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Littérature scientifique sur le sujet « Multiplex immunohistochemistry »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 14 mars 2023

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Articles de revues sur le sujet "Multiplex immunohistochemistry"

Wistuba, I., E. Parra et A. Francisco Cruz. « MS17.04 Multiplex Immunohistochemistry ». Journal of Thoracic Oncology 14, n^o 10 (octobre 2019) : S191. http://dx.doi.org/10.1016/j.jtho.2019.08.380.

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Sheng, Wenjie, Chaoyu Zhang, T. M. Mohiuddin, Marwah Al-Rawe, Felix Zeppernick, Franco H. Falcone, Ivo Meinhold-Heerlein et Ahmad Fawzi Hussain. « Multiplex Immunofluorescence : A Powerful Tool in Cancer Immunotherapy ». International Journal of Molecular Sciences 24, n^o 4 (4 février 2023) : 3086. http://dx.doi.org/10.3390/ijms24043086.

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Traditional immunohistochemistry (IHC) has already become an essential method of diagnosis and therapy in cancer management. However, this antibody-based technique is limited to detecting a single marker per tissue section. Since immunotherapy has revolutionized the antineoplastic therapy, developing new immunohistochemistry strategies to detect multiple markers simultaneously to better understand tumor environment and predict or assess response to immunotherapy is necessary and urgent. Multiplex immunohistochemistry (mIHC)/multiplex immunofluorescence (mIF), such as multiplex chromogenic IHC and multiplex fluorescent immunohistochemistry (mfIHC), is a new and emerging technology to label multiple biomarkers in a single pathological section. The mfIHC shows a higher performance in cancer immunotherapy. This review summarizes the technologies, which are applied for mfIHC, and discusses how they are employed for immunotherapy research.

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Gannot, Gallya, Michael A. Tangrea, Heidi S. Erickson, Peter A. Pinto, Stephen M. Hewitt, Rodrigo F. Chuaqui, John W. Gillespie et Michael R. Emmert-Buck. « Layered Peptide Array for Multiplex Immunohistochemistry ». Journal of Molecular Diagnostics 9, n^o 3 (juillet 2007) : 297–304. http://dx.doi.org/10.2353/jmoldx.2007.060143.

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Morrison, Larry E., Mark R. Lefever, Lauren J. Behman, Torsten Leibold, Esteban A. Roberts, Uwe B. Horchner et Daniel R. Bauer. « Brightfield multiplex immunohistochemistry with multispectral imaging ». Laboratory Investigation 100, n^o 8 (27 avril 2020) : 1124–36. http://dx.doi.org/10.1038/s41374-020-0429-0.

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Forsberg, Peter A., Andrew Hammes, Diana Abbott, Daniel W. Sherbenou, Adriana Rossi, David Jayabalan, Ruben Niesvizky, Tomer M. Mark et Scott Ely. « Cellular proliferation by multiplex immunohistochemistry identifies aggressive disease behavior in relapsed multiple myeloma ». Leukemia & ; Lymphoma 60, n^o 8 (11 janvier 2019) : 2085–87. http://dx.doi.org/10.1080/10428194.2018.1551537.

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Barrow, Emma, D. Gareth Evans, Ray McMahon, James Hill et Richard Byers. « A comparative study of quantitative immunohistochemistry and quantum dot immunohistochemistry for mutation carrier identification in Lynch syndrome ». Journal of Clinical Pathology 64, n^o 3 (22 décembre 2010) : 208–14. http://dx.doi.org/10.1136/jcp.2010.084418.

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AimsLynch Syndrome is caused by mutations in DNA mismatch repair (MMR) genes. Mutation carrier identification is facilitated by immunohistochemical detection of the MMR proteins MHL1 and MSH2 in tumour tissue and is desirable as colonoscopic screening reduces mortality. However, protein detection by conventional immunohistochemistry (IHC) is subjective, and quantitative techniques are required. Quantum dots (QDs) are novel fluorescent labels that enable quantitative multiplex staining. This study compared their use with quantitative 3,3′-diaminobenzidine (DAB) IHC for the diagnosis of Lynch Syndrome.MethodsTumour sections from 36 mutation carriers and six controls were obtained. These were stained with DAB on an automated platform using antibodies against MLH1 and MSH2. Multiplex QD immunofluorescent staining of the sections was performed using antibodies against MLH1, MSH2 and smooth muscle actin (SMA). Multispectral analysis of the slides was performed. The staining intensity of DAB and QDs was measured in multiple colonic crypts, and the mean intensity scores calculated. Receiver operating characteristic (ROC) curves of staining performance for the identification of mutation carriers were evaluated.ResultsFor quantitative DAB IHC, the area under the MLH1 ROC curve was 0.872 (95% CI 0.763 to 0.981), and the area under the MSH2 ROC curve was 0.832 (95% CI 0.704 to 0.960). For quantitative QD IHC, the area under the MLH1 ROC curve was 0.812 (95% CI 0.681 to 0.943), and the area under the MSH2 ROC curve was 0.598 (95% CI 0.418 to 0.777).ConclusionsDespite the advantage of QD staining to enable several markers to be measured simultaneously, it is of lower utility than DAB IHC for the identification of MMR mutation carriers. Automated DAB IHC staining and quantitative slide analysis may enable high-throughput IHC.

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Harmsen, Marissa J., Arda Arduç, Maaike C. G. Bleeker, Lynda J. M. Juffermans, Arjan W. Griffioen, Ekaterina S. Jordanova et Judith A. F. Huirne. « Increased Angiogenesis and Lymphangiogenesis in Adenomyosis Visualized by Multiplex Immunohistochemistry ». International Journal of Molecular Sciences 23, n^o 15 (29 juillet 2022) : 8434. http://dx.doi.org/10.3390/ijms23158434.

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There is evidence for increased angiogenesis in the (ectopic) endometrium of adenomyosis patients under the influence of vascular endothelial growth factor (VEGF). VEGF stimulates both angiogenesis and lymph-angiogenesis. However, information on lymph vessels in the (ectopic) endometrium of adenomyosis patients is lacking. In this retrospective matched case-control study, multiplex immunohistochemistry was performed on thirty-eight paraffin embedded specimens from premenopausal women who had undergone a hysterectomy at the Amsterdam UMC between 2001 and 2018 to investigate the evidence for (lymph) angiogenesis in the (ectopic) endometrium or myometrium of patients with adenomyosis versus controls with unrelated pathologies. Baseline characteristics of both groups were comparable. In the proliferative phase, the blood and lymph vessel densities were, respectively, higher in the ectopic and eutopic endometrium of patients with adenomyosis than in the endometrium of controls. The relative number of blood vessels without α-smooth muscle actinin (α SMA) was higher in the eutopic and ectopic endometrium of adenomyosis patients versus controls. The level of VEGF staining intensity was highest in the myometrium but did not differ between patients with adenomyosis or controls. The results indicate increased angiogenesis and lymphangiogenesis in the (ectopic) endometrium affected by adenomyosis. The clinical relevance of our findings should be confirmed in prospective clinical studies.

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Oscar, Brück, Sami Blom, Riku Turkki, Panu E. Kovanen, Antonio Ribeiro, Nina Linder, Johan Lundin, Olli Kallioniemi, Teijo Pellinen et Satu Mustjoki. « Immune Cell Profiling in CML Bone Marrow By Multiplex Immunohistochemistry ». Blood 128, n^o 22 (2 décembre 2016) : 1897. http://dx.doi.org/10.1182/blood.v128.22.1897.1897.

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Abstract Background In most solid tumors, CD8+ cytotoxic T-cells and type 1 T-helper cells are associated with a positive prognosis, but a strong immunosuppressive microenvironment may hamper their effectiveness. This notion has contributed to the development of new immune-activating therapies, such as immune checkpoint inhibitors. Although having demonstrated long-term remissions in many different solid tumor types, immune checkpoint inhibitors have not been evaluated comprehensively in hematological malignancies. In this study, we aimed to characterize the cellular and molecular immunological profiles of chronic myeloid leukemia (CML) patients' bone marrow (BM) samples. Methods BM biopsies were taken at the time of diagnosis from chronic phase CML patients (n=57) treated in the Helsinki University Hospital during years 2005-2015. We used non-leukemic (NL) BM biopsies (n=10) as controls. Using hematopathologic expertise, we constructed tissue microarray (TMA) blocks from duplicate BM spots characterized with high leukemic cell infiltration. We stained TMA slides using multiplexed immunohistochemistry (IHC) combining fluorescent and chromogenic staining allowing detection of up to six markers and nuclei simultaneously. Marker panels included T and B-lymphoid (CD3, CD4, CD8, CD20), myeloid dendritic (CD11c, BDCA-1, BDCA-3), macrophage (CD68, pSTAT1, c-MAF), natural killer cell (CD3 and CD56) and leukemia cell (CD34) markers. In addition, we examined immune checkpoint molecules (PD1, CTLA4, OX40, LAG3, TIM3) and their ligands in leukemic cells (HLA-G, PD-L1, PD-L2, HLA-ABC), as well as activation markers (CD25, CD27, CD57, Granzyme B and CD45RO). We analyzed leukemia patients' immune checkpoint expression profiles quantitatively using the image analysis software Cell Profiler and cell analysis software FlowJo and compared results with NL BMs' immune cell profiles. Results The proportion of CD3+ T cells of all cells was significantly higher in CML BM vs. NL BM (median 6.0% [interquartile range (IQR) 3.6-10.7] vs. 2.1% [IQR 1.5-4.5], p=0.001). There was no significant difference in CD8+ cytotoxic T cell levels, but CD4+ helper T cells were 8-fold more abundant in CML as compared to non-leukemic BM (p<0.0001). The proportion of both memory CD45RO+CD8+ T cells (62.2% [IQR 47.4-69.8] vs. 47.3% [IQR 27.9-56.2] of CD8+ T cells, p=0.03) and memory CD45RO+CD4+ T cells (61.8% [IQR 51.8-68.5] vs. 40.0% [IQR 25.6-57.9] of CD4+ T cells, p=0.004) were significantly higher in leukemic patients. Although the proportion of PD1+CD8+ T cells did not differ between CML and NL BM, there was a significantly lower proportion of PD1+CD4+ T cells in CML BM vs. NL BM (25.1% [IQR 17.0-38.7] vs. 69.5% [IQR 50.7-77.9], p<0.0001). However, as the number of CD4+ T cells was increased in CML, the absolute number of CD4+PD1+ T cells of total cell population was 3-fold higher in CML BM than in NL BM (p=0.02). Both the proportion of OX40+CD4+ T cells (42.3% [IQR 28.7-51.6] vs. 18.1% [IQR 13.2-22.9], p=0.001) and OX40+CD8+ T cells (42.6% [IQR 25.8-60.7] vs. 12.7% [IQR 5.0-15.8], p<0.0001) were increased in leukemic patients. Interestingly, also the proportion of OX40+PD1+CD8+ T cells (25.7% [IQR 15.4-36.4] vs. 11.9% [IQR 5.0-15.8], p=0.0019) was higher in CML samples. Conclusion Multiplex IHC allows detailed characterization of immune cell subtypes and their phenotypes in BM biopsy samples. Our data show significant heterogeneity in immune cell subsets between individual patients. The CML BM is characterized with an increase in CD3+ T cells, especially helper T cells and CD45RO+ memory T cells, when compared to non-leukemic BM. Phenotypically, OX40+PD1neg T cells and OX40+PD1+ cytotoxic T cells were elevated in CML patients. The analysis of other immune cell subclasses, including inhibitory immune cells, and the correlation of histologic findings to prognostic data are ongoing. Together, they will provide a detailed understanding of BM immune cell composition in CML. Disclosures Mustjoki: Novartis: Honoraria, Research Funding; Ariad: Research Funding; Bristol-Myers Squibb: Honoraria, Research Funding; Pfizer: Honoraria, Research Funding.

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Silverman, Andrew, Matthew Ingham, Robyn Denise Gartrell, Douglas Kanter Marks, Hojung Rachel Park, Thomas D. Hart, Camden L. Esancy et al. « Interrogating the sarcoma immune microenvironment (iME) using multiplex immunohistochemistry (mIHC). » Journal of Clinical Oncology 36, n^o 15_suppl (20 mai 2018) : 11536. http://dx.doi.org/10.1200/jco.2018.36.15_suppl.11536.

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Ugolini, Filippo, Elisa Pasqualini, Sara Simi, Gianna Baroni et Daniela Massi. « Bright-Field Multiplex Immunohistochemistry Assay for Tumor Microenvironment Evaluation in Melanoma Tissues ». Cancers 14, n^o 15 (28 juillet 2022) : 3682. http://dx.doi.org/10.3390/cancers14153682.

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The tumor microenvironment (TME) plays a crucial role in melanoma development, progression and response to treatment. As many of the most relevant TME cell phenotypes are defined by the simultaneous detection of more than two markers, the bright-field (BF) multiplex immunohistochemistry (IHC) technique has been introduced for the quantitative assessment and evaluation of the relative spatial distances between immune cells and melanoma cells. In the current study, we aimed to validate BF multiplex IHC techniques in the Ventana Discovery Ultra Immunostainer to be applied to the evaluation of the TME in variably pigmented melanoma tissues. The BF multiplex IHC staining was performed using different combinations of six immune-cell markers—CD3, CD4, CD8, CD20, CD68 and CD163—and the melanoma cell marker SOX10. Our results show that the BF double IHC Yellow/Purple protocol guarantees the maximum contrast in all the cell populations tested and the combination SOX10 (Green), CD8 (Yellow) and CD163 (Purple) of the BF triple IHC protocol ensures the best contrast and discrimination between the three stained cell populations. Furthermore, the labeled cells were clearly distinct and easily identifiable using the image analysis software. Our standardized BF IHC multiplex protocols can be used to better assess the immune contexts of melanoma patients with potential applications to drive therapeutic decisions within clinical trials.

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Thèses sur le sujet "Multiplex immunohistochemistry"

Akarca, Ayse. « Immunohistochemical studies for identification of biomarkers in haematological malignancies : An approach for potential novel therapeutic targets ». Doctoral thesis, Università di Siena, 2021. http://hdl.handle.net/11365/1127626.

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Lymphoid neoplasms are a subgroup of haematological malignancies that affect circulating lymphocytes. The clinical and biological heterogeneity of lymphoid neoplasms can lead to difficulty in accurate diagnosis in this group of diseases. The advancement in effective and feasible detection platforms has enabled novel biomarkers to improve diagnosis and prognosis, in addition to assist in patient stratification and personalised treatments for these diseases. Although there have been improvements in high-throughput diagnostic techniques, the conventional immunohistochemistry (IHC) remains the most widely used platform for biomarker assessment in the field of tissue pathology. As this conventional technique has certain limitations, multiplex IHC (MIHC) approaches have found ways to overcome these challenges, therefore becoming the main focus of immunotherapy for lymphoid neoplasms. This particular effective and proficient technology can simultaneously target multiple molecule/protein of interest within the tumor microenvironment to determine the status of immune cell activation and the presence of protein expression. MIHC is advantageous in providing information about the underlying immune evasion mechanisms, which play a vital role in the development of prognostic and diagnostic biomarkers. This thesis focuses on the novel use of IHC/MIHC approaches and their current role in biomarker development to be used in diagnosis, prognosis, and the potential treatment strategies within haematological malignancies in specific lymphoid neoplasms.

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Oguejiofor, Kenneth Kenechukwu. « Prognostic markers in oropharyngeal cancers ». Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/prognostic-markers-in-oropharyngeal-cancers(fda96224-657d-4049-ae6c-50db33a5388a).html.

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Introduction: Human papillomavirus (HPV) is changing the prevalence, survival and treatment paradigms in oropharyngeal squamous cell carcinoma (OPSCC). Improved survival of patients with HPV positive compared to HPV negative OPSCC has led to trials of treatment de-escalation. Current HPV detection methods are imprecise, therefore standardised assessment of transcriptionally active HPV in OPSCC is required. Furthermore, the differences in immune characteristics and/or the hypoxia response/effects could explain observed differences in prognosis between HPV positive and negative OPSCC. Rigorous HPV detection and subsequent biomarker evaluation should provide additional information required before introduction of treatment de-escalation in broad patient groupings. Methods: The study cohort was 218 patients with OPSCC who received radiotherapy with curative intent. HPV status was determined on pre-treatment, formalin-fixed paraffin-embedded blocks using: 1) polymerase chain reaction (PCR); 2) in-situ hybridisation (ISH) and 3) immuno-histochemistry (IHC). QuantiGene multiplex assay was designed to detect mRNA of reference sequences of the common high-risk HPV types (16, 18, 33, 35, 45, 52 and 58). HPV detection methods were compared with mRNA quantification. Multimarker IHC of immune cell markers using chromogenic and fluorescent staining was performed, analysed and compared with single marker IHC using automated multispectral image analysis. A validated multiplex IHC method was used for a) chromogenic (CD3, CD4, CD8, and FoxP3) and b) fluorescent (CD8, CD68 and PD1/PD-L1) evaluation in tumour and stroma compartments. Single marker IHC was used to investigate tumour hypoxia markers (HIF-1α and CA-IX) in HPV positive and negative OPSCC. Results: p16 IHC and ISH were the most sensitive and specific, respectively, for classifying HPV status. The combination of the three tests had the highest positive/negative predictive values compared with QuantiGene mRNA detection. Multiplex validation showed that, for serial sections up to 6 μm apart, there were highly significant correlations (P<0.0001) between single and multiplex counts for both chromogenic and fluorescent IHC. Overall there was less variation in cell counts with fluorescent staining when compared to chromogenic staining. Multiplex IHC of TILs in HPV positive and negative OPSCC showed higher infiltration in both tumour and stromal areas of CD3+CD4+ and CD3+CD8+ T cells but not CD4+FoxP3 Tregs in HPV positive compared with HPV negative OPSCC. Only CD3+CD8+ stromal and not tumour area infiltration was associated with increased survival (P=0.02). PD-L1 expression was higher in HPV negative OPSCC and this was related to macrophage (CD68) expression of PD-L1. In HPV negative tumours infiltration with CD68+PD-L1 was associated with a good prognosis. HPV negative patients had higher expression of HIF-1α but not CA-IX. High expression of both markers was associated with a poor prognosis irrespective of HPV status. Conclusions: There are other prognostic factors operating in the larger subdivision of HPV positive and negative OPSCC. Precise HPV detection and inclusion of other prognostic factors is required before treatment de-escalation is used. Expression of immune inhibitory factors (PD1/PD-L1) alone without contextualisation with immune cell density is insufficient for patient prognostication and potential selection for therapy using immune checkpoint inhibitors. Hypoxia modification of radiotherapy should be explored in both HPV positive and negative OPSCC.

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Pomeroy, Ian. « Neocortical lesions in an animal model of multiple sclerosis ». Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670186.

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Padrão, Ines Liguori. « Adenomas hipofisarios : estudo clinico, morfologico e morfometrico ; busca de fatores de prognostico utilizando o metodo imunoistoquimico ». [s.n.], 2007. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311565.

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Orientador: Patricia Sabino de Matos
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-09T15:50:12Z (GMT). No. of bitstreams: 1 Padrao_InesLiguori_D.pdf: 2489921 bytes, checksum: 62e17012ad64cca8cff1b95a7a39190e (MD5) Previous issue date: 2007
Resumo: Adenomas hipofisários (AH) são neoplasias epiteliais geralmente bem diferenciadas e benignas. Manifestam-se clinicamente com sintomas de excesso ou redução hormonal e/ou de massa intracraniana. São classificados conforme aspecto macroscópico/radiológico (macro x microadenomas; invasivos x não invasivos), status funcional (funcionantes x não funcionantes), citológico (acidófilos, basófilos e cromófobos) e imunoistoquímicos/ultraestruturais (somatotropinomas, prolactinomas, orticotropinomas, tireotropinomas, gonadotropinomas e de células nulas). Entre as heterogêneas formas de apresentação, evolução e manifestações clínicas, adenomas invasivos e macroadenomas não invasivos são os que limitam o tratamento cirúrgico, com recidivas determinantes de morbidade endócrina e /ou neurológica. Variantes agressivas e não agressivas podem exibir aspecto histológico semelhante, motivando a investigação imunoistoquímica, genética e de biologia molecular, com o propósito de relacionar mecanismos de tumorigênese com o comportamento biológico desses tumores, como crescimento invasivo e recorrência. Objetivos Classificação e estudo da freqüência dos AH da amostra sob o ponto de vista funcional embasada na sintomatologia clínica; Classificação anatômica/neuroradiológica baseada no tamanho tumoral e grau de invasão, utilizando a gradação de Jules Hardy; Classificação e estudo da freqüência dos subtipos hormonais, utilizando o método imunoistoquímico. Correlacionar dados clínicos, anatômicos, imunoistoquímicos, com o grau de agressividade dos AH, buscando fatores de prognóstico utilizando marcadores de atividade proliferativa (Ki 67), alteração de gene supressor tumoral (p53 e menin), angiogênese (CD 34) e expressão de neuropeptídeo (Galanina). Material e métodos Avaliamos AH de 61 pacientes submetidos à ressecção cirúrgica, sob o ponto de vista clínico, anatômico/neuroradiológico e imunoistoquímico. Utilizamos a técnica imunoistoquímica: para a determinação dos diferentes subtipos hormonais e para o Ki 67 como marcador de proliferação, o p53 e menin como marcadores de supressão tumoral, CD34 para a avaliação da angiogênese e Galanina para avaliar a presença desse neuropeptídeo. Resultados A amostra está constituída por 57 (93,4%) macroadenomas (19 invasivos e 38 não invasivos) e 4 microadenomas não invasivos; a freqüência de invasão foi de 62,3%. Vinte e cinco (41%) AH são clinicamente funcionantes (13 somatotropinomas, 6 prolactinomas , 6 corticotropinomas) e 36 (59%) não funcionantes (32 AH silenciosos e 4 de células nulas). Macroadenomas invasivos não funcionantes predominaram em relação aos macroadenomas invasivos funcionantes (p= 0,014). Houve 54,09% de recidiva. A imunoistoquímica revelou expressão positiva para hormônio do crescimento (GH) em 18 AH, 10 AH expressaram prolactina (PRL), 12 positivos para corticotropina (ACTH), 17 para gonadotrofinas e 4 AH negativos para todos os hormônios. A sintomatologia endócrina incidiu em 42,62% dos casos e os sintomas neurológicos em 88%. Homens e mulheres foram igualmente afetados e a maioria dos AH estão distribuídos nas quarta e quinta décadas de vida. O Ki 67 foi positivo em 83,69% do total da amostra e a média desse índice foi 4,39% (variação de 0 ¿ 36,9%); entre os subtipos hormonais os AH com expressão positiva para GH, mono ou pluri-hormonais, apresentaram índice de proliferação significativamente maior em relação aos demais subtipos (p=0,001). Os macroadenomas funcionantes invasivos apresentaram maior índice de proliferação em relação aos macroadenomas não funcionantes invasivos (p = 0,0328). O p53 foi positivo em 60,65% do total da amostra e a média do índice de núcleos corados foi 1,23% (variação de 0 ¿ 16%). Não houve diferença significativa da expressão do p53 quanto à invasão, fenótipo hormonal, status funcional e recidiva, entretanto houve correlação positiva entre o índice de proliferação e o p53 (p = 0,0004). Quanto à angiogênese, o CD34 mostrou que a densidade microvascular (DMV) em AH é menor em relação ao tecido adeno-hipofisário normal. A Galanina (GAL) foi positiva em 57% dos casos; os AH negativos para a GAL apresentaram índices de DMV significativamente maior em relação aos GAL positivos (p = 0,0464). A imunoreação para menin foi positiva em 41 AH (67,21%), e negativa em 20 AH (32,7%). A grande variedade de expressão de menin, tanto na intensidade da coloração quanto na localização nuclear ou citoplasmática, dificultou a interpretação dos resultados, sendo necessários estudos genéticos comparativos que possam orientar essa interpretação dos dados obtidos. Conclusões A maior freqüência de AH não funcionantes desta amostra pode estar relacionada ao diagnóstico tardio. A expressão do Ki 67 não se associou à gradação de Hardy. Os macroadenomas funcionantes e invasivos apresentaram índice de proliferação maior do que os não funcionantes, podendo indicar comportamento mais agressivo. Entre os diferentes subgrupos de AH apenas os que expressaram positividade para GH apresentaram índice de proliferação significativamente maior. A invasão nos AH = 10 mm, que apresentaram índice de proliferação igual a zero, não é dependente da atividade proliferativa. A maior expressão do p53 se correlacionou com o maior índice de proliferação (Ki 67) nesta amostra. O p53, a DMV e GAL não são marcadores de prognóstico nos AH. Os índices mais elevados da DMV em AH com ausência de expressão da GAL, podem indicar comportamento biológico mais agressivo
Abstract: Pituitary Adenomas (PA) are an easily identifiable and benign epithelial neoplasia. They are clinically detected through symptoms of an increased or decreased hormone rate and/or alterations of intra-cranial mass. They are classed in accordance with radiological / macroscopical aspects (macro versus microadenoma / invasive versus non-invasive), functional status (functional versus non-functional), cytological (acidophil, basophilic and chromophobic) and immunohistochemical / ultra-structural (somatotrophinomas, prolactinomas, corticotrophinomas, thyrotrophinomas, gonadotrophinomas and those from null cells). Amongst their various forms of disclosure, evolution, and clinical manifestation, invasive adenomas and non-invasive macroadenomas impose limits to surgical procedures, resulting in recidivist determination of endocrine and / or neurological morbidity. Aggressive and non-aggressive variants may display similar histological aspects, which require immunohistochemical, genetic and molecular-biological investigation, attempting to relate tumorigenesis mechanisms to the biological behavior of these tumors, such as invasive growth and recurrence. Objectives Classification and study of the occurrence of the sampled PA under a functional viewpoint based upon clinical symptomatology; Neuro-radiological / anatomic classification based upon tumor size and invasive rate through the Jules Hardy labeling index; Analysis and classification of the occurrence of hormonal subtypes, through the immunohistochemical method; Co-relate clinical, anatomical, and immunohistochemical data with the aggressivity of the PA, seeking prognostic factors using proliferous activity markers (Ki 67), suppressive tumorous gene alteration (p53 and menin), angiogenesis (CD 34) and neuropeptide (galanin). Materials and Methods 61 PA patients who had undergone surgical re-section were studied: clinical, anatomical / neurological, and immunohistochemical aspects were considered. The immunohistochemical technique was used to determine the different hormonal subtypes, and for the Ki 67 as a proliferation marker, the p53 and menin as a tumor suppression marker, CD34 for the assessment of the agiogenesis, and galanin to observe the presence of this neuropeptide. Results The sample contains 57 (93.4% macro-adenomas (19 invasive and 38 non-invasive) and 4 non-invasive microadenomas; the invasion rate equaled 62.3%. Twenty-five (41%) PA are clinically functional (13 somatotrophinomas, 6 prolactinomas, 6 corticotrophinomas) and 36 (59%) non-functional (32 PA silenced and 4 null cells). Invasive, non-functional macroadenomas stood out when compared to invasive, functional macroadenomas (p=0.014). 54.09% recidivists were detected. Immunohistochemistry revealed positive expression of the growth hormone (GH) in 18 PA, 10 PA expressed prolactin (PRL), 12 showed positive for corticotrophin (ACTH), 17 for gonadotrophin, and 4 PA showed negative for all hormones. Endocrine symptomatology occurred in 42.62% of the cases, and neurological symptoms were present in 88%. Male and female patients were affected indistinctly, and most PA patients were in their 40s and 50s. Ki 67 was positive in 83.69% of the total sampled, rating at an average of 4.39% (varying from 0 ¿ 36.9%); amongst hormonal subtypes, PA showing positive expression of GH (mono or plurihormonal) had a significantly increased proliferative activity when compared to other subtypes (p=0.001). Invasive, functional macroadenomas showed a higher proliferation rate than invasive, non-functional macroadenomas (p=0.0328). p53 was positive in 60.65% of the total sampled, and the average rate of dyed nuclei equaled 1.23% (varying from 0 ¿ 16%). There was no meaningful change in the expression of p53 as to the invasion, hormonal phenotype, functional and recidivist status. However, a positive co-relation between the proliferation rate and the p53 was detected (p=0.0004). Concerning the angiogenesis, CD34 showed that the microvascular density (MVD) in PA is lower when compared to the healthy adenohypophysial tissue. Galanin (GAL) was positive in 57% of the cases. The PA negative for GAL showed significantly increased MVD rates than the GAL positive (p=0.0464). Immunoreaction for menin was positive in 41 PA (67.21%) and negative in 20 PA (32.7%). The large variety of menin expression, regarding chromatic intensity and cytoplasmic or nuclear location made the interpretation of the results more difficult, which required comparative genetic studies that could guide the understanding of the data obtained. Conclusions Higher rates of non-functional PA cases may be a result of late diagnosis. Ki 67 expression could not be linked to the Hardy index. Invasive, functional macro-adenomas showed a higher proliferation rate than the rate obtained from the non-functional types ¿ which may signal increased aggressivity. Amongst the various PA subgroups, only those with GH positive expression had a significantly higher proliferation rate. The invasion of PA =10 mm, whose proliferation rate was null, is not dependent on proliferative activity. In this sample, the largest p53 expression matched the highest proliferation rate (Ki 67). p53, MVD and GAL are not PA prognostic markers. The highest MVD rates among PA combined with a null GAL expression may indicate more aggressive biological behavior
Doutorado
Ciencias Biomedicas
Mestre em Ciências Médicas

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Jorge, Uana Maria Miguel. « Tumores gástricos primários múltiplos e únicos : análise imunohistoquímica comparativa ». Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/5/5154/tde-29012007-154954/.

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Introdução: Adenocarcinomas gástricos múltiplos primários (AGMP) são encontrados em 3,5% a 10% de todos os pacientes com câncer gástrico. A multiplicidade tumoral é amplamente reconhecida como indicador de predisposição genética para o desenvolvimento de neoplasias Além disso, as rotas de carcinogênese não estão claramente definidas nestes tumores (rota mutadora, ou supressora, ou da E-caderina). Objetivo: avaliar a imunoexpressão de hMLH1, hMSH2, e hMSH6 (rota mutadora), p53 (rota supressora) e E-caderina nos AGMP comparando-se com adenocarcinomas únicos (pareados quanto ao sexo, idade, tipo histológico, localização e estádio) e sua relação com dados clínico-patológicos. Casuística: dezenove pacientes com AGMP foram comparados a 21 pacientes com tumores gástricos únicos quanto a características imunohistoquímicas. Métodos: Blocos de tecido fixados em formalina a 10% e incluídos em parafina foram submetidos a cortes histológicos de 4 mm, para as avaliações histológica e imunohistoquímica para hMLH1, hMSH2, hMSH6, p53 e E-caderina. Resultados: A média de idade dos pacientes com AGPM foi de 66 + 9,06 anos, e de 60 + 16,9 anos nos pacientes com tumor único (P=0,56). Vinte e dois tumores estavam localizados na porção distal do estômago; 14, no corpo e cinco na porção proximal. Em 14 pacientes, as lesões eram próximas (< 3 cm), enquanto que, em cinco pacientes, as lesões estavam em outra porção do estômago. O estágio final anatomopatológico pós-operatório foi: 15 no estágio T1 (37,5%) (8 múltiplos e 7 únicos), 7 no estágio T2 (17,5%) (1 múltiplo e 6 únicos), 17 no estágio T3 (42,5%) (9 múltiplos e 8 únicos) e 1 no estágio T4 (27,5%) (1 múltiplo). Segundo a classificação de Laurén, 45 dos tumores foram do tipo intestinal (29 múltiplos e 16 únicos), 16 do tipo gástrico (12 múltiplos e 4 únicos) e um tumor do tipo misto (1 único). O estádio anatomopatológico revelou 30 tumores avançados (16 múltiplos e 14 únicos) e 32 precoces (25 múltiplos e 7 únicos). Na imunohistoquímica, não houve diferença entre a imunoexpressão nos dois grupos de tumores quanto a: hMLH1 (24,3% vs. 19% P=0,64), hMSH6 (4,8% vs. 2,4%, P=0,68), p53 (39% vs. 24%, P=0,35) e E-caderina (27% vs. 19%, P=0,46). hMSH2 foi positivo em todos os casos. Não houve associação entre os imuno-marcadores e os dados clínico-patológicos. Conclusões: 1. As rotas de carcinogênese, mutatora, supressora e E-caderina parecem estar independentemente envolvidas no desenvolvimento dos AGMP; 2. Não houve diferença de imunoexpressão dos marcadores analisados quando compararam-se os AGMP e os tumores únicos.
Introduction: Multiple primary gastric adenocarcinomas (MPGA) have been reported from 3.5% to 10% of all patients with gastric cancer. Tumoral multiplicity is largely known as an indicator of genetic predisposition for the development of neoplasias. Moreover, the route of carcinogenesis has not been clearly clarified in these tumors (mutator pathway or suppressor pathway). Aim: to evaluate the immunoexpression of hMLH1, hMSH2, and hMSH6 (mutator pathway), p53 (suppressor pathway) and E-cadherin in the MPGA, comparing to solitary adenocarcinomas (similar gender, age, histological type, location and staging) and also the relation to the clinicopathological data.: Casuistics: Nineteen patients (Group 1) with MPGA were compared to 21 patients (Group 2) with solitary gastric tumors regarding clinicopathological characteristics and immunohistochemistry. Methods: Blocks of tissue fixed in 10% formalin and embedded in parafin were submitted to 4 mm sections for histological and immunohistochemistry analysis for hMLH1, hMSH2 and hMSH6 (mutator pathway), p53 (suppressor pathway) and E-cadherin. Results: The mean age for the MPGA was 66.8 + 9.06 years, and 59.0 + 16.9 years for the solitary tumor group(P = 0.27). Twenty-two tumors were in the distal stomach, 14 were in the body and five in the proximal portion. In 14 patients the lesions were close to each other (< 3 cm), while in five patients the neoplasias were distant, in another portion of the stomach.The final postoperative pathological stage was: T1 in 15 (eight multiple and seven solitary), T2 in seven (one multiple and six soliatry), T3 in 17 ( nine multiple and eight solitary) and T4 in one ( one multiple). According to the Laurén classification, 45 tumors were intestinal type (29 multiple and 16 solitary), 16 were diffuse (12 multiple and four solitart) and one mixed type ( one solitary). 30 tumors were diagnosed in advanced staging (16 multiple and 14 soliatry) and 32 were early (25 multiple and seven solitary). There was no difference between the hMLH1 immunoexpression in the two groups (24.3% vs. 19%, P=0.64), hMSH6 (4.8% vs. 2.4%, P=0.68), p53 (39% vs. 24%, P=0.35) and E-cadherin (27% v.s 19%, P=0.46). Immunostaining for hMSH2 was positive in all MPGA, indicating absence of alterations of this repair gene marker. There was no association between the immunomarkers and the clinicopathological data. Conclusions: 1. Routes of carcinogenesis, mutator, suppressor, and E-cadherin appear to be involved independently in the development of MPGA; 2. There was no difference in the markers immunoexpression in the two groups.

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Costa, Marcia Helena Soares. « Estudo da expressão dos receptores do peptídeo insulinotrópico dependente de glicose (GIPR) e do hormônio luteinizante (LHCGR) em tumores e hiperplasias do córtex adrenal ». Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-11092007-134837/.

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Introdução: Os receptores do peptídeo insulinotrópico dependente de glicose (GIPR) e do hormônio luteinizante (LHCGR) são receptores acoplados à proteína G com amplo padrão de expressão tecidual. A expressão anômala destes receptores tem sido descrita em casos de hiperplasia adrenal macronodular independente de ACTH (AIMAH) e em alguns adenomas, resultando em aumento da secreção hormonal (cortisol, andrógenos e aldosterona) pelo cortex adrenal. O papel destes receptores em outras formas de hiperplasia, como a doença adrenocortical nodular pigmentosa primária (PPNAD), aumento da adrenal associado à neoplasia endócrina múltipla tipo 1 (MEN1), e em carcinoma do córtex adrenal tem sido pouco investigado; sendo assim, considera-se relevante estudar a expressão destes receptores nos pacientes com tumores adrenocorticais esporádicos, nos pacientes com AIMAH, PPNAD e aumento adrenal associado à MEN1. Objetivos: 1) Caracterização molecular dos casos de neoplasia endócrina múltipla tipo 1 e PPNAD: pesquisa de mutações dos genes MEN1 e PRKAR1A e análise da perda de heterozigose (LOH) destes genes no tecido adrenal destes pacientes. 2) Quantificar a expressão do GIPR e do LHCGR em tecido adrenocortical normal, tumoral, hiperplásico e correlacionar a expressão destes com a classificação histológica dos tumores adrenocorticais. Pacientes: 55 pacientes (30 adultos) com tumores adrenocorticais (37 adenomas e 18 carcinomas); 7 pacientes com AIMAH, 4 com MEN1, 1 com PPNAD e tecidos controles (adrenal; testículo e pâncreas). Métodos: extração de DNA genômico, RNA e síntese de DNA complementar (cDNA); amplificação por PCR das regiões codificadoras dos genes MEN1 e PRKAR1A seguida por seqüenciamento automático. Pesquisa de LOH pela amplificação de microssatélites por PCR e análise pelo programa GeneScan. Quantificação da expressão do GIPR e do LHCGR por PCR em tempo real pelo método TaqMan e estudo de imunohistoquímica para GIPR nos tumores adrenocorticais. Resultados: identificação de 3 mutações (893+ 1G>A, W183X e A68fsX118) e dois polimorfirmos (S145S e D418D) no gene MEN1 e uma mutação (Y21X) no PRKAR1A. Ausência de LOH nos tecidos adrenais estudados. A expressão do GIPR e do LHCGR foi identificada em tecidos adrenais normais, tumorais e hiperplásicos. O nível de expressão do GIPR foi mais elevado nos tumores adrenocorticais malignos que nos benignos tanto no grupo pediátrico (mediana= 18,1 e 4,6, respectivamente; p <0,05), quanto no grupo adulto (mediana = 4,8 e 1,3 respectivamente; p <0,001). O nível de expressão do LHCGR, no grupo pediátrico, foi elevado tanto nos tumores benignos quanto nos malignos (mediana= 6,4 e 4,3, respectivamente). No grupo adulto os níveis de expressão deste receptor foram extremamente baixos nos tumores malignos em relação aos benignos (mediana= 0,06 e 2,3, respectivamente; p <0,001). A imunohistoquímica para o GIPR foi variável e não correlacionada à expressão do gene GIPR. Não houve diferença nos níveis de expressão do GIPR e do LHCGR nas hiperplasias do córtex adrenal. Conclusões: a presença de LOH e mutação em heterozigose composta do gene MEN1 e do PRKAR1A foram afastadas como mecanismos responsáveis pelo aumento adrenal tanto nos pacientes com MEN1 como no paciente com PPNAD. A hiperexpressão de GIPR está associada a malignidade nos tumores adrenocorticais nos grupos adulto e pediátrico e a baixa expressão de LHCGR está associada a malignidade nos tumores adrenocorticais somente no grupo adulto.
Introduction: The glucose- dependent insulinotropic peptide receptor (GIPR) and luteinizing hormone receptor (LHCGR) are G-protein coupled receptors with a wide tissue expression pattern. The aberrant expression of these receptors has been described in cases of ACTH-independent macronodular adrenal hyperplasia (AIMAH) and in some adenomas, resulting in the increase of adrenal cortex hormonal secretion (cortisol, androgens and aldosterone). The role of these receptors in other forms of adrenocortical hyperplasia, such as primary pigmented nodular adrenocortical disease (PPNAD), adrenal enlargement associated with multiple endocrine neoplasia type 1 (MEN1), and adrenocortical carcinoma has been scarcely investigated. Thus, the study of the expression of these receptors in patients with sporadical adrenocortical tumors, AIMAH, PPNAD and adrenal enlargement associated to MEN1 was considered important. Objectives: 1) Molecular study in patients with multiple endocrine neoplasia type 1 and PPNAD: mutation screening of MEN1 and PRKAR1A genes and analysis of the loss of heterozygosis (LOH) of these genes in the adrenal lesions of these patients. 2) To quantify the GIPR and LHCGR expression, in normal, tumor and hyperplasic tissue and to correlate the expression of these receptors with the adrenocortical tumor histology. Patients: 55 patients (30 adults) with adrenocortical tumors (37 adenomas and 18 carcinomas); 7 patients with AIMAH, 4 with MEN1, 1 with PPNAD and control tissue (adrenal, testis and pancreas). Methods: Extraction of genomic DNA, RNA and synthesis of complementary DNA (cDNA); PCR-amplification of the coding regions of MEN1 and PRKAR1A, followed by direct sequencing. LOH study using polymorphic marker amplification by PCR and GeneScan software analysis. Quantification of GIPR and LHCGR expression using realtime PCR -TaqMan method and GIPR immunohistochemistry study in adrenocortical tumors. Results: Identification of 3 mutations (893+ 1G>A, W183X and A68fsX118) and two polymorphic alterations (S145S and D418D) in MEN1 and a mutation (Y21X) in the PRKAR1A gene; LOH was not identified in adrenal tissue. The GIPR and LHCGR expression was identified in normal, tumor and hyperplasic adrenal tissues; the GIPR expression level was more elevated in malignant tumors compared to benign tumors in pediatric (median = 18.1 and 4.6, respectively; p <0.05) and adult patients (median = 4.8 and 1.3 respectively; p <0.001). The LHCGR expression in pediatric patients was elevated in benign as well as in malignant tumors (median = 6.4 and 4.3, respectively). In the adult group, the expression level of these receptors was extremely low in malignant tumors in relation to benign ones (median = 0.06 and 2.3, respectively; p <0.001). The GIPR immunohistochemistry was variable and did not correlate with GIPR gene expression. No difference between GIPR and LHCGR expression levels was observed in the different forms of hyperplasia. Conclusions: The presence of LOH and mutations in compound heterozygosis of MEN1 and PRKAR1A genes were ruled out as the mechanisms responsible for the adrenal enlargement in patients with multiple endocrine neoplasia type 1. GIPR overexpression is associated with malignant adrenocortical tumors in the adult and pediatric patients and low LHCGR expression is associated with malignant adrenocortical tumors only in the adult patients.

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Sekiya, Tomoko. « Análise do gene CDKN1B/p27kip1 em pacientes com neoplasia endócrina múltipla tipo 2 ». Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-26022014-112355/.

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INTRODUÇÃO: Na Neoplasia Endócrina Múltipla tipo 2 (NEM2), o desenvolvimento do Carcinoma Medular de Tireoide (CMT), Feocromocitoma (FEO) e Hiperparatireoidismo primário (HPT) está associado à mutações germinativas ativadoras no proto-oncogene RET. Casos de CMT esporádico podem apresentar mutações somáticas no RET (~40%). A variabilidade fenotípica observada em casos de CMT e FEO familiais associados à NEM2 indica o envolvimento de eventos genéticos adicionais que seriam responsáveis pelas diferenças clínicas observadas nos indivíduos afetados (idade de desenvolvimento, progressão e agressividade do tumor). Outras alterações genéticas no RET como duplas mutações, SNPs e haplótipos específicos podem influenciar na susceptibilidade, agressividade e modulação do fenótipo NEM2. Entretanto, os estudos de outros genes envolvidos no processo da tumorigênese NEM2 ainda estão em andamento. Recentemente foi mostrado que RET ativado controla a expressão de proteínas inibidoras do ciclo celular (p18 e p27). Mutações germinativas no gene p27 foram recentemente associadas à susceptibilidade de tumores neuroendócrinos e estão associadas à síndrome NEM4 (Neoplasia endócrina múltipla tipo 4). Mutações somáticas, inativadoras de p27, são raramente encontradas em vários tipos de tumores. Entretanto, diversos estudos documentaram que a redução na expressão e a sublocalização citoplamática de p27 são controladas por alterações pós-transducionais e/ou epigenéticas. OBJETIVOS: o estudo teve como objetivos avaliar a participação de genes, recentemente associados ao RET ativado, em tumores de pacientes com NEM2 e também verificar se polimorfismos no gene p27 estariam atuando como moduladores de fenótipo em uma grande família com NEM2. CASUÍTICA: foram analisadas 66 amostras tumorais advindas de 36 pacientes com diagnóstico clínico e genético de NEM2 e 28 indivíduos pertencentes a uma grande família com NEM2A-CMTF e mutação C620R no gene RET. MÉTODOS: As análises somáticas do p27 e também de p15, p18 e RET foram realizadas por PCR e sequenciamento direto de DNA e análise de microssatélites para p27 foi realizada por PCR e eletroforese capilar. Análises de expressão e localização da proteína p27 celular foram realizadas por Western blot e imunohistoquímica. A análise da modulação de fenótipo na família com NEM2A foi realizada por meio da amplificação do éxon 1 do gene p27 na amostra de sangue total. RESULTADOS: Não foram encontradas mutações somáticas no gene p27 e também nos genes p15 e p18. Entretanto, verificamos baixa expressão proteica de p27 em tumores CMT e FEO, a qual se encontrava relacionada com o tipo e agressividade do códon mutado no RET, principalmente em tumores que apresentavam mutação RET no códon 634 (controle x 634 p=0,05; controle x 634/791 p= 0,032; 620 x 634 p=0,045; 620 x 634/791 p= 0,002; 620 x 634 + 634/791 p=0,036). Notou-se também correlação positiva entre os níveis de expressão de p27 na localização nuclear, analisada por imunohistoquímica, e o genótipo TT do SNP p27 p.V109G (p=0,03). CONCLUSÕES: Alterações moleculares somáticas no gene p27 nos tumores NEM2 não são frequentes. Entretanto, a redução na expressão e a localização citoplasmática de p27 provavelmente estão associadas a alterações somáticas em outros genes que controlam os processos de fosforilação da proteína p27 (eventos pós-transducionais)
INTRODUCTION: In Multiple Endocrine Neoplasia type 2 (MEN2) the development of medullary thyroid carcinoma (MTC), pheochromocytoma (PHEO) and primary hyperparathyroidism (HPT) are associated with activating germline mutations in RET proto-oncogene. Cases of sporadic MTC may have somatic RET mutations (~ 40%). The phenotypic variability observed in cases with familial MTC/MEN2 and PHEO/MEN2 indicates the probable involvement of additional genetic events that could be responsible for the clinical differences observed in the affected individuals (age development, progression and aggressiveness of the tumor). Other genetic alterations such as RET double mutations, SNPs and specific haplotypes may influence susceptibility, aggressiveness and MEN2 phenotype modulation. However, studies of other genes involved in the tumorigenesis of MEN2 are still in progress. Recently, it was shown that the activated RET controls the expression of cell cycle inhibitory proteins (p18 and p27). Germline mutations in the p27 gene have recently been associated with the susceptibility to neuroendocrine tumors and are associated with the MEN4 syndrome (Multiple endocrine neoplasia type 4). Somatic inactivating mutations p27 are rarely found in many types of tumors. However, several studies have documented that reduced expression and subcellular location of p27 is controlled by post-transductional changes and/or epigenetic factors. OBJECTIVES: This study aimed to evaluate the role of genes recently associated with RET activated in tumors from MEN2 patients and also check whether polymorphisms in the p27 gene would be acting as modulators of phenotype in a large MEN2 family. PATIENTS: We analyzed 66 tumor samples from 36 patients with clinical and genetic diagnosis of MEN2 and from 28 individuals belonging to a large family with FMTC/MEN2A and RET C620R mutation. METHODS: The analyses of somatic p27, p15, p18 and RET were performed by PCR and direct sequencing of DNA and microsatellite analysis was performed for p27 by PCR and capillary electrophoresis. Expression analysis and subcellular localization of p27 protein were performed by Western blot and immunohistochemistry. The analysis of phenotype modulation in MEN2A families was performed by the amplification of exon 1 of the p27 gene in a whole blood sample. RESULTS: There were no somatic mutations in the p27 gene and also in the p15 and p18 genes. However, we verified a low p27 protein expression in MTC/MEN2 and PHEO/MEN2 that showed a definite correlation with the type and aggressiveness of the mutated RET codon, mainly in those tumors from cases with germline RET codon 634 mutations (control vs 634, p=0,05; control vs 634/791, p= 0,032; 620 vs 634, p=0,045; 620 vs 634/791, p= 0,002; 620 vs 634 + 634/791, p=0,036). It was also verified a positive correlation between the immunohistochemistry expression of nuclear p27 subcellular location and the p27 p.V109G TT genotype (p=0,03). CONCLUSIONS: The reduction in the expression of p27 and its subcellular localization are likely to be associated with somatic changes in other genes that control the processes of phosphorylation of p27 protein through post-transductional events

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Livres sur le sujet "Multiplex immunohistochemistry"

C. M. van der Loos. Immunoenzyme multiple staining methods. Oxford, UK : Bios Scientific Publishers in association with the Royal Microscopical Society, 1999.

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Immunoenzyme multiple staining methods. Oxford, UK : Bios Scientific Publishers, 1999.

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Yeong, Joe, Bernard A. Fox, Houssein A. Sater, Jaime A. Rodriguez-Canales et Trevor David McKee, dir. Multiplex Immunohistochemistry/Immunofluorescence Technique : The Potential and Promise for Clinical Application. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-718-4.

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L, CHRIS VAN DER. Immunoenzyme Multiple Staining Methods. Garland Science, 1999.

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Chapitres de livres sur le sujet "Multiplex immunohistochemistry"

Kalra, Jessica, et Jennifer Baker. « Multiplex Immunohistochemistry for Mapping the Tumor Microenvironment ». Dans Methods in Molecular Biology, 237–51. New York, NY : Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6759-9_17.

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Nguyen, Thu, Nikolce Kocovski, Sean Macdonald, Han Xian Aw Yeang, Minyu Wang et Paul J. Neeson. « Multiplex Immunohistochemistry Analysis of Melanoma Tumor-Infiltrating Lymphocytes ». Dans Methods in Molecular Biology, 557–72. New York, NY : Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1205-7_39.

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Kang, Wenfei, Anthony Santella, Eric Rosiek, Maria Pulina, Eric Chan, Ning Fan, Murray J. Tipping, Afsar Barlas, Yevgeniy Romin et Katia Manova-Todorova. « Multiplex Spatial Protein Detection by Combining Immunofluorescence with Immunohistochemistry ». Dans Methods in Molecular Biology, 233–44. New York, NY : Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2811-9_15.

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Steele, Keith E., et Charles Brown. « Multiplex Immunohistochemistry for Image Analysis of Tertiary Lymphoid Structures in Cancer ». Dans Tertiary Lymphoid Structures, 87–98. New York, NY : Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8709-2_6.

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Pang, Lokman, Matthias Ernst et Jennifer Huynh. « Spatially Characterizing the Immune Contexture in Mouse Tissue Using Multiplex Immunohistochemistry ». Dans Methods in Molecular Biology, 307–16. New York, NY : Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2811-9_20.

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Hagos, Yeman Brhane, Priya Lakshmi Narayanan, Ayse U. Akarca, Teresa Marafioti et Yinyin Yuan. « ConCORDe-Net : Cell Count Regularized Convolutional Neural Network for Cell Detection in Multiplex Immunohistochemistry Images ». Dans Lecture Notes in Computer Science, 667–75. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-32239-7_74.

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van Diest, Paul J., C. B. Moelans, D. Purnomosari, G. Pals et R. A. de Weger. « Invasive Breast Cancer : Overexpression of HER-2 Determined by Immunohistochemistry and Multiplex Ligation-Dependent Probe Amplification ». Dans Methods of Cancer Diagnosis, Therapy and Prognosis, 291–304. Dordrecht : Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-8369-3_22.

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Muñoz-Castro, Clara, Ayush Noori, Bradley T. Hyman et Alberto Serrano-Pozo. « Cyclic Multiplex Fluorescent Immunohistochemistry Protocol to Phenotype Glial Cells in Formalin-Fixed Paraffin-Embedded Human Brain Sections ». Dans Methods in Molecular Biology, 283–305. New York, NY : Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2811-9_19.

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Buchwalow, Igor B., et Werner Böcker. « Multiple Immunofluorescence Staining ». Dans Immunohistochemistry : Basics and Methods, 69–76. Berlin, Heidelberg : Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-04609-4_8.

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Buchwalow, Igor B., et Werner Böcker. « Multiple Multicolor Immunoenzyme Staining ». Dans Immunohistochemistry : Basics and Methods, 61–67. Berlin, Heidelberg : Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-04609-4_7.

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Actes de conférences sur le sujet "Multiplex immunohistochemistry"

Bauer, Daniel R., Mark Lefever, Torsten Leibold, Lauren Behman, Esteban Roberts, Julia Ashworth-Sharpe et Larry Morrison. « Abstract 4250 : Multispectral imaging of brightfield multiplex immunohistochemistry ». Dans 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.am2020-4250.

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Lorsakul, Auranuch N., Joerg Bredno, Robert L. Ochs, Larry Morrison et William Day. « Validation of multiplex immunohistochemistry assays using automated image analysis ». Dans Digital Pathology, sous la direction de Metin N. Gurcan et John E. Tomaszewski. SPIE, 2018. http://dx.doi.org/10.1117/12.2293168.

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zheng, Yi, Carla Coltharp, Ryan Dilworth, Linying Liu, Darryn Unfricht, Cliff Hoyt, Milind Rajopadhye et Peter Miller. « Abstract 3832 : Optimization strategy for fluorescent multiplex immunohistochemistry tissue staining ». Dans Proceedings : AACR Annual Meeting 2017 ; April 1-5, 2017 ; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3832.

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Sobhani, Faranak, Azam Hamidinekoo, Allison H. Hall, Lorraine King, Jeffrey R. Marks, Carlo Maley, Hugo M. Horlings, E. Shelley Hwang et Yinyin Yuan. « Automated Dcis Identification From Multiplex Immunohistochemistry Using Generative Adversarial Networks ». Dans 2022 IEEE 19th International Symposium on Biomedical Imaging (ISBI). IEEE, 2022. http://dx.doi.org/10.1109/isbi52829.2022.9761413.

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Cooper, Lee A. D., Rami Yacoub, David A. Gutman, Fusheng Wang, Carlos S. Moreno, Daniel J. Brat, Roberd M. Bostick et Joel H. Saltz. « Abstract LB-101 : Quantitative imaging of protein expression using multiplex quantum dot immunohistochemistry ». Dans Proceedings : AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012 ; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-101.

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Chachi, Latifa, Joao Sousa, Chris Brightling et Yassine Amrani. « Multiplex immunohistochemistry to investigate inflammatory cell spatial organisation and interactions in severe asthma ». Dans ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2297.

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Dauffenbach, Lisa M., Christopher A. Kerfoot, Gela Sia, Anthony Masci, Johannes Zimmermann, Jan Lesniak, Alexei Budco et al. « Abstract B069 : Characterization of inflammatory cell patterns and densities using multiplex immunohistochemistry immuno-oncology assays ». Dans Abstracts : AACR-NCI-EORTC International Conference : Molecular Targets and Cancer Therapeutics ; October 26-30, 2017 ; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-b069.

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Vargas, Joseph, David Tacha, Sara Figueroa et Cristin Douglas. « Abstract 3860 : Rodent multispecies multiplex immunohistochemistry using digoxigenin and polymer detection methods in mouse tissues ». Dans 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.am2018-3860.

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Ziello, Jennifer, Sarah Klein et Katherine Crosby. « Abstract B33 : Coexpression and frequency of immune checkpoint proteins in the tumor microenvironment analyzed via multiplex immunohistochemistry ». Dans Abstracts : AACR Special Conference on Tumor Immunology and Immunotherapy ; October 1-4, 2017 ; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-b33.

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Rapports d'organisations sur le sujet "Multiplex immunohistochemistry"

Fields, Michael J., Mordechai Shemesh et Anna-Riitta Fuchs. Significance of Oxytocin and Oxytocin Receptors in Bovine Pregnancy. United States Department of Agriculture, août 1994. http://dx.doi.org/10.32747/1994.7568790.bard.

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Oxytocin has multiple actions in bovine reproductive tract and it was our purpose to determine the nature of these actions and their significance for the physiology of bovine reproduction. The bovine oxytocin receptors (OTR) gene was cloned and its expression studied during the cycle and pregnancy. OTR mRNA changed in parallel with OTR with control occurring mainly at the transcriptional level. However, the endocrine regulation of OTR were found in endometrium and cervical mucosa at estrus and at parturition. In both tissues OTR were suppressed in the luteal phase and early pregnancy. Whereas cervical OTR remained suppressed throughout pregnancy, endometrial OTR began to increase soon after implantation and reached higher concentrations in midpregnancy than at estrus. OTR in caruncles did not increase until third trimester, and OTR in cervical mucosa, cotyledons and fetal membranes increased only at term. Myometrial OTR showed less variation and OTR were present throughout the cycle and pregnancy but increased significantly during mid- and late pregnancy. OTR were localized in endometrial epithelial cells and lumina epithelial cells of cervical mucosa as determined by immunohistochemistry. Endometrial OTR were functional throughout pregnancy and mediated PGF release from day 50 onwards in a receptor density related manner. OTR in cervical mucosa mediated PGE release both in vivo and in vitro, as shown in cyclic cows. The ontogeny of uterine OTR was studied from third trimester fetal stage until puberty. OTR were present in endometrium and cervical mucosa in high concentrations throughout this period; myometrial OTR began to increase somewhat later but also reached adult values by 6-mo of age. In the prepuberal heifers OT injections failed to initiate PGF2a, release. The influence of steroids on the effect of OT was examined. Ovariectomy and E2 were without effect, but P4 with or without E2 induced a massive PGF2a release in response to OT in spite of reduced OTR. Bovine cyclooxygenases (COX-1 and COX-2) were cloned and their expression studied in the endometrium of prepuberal heifers and pregnant cows. Untreated and E2 treated prepuberal heifers did not express COX-2 but P4 treated heifers did express the mRNA for COX-2, albeit weakly. During the second half of pregnancy COX-2 mRNA was strongly expressed in cotyledons and somewhat less in caruncles, whereas endometrium, myometrium and cervical mucosa showed only weak, if any, COX-2 mRNA under basal conditions. However, 2 h after OT injection significant increases in COX-2 mRNA were found in endometrial RNA. Thus OT is capable of inducing the expression of the inducible COX-2 gene, and hence the conversion of arachidonic acid to prostanoids. The results indicate that the functions of OT are numerous and probably essential for successful pregnancy and parturition.

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