Choi, Hyun Jung Choi, Seung Jung Kee, Jong Hee Shin, and Myung-Geun Shin. "Diagnostic Validation of a Clinical Laboratory-Oriented Targeted RNA Sequencing System As a Comprehensive Assay for Hematologic Malignancies." Blood 136, Supplement 1 (November 5, 2020): 38–39. http://dx.doi.org/10.1182/blood-2020-142264.

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Introduction Targeted RNA sequencing (RNA-seq) is a highly accurate method for sequencing transcripts of interest and can overcome limitations regarding resolution, throughput, and multistep workflow. However, RNA-seq has not been widely performed in clinical molecular laboratories due to the complexity of data processing and interpretation. We developed a customized targeted RNA-seq panel with a data processing protocol and validated its analytical performance for gene fusion detection using a subset of samples with different hematologic malignancies. Additionally, we investigated its applicability for identifying transcript variants and expression analysis using the targeted panel. Methods The target panel and customized oligonucleotide probes were designed to capture 84 genes associated with hematologic malignancies. Libraries were prepared from 800 to 1,500 ng of total RNA using GeneMediKit NGS-Leukemia-RNA kit (GeneMedica, Gwangju, Korea) and sequenced using Miseq reagent kit v3 (300 cycles) and MiseqDx (Illumina, San Diego, CA, USA). The diagnostic samples included one reference DNA (NA12878), one reference RNA (Cat no. 740000, Agilent Technologies), 14 normal peripheral blood (PB) samples, four validation bone marrow (BM) samples with known gene fusions, and 30 clinical BM or PB samples from seven categories of hematologic malignancies. The clinical samples included 27 BM aspirates and three PB samples composed of six acute myeloid leukemia, nine B-lymphoblastic leukemia/lymphoma, four T-lymphoblastic leukemia/lymphoma, three mature B-cell neoplasms, six MPN, one myelodysplastic/myeloproliferative neoplasm, and one myeloid/lymphoid neoplasm with eosinophilia and gene rearrangement. For the analytical validation of fusion detection, target gene coverage, between-run and within-run repeatability, and dilution tests (1:2 to 1:8 dilution) were performed. For the comparative analysis of fusion detection, the RNA-seq data were analyzed by STAR-Fusion and FusionCatcher and processed with stepwise filtering and prioritization strategy (Figure 1), and the result was compared to those of multiplex RT-PCR (HemaVision kit; DNA Technology, Aarhus, Denmark) or FISH (MetaSystems Gmbh, Althusseim, Germany) using 30 clinical samples. The RNA-seq data from clinical samples were additionally analyzed by FreeBayes for variant detection and by StringTie for expression profiling (Figure 1). Results First, the analytical validation showed reliable results in target gene coverage, between-run and within-run repeatability, and linearity tests. The uniformity of coverage (% of base pairs higher than 0.2 × total average depth) was calculated to be 99.8%, which revealed even coverage for the target genes in the panel using the reference DNA. Both in the within-run and between-run tests, the read counts and FFPM (fusion fragments per million) of all replicates showed reliable repeatability (r2 = 0.9655 and 0.9874, respectively). The FFPM of the diluted analytical samples including BCR-ABL1 and PML-RARA showed linear log2-fold-changes (r2 = 0.9852 and 0.9447, respectively). Second, compared to multiplex RT-PCR and FISH using 30 clinical samples, targeted RNA-seq combined with filtering and prioritization strategies detected all 13 known fusions and newly detected 17 fusions. Finally, 16 disease- and drug resistance-associated variants on the expressed transcripts of ABL1, GATA2, IKZF1, JAK2, RUNX1, and WT1 were simultaneously designated and expression analysis showed distinct four clusters of clinical samples according to the cancer subtypes and lineages. Conclusions Our customized targeted RNA-seq system provided a stable analytical performance and a more sensitive identification of gene fusions than conventional molecular methods in various clinical samples. In addition, clinically significant variants in the transcripts and expression profiling could be simultaneously identified directly from the RNA-seq data without the need for additional parallel testing. Our study identified the advantages of the clinical laboratory-oriented targeted RNA-seq system to enhance the diagnostic yield for gene fusion detection and to simplify the diagnostic steps as providing a comprehensive tool for analyzing hematologic malignancies in the clinical laboratory. Figure 1 Disclosures Lee: National Research Foundation of Korea: Research Funding.
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Dissertations / Theses on the topic "Neoplasm RNA"

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Velázquez-Fernández, David. "Differential RNA expression in benign and malignant adrenocortical tumours /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-578-X/.

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Moore, Lakisha Dionne. "Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2008p/ldmoore.pdf.

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Farnebäck, Malin. "Quantitative analysis of melanoma transcripts : with emphasis on methodological and biological variation /." Linköping : Univ, 2004. http://www.bibl.liu.se/liupubl/disp/disp2004/med843s.pdf.

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Ménard, Isabelle. "Exploring the many facets of cell death." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111878.

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This thesis summarises research performed with the intent of exploring the many facets of cell death. In the first part of the thesis, the fate of the formin-homology domain containing protein FHOD1 during apoptosis is examined (research performed in the laboratory of Dr. Sophie Roy) and evidence for the cleavage of FHOD1 by caspase-3 at the SVPD616 site is demonstrated. Moreover, the C-terminal FHOD1 cleavage product is shown to translocate to the nucleolus where it inactivates RNA polymerase I transcription.
In the second part of the thesis, the role of the RNA-binding protein HuR in cancer cell migration and invasion, as well as in multidrug resistance is determined using RNA interference to knockdown the expression of HuR in HeLa and KB-V1 cells respectively (research performed in the laboratory of Dr. Imed Gallouzi). In this part of the thesis, HuR is shown to promote cancer cell migration and invasion by stabilizing the beta-actin mRNA in a U-rich-dependent manner. Moreover, evidence is shown for the potential involvement of HuR in the phenomenon of multidrug resistance possibly through the post-transcriptional regulation of the multidrug resistance 1 gene.
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Gouvea, Mirian Nakamura. "Análise comparativa dos transcritomas do córtex adrenal normal e adenocarcinoma do córtex adrenal." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5144/tde-29042008-132519/.

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A carcinogênese do córtex da supra-renal é um processo complexo que envolve alterações genéticas múltiplas e seqüenciais. Embora algumas dessas alterações já tenham sido caracterizadas, de modo geral estes mecanismos permanecem pouco compreendidos. Um conhecimento mais aprofundado dos mesmos não só levaria à descoberta de novos marcadores de prognóstico como também a alvos terapêuticos em potencial. A fim de melhor caracterizarmos os mecanismos envolvidos na progressão maligna do tumor e selecionarmos genes candidatos a serem marcadores de malignidade e alvos terapêuticos, nós estudamos os RNAs de uma linhagem celular derivada de um tumor adrenocortical maligno (NCI-H295A) e um espécime de tumor do córtex da supra-renal por \"Differential Display\" (DDRT-PCR). Foi selecionado um total de 317 transcritos únicos diferencialmente expressos, com base na análise densitométrica digital dos géis de DDRTPCR. A anotação funcional dos genes hiper-expressos mostrou relação com motilidade celular e proliferação. Entre os hipo-expressos foram identificados genes envolvidos na regulação de transcrição, síntese e processamento de RNA e remodelamento da cromatina. A expressão de dois genes entre os transcritos selecionados foi verificada por RT-PCR semi-quantitativa em 19 tumores adrenocorticais adultos e pediátricos, metastáticos e não metastáticos. Os genes da fucosiltransferase-11 e do supressor tumoral BCSC-1 (hiper- e hipo-regulado, respectivamente) encontraram-se diferencialmente expressos nos subgrupos específicos das 19 amostras tumorais. Em suma, o DDRT-PCR revelou-se uma ferramenta valiosa para uma análise global dos transcritomas do córtex da supra-renal e para selecionar genes com possível envolvimento na tumorigênese adrenocortical. Novos aspectos da biologia, progressão e possíveis alvos terapêuticos moleculares puderam ser vislumbrados.
There are important gaps in the present knowledge about adrenocortical tumorigenesis. For this reason we compared by Differential Display RNAs from a carcinoma-derived cell line (NCI-H295A) and a metastatic adrenocortical tumor and characterized 317 differentially expressed transcripts. The up-regulated genes are mainly related to cell motility and proliferation. Among the down-regulated genes, those involved in regulation of transcription, RNA synthesis and processing and chromatin remodeling were identified. Differential expression of FUTT11 and BCSC-1 tumor suppressor gene were confirmed in specific subsets of 19 adult and pediatric adrenocortical tumors and might serve as marker for malignancy. Our data revealed previously unknown aspects of adrenal tumorigenesis.
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Ruiz, Jorge Luis Maria. "Caracterização de uma nanopartícula lipídica semelhante à LDL (LDE) como vetor para RNA de interferência." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/5/5167/tde-14062011-154226/.

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As nanopartículas são consideradas promissores vetores para a liberação eficaz e segura de ácidos nucléicos para tipos específicos de célula ou tecido, proporcionando uma alternativa aos vetores virais para terapia gênica. No entanto, com a maioria destes sistemas não torna possível a entrega de oligonucleotídeos nas células in vivo de forma especifica. O uso de uma nanoemulsão funcionalmente semelhante à lipoproteina de baixa densidade poderia resolver esse problema, pois esta particula é capaz de direcionar o transporte das moléculas para a internalização celular através de receptores de LDL. Aqui, descreve-se um sistema lipidico semelhante à lipoproteína de baixa densidade, LDE, capaz de direcionar e liberar RNA de interferência (RNAi) para as células tumorais in vitro e in vivo em um modelo celular que expressa resistência a múltiplas drogas (células de sarcoma uterino; MESSA/ Dx5). Estudou-se também as caracteristicas de captação do complexo LDE-RNAi e a regulação especifica do gene mdr-1. Os resultados sugerem que a LDE é estavel e liga-se com alta afinidade aos RNAis permitindo que eles entrem nas células tumorais, com localização citoplasmática. Em conclusão, a LDE, por direcionar o RNAi a receptores de LDL favorece o silenciamento do gene mdr-1 por RNAi nas células MES-SA/Dx5 aumentando sua sensibilidade a quimioterápicos
Nanoparticles are considered promising vectors for efficient and safe delivery of nucleic acids to specific types of cell or tissue, providing an alternative to viral vectors for gene therapy. However, most of these systems cannot target and deliver oligonucleotides to specific cells in vivo. The use of nanoemulsion functionally resemble low density emulsion could solve this problem, once particle is capable of direct the molecules transport to the cell through internalization in LDL receptors. Here, we describe a lipid system similar to low density lipoprotein, LDE, capable of targeting and release small interfering RNA (siRNA) to tumor cells in vitro and in vivo in a cell model that expresses multidrug resistance (sarcoma uterine cell line; MES-SA/Dx5). Were also studied the characteristics of uptake of the complex LDE-siRNA, as well as the downregulation of mdr-1 gene. The results suggest that LDE is stable and bind with high affinity to siRNAs allowing them to enter tumor cells, with cytoplasmic localization enhanced. In conclusion, LDE, binds to siRNA through LDL receptors, and promotes mdr-1 silenciament by RNAi in MES-sa/Dx5 cells, increasing their sensitivity to chemotherapeutics agents
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Ghezzi, Tiago Leal. "Comparação da expressão gênica do KRAS mutante, KU70, TACSTD2 e SERIN1 em tecidos tumoral e normal de pacientes com câncer colorretal pela técnica de PCR em tempo real." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2010. http://hdl.handle.net/10183/22996.

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INTRODUÇÃO: O estudo das vias moleculares e das alterações específicas responsáveis pela progressão desfavorável de pacientes com CCR parece essencial para o desenvolvimento de terapias mais efetivas. OBJETIVO: Comparar a expressão quantitativa dos genes TACSTD2, Ku70, KRAS mutante e SERIN1 em amostras de tecidos normal e tumoral de pacientes com CCR e relacionar sua expressão com variáveis clínico-patológicas. MÉTODOS: Foram estudados 37 pacientes com CCR submetidos à ressecção cirúrgica entre julho de 2005 e julho de 2009 e cujas amostras congeladas de tecidos tumoral e normal foram armazenadas em um banco de tecidos. Através da RT-PCR foi sintetizado o cDNA a partir do RNA extraído das amostras teciduais. A expressão dos genes TACSTD2, KRAS mutante, Ku70 e SERIN1 foi quantificada pela técnica de PCR em tempo real. RESULTADOS: A expressão do KRAS mutante foi maior no tecido tumoral do que no normal (p = 0,024). A expressão tumoral dos genes Ku70, TACSTD2 e SERIN1 foi respectivamente menor, igual e maior que o tecido normal, porém sem significância estatística. Associação estatisticamente significativa também foi observada entre idade e expressão de KRAS mutante no tecido normal e tumores pouco diferenciados e expressão de Ku70 no tecido normal. Não foram observadas outras associações estatisticamente significativas. CONCLUSÕES: A expressão do KRAS mutante no tecido tumoral é maior do que no tecido normal (p = 0,024) na casuística de 37 pacientes com CCR estudados através da técnica de PCR em tempo real.
INTRODUCTION: Knowledge of the molecular pathways and of the specific alterations responsible for the unfavorable progression of patients with CCR appears essential for the development of more effective therapies. PURPOSE: To compare the quantitative expression of the genes TACSTD2, mutant KRAS, Ku70 and SERIN1 in samples of normal and tumoral tissues of patients with CCR and to relate their expression to clinicopathologic characteristics. METHODS: 37 patients with CCR were studied. The patients had been operated on between July 2005 and July 2009, and their frozen samples of tumoral and normal tissues had been stored in a tissue bank. The expression of the genes TACSTD2, mutant KRAS, Ku70 and SERIN1 was quantified through the technique of real time polymerase chain reaction. RESULTS: The mutant KRAS expression was higher in the tumoral tissue than in the normal tissue (p = 0,024). Although not significant, the tumoral expression of the genes Ku70, TACSTD2 and SERIN1 was respectively lower, equal to, and higher than in the normal tissue. Statistically significant association was also observed between age and mutant KRAS expression in normal tissue and between poorly-differentiated tumors and Ku70 expression in normal tissue. No other statistically significant associations were observed. CONCLUSIONS: Tumoral tissues express mutant KRAS at higher levels than normal tissues in the casuistic of 37 patients with CCR studied through the technique of PCR real time.
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Higgins, Geoffrey David. "Human papillomavirus RNA transcripts in anogenital neoplasia /." Title page, contents and outline only, 1991. http://web4.library.adelaide.edu.au/theses/09PH/09phh6358.pdf.

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Hoghoughi, Neda. "Caractérisation fonctionnelle d'une nouvelle translocation t(3;5)(q21;q31), ciblant le gène du récepteur aux glucocorticoïde et un ARN non-codant, dans la leucémie aigüe à cellules plasmocytoides dendritiques." Thesis, Grenoble, 2014. http://www.theses.fr/2014GRENV073/document.

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La leucémie aiguë à cellules dendritiques plasmacytoïdes (BPDCN) fait partie des cancers incurables pour lesquels les mécanismes impliqués dans la pathogénèse restent inconnus. Dans ce travail, nous avons identifié le gène NR3C1 (5q31), qui code pour le récepteur des glucocorticoïdes (GCR), et un long ARN non-codant inter-génique (appelé ici lincRNA-3q), comme étant des cibles d'altération géniques ou de dérégulation transcriptionnelles dans les BPDCN. La translocation/délétion de NR3C1 est associée avec un temps de survie extrêmement court et des activités anormales du réseau de régulation des gènes GCR, EZH2 et FOXP3. Nous avons découvert que lincRNA-3q code pour une forme nucléaire d'ARN non-codant qui est activé de façon ectopique dans les BPDCN et les AML à haut risque. Dans les cancers myéloïdes, une déplétion de lincRNA-3q induit un arrêt du cycle cellulaire qui coïncide avec la suppression des signatures d'expression génique de E2F1/Rb et des gènes spécifiques aux cellules souches leucémiques. Nos résultats démontrent qu'une inhibition des protéines à bromodomaine BET supprime sélectivement l'expression lincRNA-3q, indiquant une stratégie thérapeutique potentielle pour contrer l'activité oncogénique de cet ARN non-codant. Ce travail défini, un nouveau cadre de recherche pour comprendre la pathogénèse et la résistance au traitement dans les BPDCN
Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is an incurable malignancy for which disease mechanisms are unknown. Here, we identify the NR3C1 gene (5q31), encoding the glucocorticoid receptor (GCR), and a long, intergenic, non-coding RNA gene (named here lincRNA-3q), respectively, as targets for genetic alteration or transcriptional deregulation in BPDCN. NR3C1 translocation/deletion was associated to critically short survival in BPDCN and to abnormal activity of GCR, EZH2, and FOXP3 gene regulatory networks. LincRNA-3q, was found to encode a nuclear, non- coding RNA that is ectopically activated in BPDCN and high-risk AML. Depletion of lincRNA-3q in myeloid cancer cells induced cell cycle arrest, coincident to suppression of E2F1/Rb and leukemia stem cell-specific gene expression signatures. BET bromodomain protein inhibition could selectively suppress lincRNA-3q indicating a treatment strategy for counteracting oncogenic activity of this non- coding RNA. Thus, this work defines a new framework for understanding disease pathogenesis and treatment resistance in BPDCN
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Faria, André Murad. "Papel do LIN28, uma proteína ligadora de RNAs, na tumorigênese adrenocortical." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-26022015-095301/.

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INTRODUÇÃO: O carcinoma adrenocortical é uma neoplasia rara que carreia um prognóstico reservado. Recentemente, uma série de estudos demonstrou o potencial do perfil de miRNAs na diferenciação entre adenomas e carcinomas adrenocorticais, estratificação de risco e prognóstico. Entretanto, pouco se sabe ainda sobre a regulação pós-transcricional de miRNAs. Nesse contexto, o LIN28 é uma proteína ligadora de RNAs altamente conservada que surgiu como um modulador do let-7, uma importante família de miRNAs amplamente conhecida por seus efeitos supressivos tumorais. Além do let-7, o LIN28 também mostrou regular e ser regulado pelo mir-9, mir-30 e mir-125. OBJETIVOS: Analisar a expressão gênica e proteica do LIN28 em uma grande coorte de tumores adrenocorticais (TACs) de adultos e pediátricos, além de investigar a variação no número de cópias dos genes LIN28A e LIN28B e a expressão dos miRNAs regulatórios do LIN28 (família let-7, mir-9, mir-30 e mir-125) em um subgrupo desta coorte. MÉTODOS: A expressão proteica do LIN28 foi avaliada em um total de 266 TACs de adultos (78 adenomas e 188 carcinomas) e 44 pediátricos (35 clinicamente benignos e 9 clinicamente malignos). A expressão dos genes LIN28A e LIN28B foi avaliada em um subgrupo de 86 TACs adultos e pediátricos e a análise da variação no número de cópias destes genes em 58 TACs. O estudo de expressão das famílias dos miRNAs let-7, mir-9, mir-30 e mir-125 foi realizado em 28 carcinomas adrenocorticais de adultos. RESULTADOS: Em adultos, o gene LIN28A mostrou-se hiperexpresso em carcinomas agressivos quando comparado a adenomas [7,0 (0 a 174,3) vs. 3,6 (0 a 18,3); p = 0,006, respectivamente] e observou-se uma tendência a maior expressão quando comparados a carcinomas não agressivos [7,0 (0 a 174,3) vs. 7,1 (0 a 17,1); p = 0,092]. A expressão do LIN28B foi negativa na grande maioria (92%) dos TACs de adultos. Curiosamente, uma imunorreatividade fraca para o LIN28 foi significativamente associada com diminuição da sobrevida livre de doença nessa população (p = 0,01), mas para sobrevida global apenas uma tendência foi observada (p = 0,117). Na análise multivariada, somente o índice Ki67 >= 10% (RR 5,7, 95% IC 3,0-10,8; p= 0,0001) e imunorreatividade fraca para o LIN28 (RR 2,3, 95% IC 1,2-4,4; p = 0,008) foram preditores independentes de recorrência em adultos. De forma interessante, a expressão do mir-9, um regulador negativo do LIN28A/B, foi significativamente maior em carcinomas agressivos quando comparados a não agressivos [2076 (36 a 9307) vs. 133,4 (2,4 a 5193); p = 0,011] e fortemente associada com a redução da sobrevida global (p = 0,01) e livre de doença (p = 0,01). Na população pediátrica, não se observou diferença significativa entre expressão da proteína LIN28, assim como dos genes LIN28A e mir-9, entre tumores clinicamente benignos e malignos. Nas crianças, a hiperexpressão do LIN28B foi significativamente associada com redução da sobrevida livre de doença (p = 0,026), mas não da sobrevida global (p = 0,406). A análise da variação do número de cópias mostrou que somente uma criança com tumor virilizante benigno apresentou amplificação do LIN28B e uma mulher com carcinoma adrenocortical metastático apresentou deleção do LIN28B. Não houve variação no número de cópias para o gene LIN28A. Um índice de Ki67 >= 20% nas crianças foi capaz de discriminar pacientes com pior prognóstico: houve uma associação significativa tanto com diminuição da sobrevida global (p = 0,015) como da sobrevida livre de doença (p = 0,001) em 36 TACs pediátricos com Weiss >- 3. CONCLUSÕES: A imunorreatividade fraca para o LIN28 foi associada à diminuição da sobrevida livre de doença em uma grande coorte de carcinomas adrenocorticais de adultos. O gene LIN28A teve expressão aumentada em carcinomas agressivos de adultos, sugerindo uma regulação pós-transcricional negativa da expressão proteica do LIN28. A hiperexpressão do mir-9, um regulador negativo do LIN28, mostrou-se um importante preditor de desfecho desfavorável nos adultos. Adicionalmente, a hiperexpressão do gene LIN28B mostrou-se um potencial marcador de mau prognóstico na população pediátrica. Um índice de Ki67 >= 10% em adultos e >= 20% em crianças foram associados a mau prognóstico
INTRODUCTION: Adrenocortical carcinoma is a rare neoplasm with overall poor prognosis. Recently, several studies demonstrated the potential of miRNA profiling in differentiating between adrenocortical adenomas and carcinomas, risk stratification and prognosis. Nevertheless, little is known about posttranscriptional regulation of miRNAs. LIN28 is a highly conserved RNA-binding protein that has emerged as a modulator of the processing of let-7, an important family of miRNAs widely known for its tumor-suppressive effects. Besides from let-7, LIN28 has also shown to regulate and be regulated by mir-9, mir-30 and mir-125. OBJECTIVES: To analyze LIN28 gene and protein expression in a large cohort of adult and pediatric adrenocotical tumors (ACTs), and investigate the copy number variation analysis for LIN28A and LIN28B genes and the expression of LIN28 regulatory microRNAs (let-7 family, mir-9, mir-30 e mir-125) in a subgroup of this cohort. METHODS: LIN28 protein expression was assessed in a total of 266 adult (78 adenomas and 188 carcinomas) and 44 pediatric ACTs (35 clinically benign and 9 clinically malignant). LIN28A and LIN28B gene expression was evaluated in a subgroup of 86 adult and pediatric ACTs and copy number variation analysis of these genes in 58 ACTs. The expression of let-7 family, mir-9, mir-30 and mir-125 was performed in 28 adult carcinomas. RESULTS: In adults, LIN28A gene was overexpressed in aggressive carcinomas when compared with adenomas [7.0 fold change (from 0 to 174.3) vs. 3.6 (from 0 to 18.3); p = 0.006, respectively] and a trend towards greaten expression when compared with non-aggressive carcinomas [7.0 (from 0 to 174.3) vs. 7.1 (from 0 to 17.1); p = 0.092]. LIN28B expression was undetectable in the great majority (92%) of adult ACTs. Surprisingly, weak LIN28 staining was significantly associated with reduced disease-free survival in this population (p = 0.01), but for overall survival only a trend was detectable (p= 0.117). In the multivariate analysis, only Ki67 index >- 10% (HR 5.7, 95% CI 3.0-10.8; p = 0,0001) and weak LIN28 staining (HR 2.3, 95% CI 1.2-4.4; p = 0,008) were independent predictors of recurrence in adult patients. Interestingly, mir-9 expression, a negative LIN28A/B regulator, was significantly higher in aggressive than in non-aggressive ACCs [2076 (from 36 to 9307) vs. 133.4 (from 2.4 to 5193); p = 0.011] and was highly associated with reduced overall survival ( p= 0.01) and disease-free survival (p = 0.01). In the pediatric population, no significant difference was observed in the expression of LIN28 protein and LIN28A and mir-9 gene expression between clinically benign and clinically malignant tumors. Additionally. overexpression of LIN28B was significantly associated with reduced disease-free survival (p = 0.026), but not with overall survival (p = 0.406). Copy number variation analysis showed that only a child with a virilizing benign tumor had LIN28B amplification and a woman with a metastatic adrenocortical carcinoma had LIN28B deletion. No LIN28A copy number variation was detected. A Ki67 >= 20% in children was able to discriminate patient with worse prognosis: there was a significant associtation with reduced overall (p = 0,015) and disease-free survival (p = 0,001) in 36 pediatric ACTs with Weiss >- 3. CONCLUSIONS: Weak LIN28 staining was associated with reduced disease-free survival in a large cohort of adult adrenocortical carcinoma. LIN28A had higher expression in aggressive carcinomas in adults, suggesting there might be negative posttranscriptional regulation of LIN28 protein expression. Interestingly, overexpression of mir-9, a negative LIN28A regulator, predicted poor outcome in adult patients. In addition, LIN28B overexpression was an potential marker of poor prognosis in the pediatric population. A Ki67 index >- 10% in adults and >- 20% in children were associated with poor prognosis
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Books on the topic "Neoplasm RNA"

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RNA therapeutics: Function, design, and delivery. New York: Humana Press, 2010.

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Venables, Julian P. Alternative splicing in cancer. Trivandrum, Kerala, India: Transworld Research Network, 2006.

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1946-, Furmanski Philip, Hager Jean Carol 1943-, and Rich Marvin A, eds. RNA tumor viruses, oncogenes, human cancer, and AIDS: On the frontiers of understanding : proceedings of the International Conference on RNA Tumor Viruses in Human Cancer, Denver, Colorado, June 10-14, 1984. Boston: M. Nijhoff, 1985.

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Slabý, Ondřej. MicroRNAs in solid cancer: From biomarkers to therapeutic targets. Hauppauge, N.Y: Nova Science, 2011.

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Slack, Frank J. MicroRNAs in development and cancer. London: Imperial College Press, 2011.

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Metagenomics: Methods and protocols. New York, NY: Humana Press, 2010.

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1949-, Müller S. C., ed. Synthetic peptides as antigens. Amsterdam: Elsevier, 1999.

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Kwang, Lee B. New Messenger RNA Research Communications. Nova Science Pub Inc, 2006.

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Barciszewski, Jan, and Volker A. Erdmann. DNA and RNA Nanobiotechnologies in Medicine: Diagnosis and Treatment of Diseases. Springer, 2013.

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Barciszewski, Jan, and Volker A. Erdmann. DNA and RNA Nanobiotechnologies in Medicine: Diagnosis and Treatment of Diseases. Springer, 2015.

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Book chapters on the topic "Neoplasm RNA"

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Lane, M. A., H. A. F. Stephens, M. B. Tobin, and Kevin Doherty. "Stage Specific Transforming Genes in Lymphoid Neoplasms." In RNA Tumor Viruses, Oncogenes, Human Cancer and AIDS: On the Frontiers of Understanding, 127–32. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2583-3_11.

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Chan, Daniel K., Cadman L. Leggett, and Kenneth K. Wang. "RFA for early esophageal neoplasia." In Esophageal cancer and barrett's esophagus, 151–60. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118655153.ch16.

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DiPaolo, J. A., and C. D. Woodworth. "Molecular Control of Human Papillomavirus RNA Expression in Neoplasia." In Antimutagenesis and Anticarcinogenesis Mechanisms III, 239–46. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2984-2_21.

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Croce, Carlo M., and Peter C. Nowell. "Molecular Basis of Human B Cell Neoplasia." In RNA Tumor Viruses, Oncogenes, Human Cancer and AIDS: On the Frontiers of Understanding, 116–26. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2583-3_10.

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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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Alahari, S. V., S. C. Eastlack, and S. K. Alahari. "Role of Long Noncoding RNAs in Neoplasia: Special Emphasis on Prostate Cancer." In International Review of Cell and Molecular Biology, 229–54. Elsevier, 2016. http://dx.doi.org/10.1016/bs.ircmb.2016.01.004.

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Conference papers on the topic "Neoplasm RNA"

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Ma, Wenxue, Larisa Balaian, Cayla Mason, Raymond Diep, Jessica Pham, Qingfei Jiang, Jeremy Lee, et al. "Abstract 3792: Imetelstat inhibits RNA-editing mediated myeloproliferative neoplasm stem cell self-renewal." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-3792.

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Khan, H., and S. Cochrane. "PTH-007 Real world experience with rfa/emr in early oesophageal neoplasia." In British Society of Gastroenterology, Annual General Meeting, 19–22 June 2017, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2017. http://dx.doi.org/10.1136/gutjnl-2017-314472.404.

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Carter, Jane, Vanessa States, Uri Netz, Jianmin Pan, Shesh Rai, and Susan Galandiuk. "Abstract B32: Longitudinal changes in plasma miRNA in patients with benign and malignant colorectal neoplasia." In Abstracts: AACR Special Conference on Noncoding RNAs and Cancer: Mechanisms to Medicines; December 4-7, 2015; Boston, MA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.nonrna15-b32.

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Krishnamoorthy, Yuthiesshan, Paul Brennan, and Elaine Henry. "PTH-017 long-term outcomes for RFA in early barrett’s-associated neoplasia – are we succeeding?" In British Society of Gastroenterology, Annual General Meeting, 4–7 June 2018, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-bsgabstracts.39.

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Dancour, A., M. Rottenstreich, G. Sheynkman, E. Tahover, D. Wengrower, E. Goldin, T. Golan, and D. Livovsky. "EUS-GUIDED, RFA ABLATION OF BENIGN AND MALIGNANT PANCREATIC NEOPLASMS AND EXTRA PANCREATIC METASTASIS IS FEASIBLE AND SAFE." In ESGE Days 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1681348.

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Santiago-Garcia, J., J. Ortiz Fernández-Sordo, M. Pana, S. Beg, and K. Ragunath. "OESOPHAGEAL STRICTURES AFTER RADIOFREQUENCY ABLATION (RFA) FOR EARLY BARRETT'S NEOPLASIA: STANDARD VS. SIMPLIFIED PROTOCOL. A RETROSPECTIVE STUDY IN A SINGLE TERTIARY REFERRAL CENTRE." In ESGE Days 2018 accepted abstracts. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1637131.

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Younis, F., O. Shibolet, A. Philips, E. Santo, and E. Scapa. "SAFETY AND EFFICACY OF ENDOSCOPIC ULTRASOUND-GUIDED RADIOFREQUENCY ABLATION (EUS-RFA) OF PANCREATIC CYSTIC NEOPLASMS (PCNS) AND PANCREATIC NEUROENDOCRINE TUMORS (PNETS): PRELIMINARY REPORT OF A PROSPECTIVE COHORT." In ESGE Days 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1681344.

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Bohm, Emanuelle Fick, and Ernesto de Paula Guedes Neto. "Metástase de carcinoma de sítio primário de mama para o trato genital feminino: relato de caso e revisão de literatura." In 44° Congresso da SGORJ - XXIII Trocando Ideias. Zeppelini Editorial e Comunicação, 2020. http://dx.doi.org/10.5327/jbg-0368-1416-2020130245.

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Introdução: Os sítios mais comuns de metástases de câncer de mama são pulmões, ossos, fígado e cérebro. Sítios menos comuns incluem trato gastrointestinal, pâncreas, baço, tireoide, adrenais, rins, coração e trato genital feminino (TGF). As metástases no TGF de sítios primários distantes são incomuns, mas quando se apresentam, tendem a estar envolvidas com os ovários ou o endométrio. O relato deste estudo retrata a ocorrência de neoplasia maligna metastática paratubária em paciente com carcinoma primário de mama. Objetivos: Relatar o caso de uma paciente com metástase de carcinoma de sítio primário de mama para o TGF e revisar na literatura disponível tal ocorrência. Material e Métodos: As informações do caso foram obtidas a partir da revisão de prontuário, registro fotográfico diagnóstico da paciente e revisão de literatura. A revisão foi realizada na base de dados do PubMed, em estudos publicados nos últimos 20 anos (2000‒2020), com os termos “breast cancer” AND “metastasis” AND “female genital tract”. Os artigos selecionados foram estudos meta-analíticos, casos clínicos e revisões na língua inglesa. Resultados e Conclusão: Paciente, sexo feminino, 70 anos, G1P1. Há 20 anos submetida à mastectomia esquerda apresentando carcinoma ductal invasor (CDI), com RE e RP positivo e Human Epidermal growth factor Receptor-type 2 (HER2) negativo. Realizou histerectomia com anexotomia profilática com diagnóstico de neoplasia maligna metastática em tuba esquerda com 1:1 cm no maior eixo. Exame imuno-histoquímico apresentando GATA3 negativo, CK7, Mamoglobina, PAX8, RP e RE positivos. Exames laboratoriais e de imagem pré-operatórios negativos para neoplasia. O CDI é o tipo mais comum de câncer de mama invasivo, seguido pelo carcinoma lobular invasivo (CLI). Contudo, metástases para o TGF são mais frequentemente associadas ao CLI do que ao CDI. Estima-se que mais de 80% dos cânceres de mama que metastatizam para o TGF são CLI. Um estudo realizado em mulheres com metástase ginecológica (n=54) demonstrou que 42,6% tinham câncer de mama correspondente a CLI; 48,1%, carcinoma invasor sem tipo específico; e 9,3%, outros. Além disso, o estudo revelou que os sítios de metástases ginecológicas mais envolvidos foram os ovários, seguido das tubas e do útero. A respeito da expressão de biomarcadores de tumores primários que se espalharam para sítios ginecológicos, 93,5% expressou RE positivo; 65,7%, RP positivo; e 0%, HER2 positivo. Uma avaliação de 13 casos mostrou que, enquanto a expressão de RE e FOXA1 foi mantida ou aumentada durante a progressão para órgãos ginecológicos, a expressão de proteínas acessórias envolvidas com a regulação hormonal diminuiu. Conforme o aumento do tumor, as células que expressam RP, RA e GATA3 em metástases distantes diminuíram em 69,2, 38,5 e 46% dos casos, respectivamente. O relato em questão confirma os resultados obtidos nos estudos, já que apresenta semelhança na expressão gênica de carcinomas primários de mama com metástase para o TGF. No entanto, apresenta um histotipo incomum para metástases ginecológicas.
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