Relevant bibliographies by topics / Cell carcinomas

Academic literature on the topic 'Cell carcinomas'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Cell carcinomas"

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Sica, Gabriel, Patrick L. Wagner, Nassar Altorki, Jeffrey Port, Paul C. Lee, Madeline F. Vazquez, and Anjali Saqi. "Immunohistochemical Expression of Estrogen and Progesterone Receptors in Primary Pulmonary Neuroendocrine Tumors." Archives of Pathology & Laboratory Medicine 132, no. 12 (December 1, 2008): 1889–95. http://dx.doi.org/10.5858/132.12.1889.

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Abstract Context.—Lung and breast carcinomas are among the most prevalent cancers. Advances in cancer therapies can provide survival benefit and be potentially curative, even in metastatic disease. Due to the high prevalence of these carcinomas, it is not unusual to encounter lung nodule(s) in a patient with breast carcinoma, and distinguishing between primary and metastatic disease is critical for management/treatment. Occasionally neuroendocrine differentiation is present in breast carcinoma, making its distinction from pulmonary/nonpulmonary neuroendocrine tumors in the lung difficult. Objective.—To assess estrogen and progesterone receptor expression in the entire spectrum of pulmonary neuroendocrine tumors. Design.—Seventy-one neuroendocrine neoplasms including typical carcinoids (42), atypical carcinoids (7), small cell carcinomas (14), large cell neuroendocrine carcinomas (2), and combined small cell carcinomas (6) were evaluated for estrogen and progesterone receptors. Mammary and non–small cell lung carcinomas were also stained for comparison. Results.—The entire spectrum of neuroendocrine neoplasms demonstrated focal to diffuse estrogen (typical carcinoid, 23; atypical carcinoid, 6; small cell carcinoma, 8; large cell neuroendocrine carcinoma, 2; combined small cell carcinoma, 4) and progesterone (typical carcinoid, 11; atypical carcinoid, 2; small cell carcinoma, 7; large cell neuroendocrine carcinoma, 0; combined small cell carcinoma, 2) expression. There was no correlation between sex and estrogen/progesterone status. Estrogen and progesterone staining were also noted in endothelial cells. Relative to neuroendocrine carcinomas, mammary carcinomas expressed estrogen and progesterone more frequently. Non–small cell carcinomas had greater and similar immunoreactivity for estrogen and progesterone, respectively. Conclusions.—Although estrogen and progesterone receptor staining is frequently associated with breast and gynecologic primaries, it can also be observed in “nontarget” organs. Therefore, presence of estrogen and/or progesterone expression in neuroendocrine tumors involving the lung should not exclude a primary pulmonary neoplasm.
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Capelli, Marco, Giulia Bertino, Patrizia Morbini, Chiara Villa, Stefano Zorzi, and Marco Benazzo. "Neuroendocrine Carcinomas of the Upper Airways: A Small Case Series with Histopathological Considerations." Tumori Journal 93, no. 5 (September 2007): 499–503. http://dx.doi.org/10.1177/030089160709300517.

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Neuroendocrine carcinomas are rare tumors. In the head and neck region they are most common in the larynx, where they represent 0.5-1% of epithelial cancers. Diagnosis requires the recognition of the typical neuroendocrine architecture and morphology and the immunohistochemical confirmation of neuroendocrine differentiation. In the 1991 WHO classification laryngeal neuroendocrine carcinomas have been divided into carcinoids, atypical carcinoids, small cell carcinomas and paragangliomas. Atypical carcinoids in the head and neck region usually show an aggressive behavior analogous to poorly differentiated carcinomas, and are resistant to chemo- and radiotherapy. For this reason, it was recently proposed to change their designation to “moderately differentiated neuroendocrine carcinomas”. We present the clinical and histopathological features of 2 moderately differentiated neuroendocrine carcinomas of the larynx, one large cell poorly differentiated neuroendocrine carcinoma of the oropharynx, and one small cell carcinoma of the minor salivary glands of the tongue. The patient with small cell carcinoma was free from disease 26 months after radical surgery, while the other patients showed liver, lung and bone metastases 18, 26 and 24 months after the diagnosis despite radical surgery or concomitant intra-arterial chemotherapy and radiotherapy.
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Shilo, Konstantin, Tatiana Dracheva, Haresh Mani, Junya Fukuoka, Isabell A. Sesterhenn, Wei-Sing Chu, Joanna H. Shih, Jin Jen, William D. Travis, and Teri J. Franks. "α-Methylacyl CoA Racemase in Pulmonary Adenocarcinoma, Squamous Cell Carcinoma, and Neuroendocrine Tumors: Expression and Survival Analysis." Archives of Pathology & Laboratory Medicine 131, no. 10 (October 1, 2007): 1555–60. http://dx.doi.org/10.5858/2007-131-1555-mcripa.

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Abstract Context.—α-Methylacyl CoA racemase (AMACR) is an oxidative enzyme involved in isomeric transformation of fatty acids entering the beta-oxidation pathway. AMACR serves as a useful marker in establishing a diagnosis of prostatic malignancy; however, limited information is available in regard to its presence in pulmonary neoplasms. Objective.—To investigate AMACR expression within a spectrum of lung carcinomas and its correlation with patients' survival. Design.—Four hundred seventy-seven pulmonary carcinomas, including 150 squamous cell carcinomas, 150 adenocarcinomas, 46 typical carcinoids, 31 atypical carcinoids, 28 large cell neuroendocrine carcinomas, and 72 small cell carcinomas, were studied immunohistochemically using tissue microarray–based samples. Results.—Overall, pulmonary tumors were positive for AMACR in a significant percentage (47%) of cases. Among tumor types, 22% of squamous cell carcinoma, 56% of adenocarcinoma, 72% of typical carcinoid, 52% of atypical carcinoid, 70% of large cell neuroendocrine carcinoma, and 51% of small cell lung carcinoma were positive for AMACR. Furthermore, the Kaplan-Meier analysis revealed that the patients with AMACR-positive small cell carcinoma had better survival (19% vs 5% after 5 years, P = .04) than patients with AMACR-negative tumors. Such survival advantage was seen for patients with stage I–II (P = .01) but not stage III–IV small cell carcinomas (P = .58). Conclusions.—These results indicate that, similar to prostate cancer, the overexpression of AMACR frequently occurs in pulmonary carcinomas. Additionally, its positive correlation with outcome of stage I–II small cell lung carcinoma warrants further investigation of the AMACR role in the prognosis of this tumor.
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Frixen, U. H., J. Behrens, M. Sachs, G. Eberle, B. Voss, A. Warda, D. Löchner, and W. Birchmeier. "E-cadherin-mediated cell-cell adhesion prevents invasiveness of human carcinoma cells." Journal of Cell Biology 113, no. 1 (April 1, 1991): 173–85. http://dx.doi.org/10.1083/jcb.113.1.173.

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The ability of carcinomas to invade and to metastasize largely depends on the degree of epithelial differentiation within the tumors, i.e., poorly differentiated being more invasive than well-differentiated carcinomas. Here we confirmed this correlation by examining various human cell lines derived from bladder, breast, lung, and pancreas carcinomas. We found that carcinoma cell lines with an epithelioid phenotype were noninvasive and expressed the epithelium-specific cell-cell adhesion molecule E-cadherin (also known as Arc-1, uvomorulin, and cell-CAM 120/80), as visualized by immunofluorescence microscopy and by Western and Northern blotting, whereas carcinoma cell lines with a fibroblastoid phenotype were invasive and had lost E-cadherin expression. Invasiveness of these latter cells could be prevented by transfection with E-cadherin cDNA and was again induced by treatment of the transfected cells with anti-E-cadherin mAbs. These findings indicate that the selective loss of E-cadherin expression can generate dedifferentiation and invasiveness of human carcinoma cells, and they suggest further that E-cadherin acts as an invasion suppressor.
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Cheuk, W., M. Y. Kwan, Saul Suster, and John K. C. Chan. "Immunostaining for Thyroid Transcription Factor 1 and Cytokeratin 20 Aids the Distinction of Small Cell Carcinoma From Merkel Cell Carcinoma, But Not Pulmonary From Extrapulmonary Small Cell Carcinomas." Archives of Pathology & Laboratory Medicine 125, no. 2 (February 1, 2001): 228–31. http://dx.doi.org/10.5858/2001-125-0228-ifttfa.

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Abstract Objective.—To study the expression of thyroid transcription factor 1 (TTF-1) and cytokeratin 20 (CK20) in pulmonary small cell carcinomas, extrapulmonary small cell carcinomas, and Merkel cell carcinomas, and thereby determine whether these markers are helpful in distinguishing these 3 groups of small cell neuroendocrine carcinomas. Materials and Methods.—Immunostaining for TTF-1 and CK20 was performed in 102 cases of small cell carcinoma (pulmonary, 52; extrapulmonary, 50) and 23 cases of Merkel cell carcinoma. The results for the 3 groups were compared. Results.—Thyroid transcription factor 1 was expressed in 82.7% of pulmonary small cell carcinomas, 42.0% of extrapulmonary small cell carcinomas (range, 33.3–53.3% for the various sites), and 0% of Merkel cell carcinomas. Cytokeratin 20 staining was consistently negative in pulmonary small cell carcinomas, and positive in 4.0% of extrapulmonary small cell carcinomas and 100% of Merkel cell carcinomas. Conclusions.—Immunostaining for TTF-1, especially when combined with immunostaining for CK20, can aid in the distinction between Merkel cell carcinoma and small cell carcinoma (both pulmonary and extrapulmonary). However, in individual cases, these markers cannot be used to distinguish between pulmonary and extrapulmonary small cell carcinomas due to the extensive overlap in immunophenotypes.
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Liddell, Heath, Anton Mare, Sean Heywood, Genevieve Bennett, and Hin Fan Chan. "Clear Cell Papillary Renal Cell Carcinoma: A Potential Mimic of Conventional Clear Cell Renal Carcinoma on Core Biopsy." Case Reports in Urology 2015 (2015): 1–4. http://dx.doi.org/10.1155/2015/423908.

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Clear cell papillary renal cell carcinoma (CCP-RCC) is a recently described, relatively uncommon variant of renal cell carcinoma (RCC) with a reported incidence of 4.1%. Thought to only arise in those with end stage renal disease, CCP-RCC is increasingly identified in those without renal impairment. CCP-RCCs have unique morphologic, genetic, and immunohistochemical features distinguishing them from both conventional clear cell renal cell carcinomas and papillary renal cell carcinomas. Immunohistochemically, these tumors are positive for CK7 and negative for CD10 and racemase. This is in contrast to conventional cell renal cell carcinomas (CK7 negative, CD10 positive) and papillary cell carcinomas (CK7, CD10, and racemase positive). These tumours appear to be indolent in nature, with no current documented cases of metastatic spread. We present the case of a 42-year-old female who presented with an incidental finding of a renal mass that on a core biopsy was reported as clear cell carcinoma, Fuhrman grade 1. She subsequently underwent a radical nephrectomy and further histological examination revealed the tumor to be a clear cell papillary renal cell carcinoma, Fuhrman grade 1.
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Milroy, C. M., P. J. Robinson, and H. R. Grant. "Primary composite squamous cell carcinoma and large cell neuroendocrine carcinoma of the hypopharynx." Journal of Laryngology & Otology 103, no. 11 (November 1989): 1093–96. http://dx.doi.org/10.1017/s0022215100111107.

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AbstractNeuroendocrine carcinomas are rare neoplasms of the larynx and hypopharynx. Tumours composed of both neuroendocrine and Squamous cell elements are very rare. We report a case of a primary hypopharyngeal carcinoma composed of both squamous cell and large cell neuroendocrine carcinoma and discuss the treatment of this patient and management of neuroendocrine carcinomas of the larynx and hypopharynx.
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Nikiforova, Marina N., Edna T. Kimura, Manoj Gandhi, Paul W. Biddinger, Jeffrey A. Knauf, Fulvio Basolo, Zhaowen Zhu, et al. "BRAF Mutations in Thyroid Tumors Are Restricted to Papillary Carcinomas and Anaplastic or Poorly Differentiated Carcinomas Arising from Papillary Carcinomas." Journal of Clinical Endocrinology & Metabolism 88, no. 11 (November 1, 2003): 5399–404. http://dx.doi.org/10.1210/jc.2003-030838.

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Abstract Activating point mutations of the BRAF gene have been recently reported in papillary thyroid carcinomas. In this study, we analyzed 320 thyroid tumors and six anaplastic carcinoma cell lines and detected BRAF mutations in 45 (38%) papillary carcinomas, two (13%) poorly-differentiated carcinomas, three (10%) anaplastic carcinomas, and five (83%) thyroid anaplastic carcinoma cell lines but not in follicular, Hürthle cell, and medullary carcinomas, follicular and Hürthle cell adenomas, or benign hyperplastic nodules. All mutations involved a T→A transversion at nucleotide 1796. In papillary carcinomas, BRAF mutations were associated with older age, classic papillary carcinoma or tall cell variant histology, extrathyroidal extension, and more frequent presentation at stages III and IV. All BRAF-positive poorly differentiated and anaplastic carcinomas contained areas of preexisting papillary carcinoma, and mutation was present in both the well-differentiated and dedifferentiated components. These data indicate that BRAF mutations are restricted to papillary carcinomas and poorly differentiated and anaplastic carcinomas arising from papillary carcinomas. They are associated with distinct phenotypical and biological properties of papillary carcinomas and may participate in progression to poorly differentiated and anaplastic carcinomas.
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Wysocki, John, Rishi Agarwal, Laura Bratton, Jeremy Nguyen, Mandy Crause Weidenhaft, Nathan Shores, and Hillary Z. Kimbrell. "Mixed Large Cell Neuroendocrine Carcinoma and Adenocarcinoma with Spindle Cell and Clear Cell Features in the Extrahepatic Bile Duct." Case Reports in Pathology 2014 (2014): 1–4. http://dx.doi.org/10.1155/2014/347949.

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Mixed adenoneuroendocrine carcinomas, spindle cell carcinomas, and clear cell carcinomas are all rare tumors in the biliary tract. We present the first case, to our knowledge, of an extrahepatic bile duct carcinoma composed of all three types. A 65-year-old man with prior cholecystectomy presented with painless jaundice, vomiting, and weight loss. CA19-9 and alpha-fetoprotein (AFP) were elevated. Cholangioscopy revealed a friable mass extending from the middle of the common bile duct to the common hepatic duct. A bile duct excision was performed. Gross examination revealed a 3.6 cm intraluminal polypoid tumor. Microscopically, the tumor had foci of conventional adenocarcinoma (CK7-positive and CA19-9-postive) surrounded by malignant-appearing spindle cells that were positive for cytokeratins and vimentin. Additionally, there were separate areas of large cell neuroendocrine carcinoma (LCNEC). Foci of clear cell carcinoma merged into both the LCNEC and the adenocarcinoma. Tumor invaded through the bile duct wall with extensive perineural and vascular invasion. Circumferential margins were positive. The patient’s poor performance status precluded adjuvant therapy and he died with recurrent and metastatic disease 5 months after surgery. This is consistent with the reported poor survival rates of biliary mixed adenoneuroendocrine carcinomas.
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Rudland, P. S., S. J. Leinster, J. Winstanley, B. Green, M. Atkinson, and H. D. Zakhour. "Immunocytochemical identification of cell types in benign and malignant breast diseases: variations in cell markers accompany the malignant state." Journal of Histochemistry & Cytochemistry 41, no. 4 (April 1993): 543–53. http://dx.doi.org/10.1177/41.4.8450194.

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We performed immunocytochemical staining of benign, in situ, and malignant breast disease to identify antigens related to the presence of the major parenchymal cell types of the normal breast. Markers for the epithelial cells, antiserum to epithelial membrane antigen, and three monoclonal antibodies (MAb) to milk-fat globule membranes stained most of the inner cells in benign breast lesions, carcinoma in situ, and invasive carcinomas, but the peripheral cells in benign lesions, as well as in carcinoma in situ, were unstained. MAb to epithelium-specific keratin 18 stained the majority of inner cells in benign breast lesions but comparatively fewer such cells in carcinoma in situ and invasive carcinoma. Markers for the myoepithelial cells, antisera, and MAb to smooth muscle actin and vimentin stained most of the peripheral cells in benign breast lesions and in carcinoma in situ but failed to stain virtually any neoplastic cells in invasive carcinomas. Markers for the basement membrane adjacent to the myoepithelial cells, antiserum, and MAb to laminin and Type IV collagen delineated an intact basement membrane around benign lesions and carcinoma in situ, and fragmented structures in 5-10% of invasive carcinomas; the remaining carcinomas were largely unstained. Markers for both myoepithelial and epithelial cells, keratin MAb PKK2 and LP34, stained most of the inner cells in benign lesions but usually only relatively few malignant cells in carcinoma in situ and invasive carcinomas. Markers for the secretory alveolar cell, MAb to beta- and kappa-casein, stained a few isolated cells in benign lesions, many more inner cells in two such lesions in pregnant females, and none in invasive carcinomas. In conclusion, the myoepithelial cell and, under suitable hormonal conditions, the secretory alveolar cell, are retained in most benign lesions, but they are largely lost in invasive carcinomas.
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Dissertations / Theses on the topic "Cell carcinomas"

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Spandidos, Athanasia. "Proteomic methods applied to renal cell carcinomas." Thesis, University of Cambridge, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620561.

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Llewelyn, Jenefer Kirstin. "Analysis of gene expression in squamous cell carcinomas." Thesis, King's College London (University of London), 2006. https://kclpure.kcl.ac.uk/portal/en/theses/analysis-of-gene-expression-in-squamous-cell-carcinomas(4ce3ae48-c239-4bc0-918e-e4aa691bd0d2).html.

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Xinarianos, George. "Genetic alterations in non-small cell lung carcinomas." Thesis, University of Liverpool, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343688.

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Dowlatshahi, Mitra. "Suppressed Activity of Tumor-Specific T Cells in Human Merkel Cell Carcinomas." Thesis, Harvard University, 2017. http://nrs.harvard.edu/urn-3:HUL.InstRepos:32676135.

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Merkel cell carcinomas (MCC) are rare but highly malignant skin cancers associated with a novel polyomavirus. We studied T cells in MCC to determine how these virally mediated tumors evade immune responses. MCC tumors were infiltrated by T cells, including effector, central memory and increased numbers of CD4 and CD8 FOXP3+ regulatory T cells. Infiltrating T cells showed markedly reduced activation as evidenced by reduced expression of CD69 and CD25. Treatment of MCC tumors in vitro with IL-2 and IL-15 led to T cell activation, proliferation, enhanced cytokine production and loss of viable tumor cells from cultures. Expanded tumor-infiltrating lymphocytes showed TCR repertoire skewing and upregulation of CD137. MCC tumors implanted into immunodeficient NOD/SCID/IL2 receptor g chainnull mice failed to grow unless human T cells in the tumor grafts were depleted with denileukin diftitox, suggesting tumor-specific T cells capable of controlling tumor growth were present in MCC. 50% of non-activated T cells in MCC expressed PD-1, a marker of T cell exhaustion, and PD-L1 and PD-L2 were expressed by a subset of tumor dendritic cells and macrophages. In summary, we observed tumor-specific T cells with suppressed activity in MCC tumors. Agents that stimulate T cell activity, block Treg function or inhibit PD-1 signaling may be effective in the treatment of this highly malignant skin cancer.
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Hudon, Valerie. "Investigating tumor suppressor genes involved in renal cell carcinomas." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86607.

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Kidney cancer is a complex disease comprising several types of renal carcinomas, which are classified in different subtypes based on their histological characteristics. A small number of cases of renal cancers are due to hereditary predispositions and nearly all the knowledge on the molecular pathogenesis of kidney cancers was learned by the investigation of these hereditary forms of renal carcinomas. In this thesis, we studied two hereditary diseases predisposing to the development of kidney cancer, von Hippel Lindau (VHL) and Birt-Hogg-Dubé (BHD) syndromes, and their causative genes, VHL and FLCN respectively. First, we investigated the role of the extracellular matrix (ECM) regulation by VHL during tumorigenesis and angiogenesis, and we demonstrated that inactivation of the VHL-ECM assembly pathway results in highly vascularized tumors with a disrupted ECM. We concluded that loss of the ECM assembly promotes and maintains tumor angiogenesis by providing a way for new blood vessels to invade the tumor tissue. In the second part of this thesis, we developed a novel VHL mouse model to investigate the possible cooperation between VHL and p53 during tumorigenesis. We observed that inactivation of both tumor suppressor genes accelerate the formation of liver hemangiomas and splenic hemangiosarcomas. Furthermore, concomitant deletion of VHL and p53 abolished the development of lymphoma usually associated with loss of p53. Our results indicate that the phenotypes arising following the inactivation of VHL and p53 is organ-dependent. Finally, to study the pathogenesis of the BHD syndrome, we developed a new mouse model using an established embryonic stem cell line. We described the murine Flcn expression pattern and noticed that homozygous disruption of Flcn was embryonically lethal early during development. Furthermore, we observed a continuum of kidney lesions from renal tubules hyperproliferation to rare adenoma. FLCN tumor suppressor role was also substantiated usi
Le cancer du rein est une maladie complexe qui comprend différents types de cancers classifiés selon leurs caractéristiques histologiques. Certains cas de cancers rénaux sont attribuables à une prédisposition héréditaire et l'étude de ces formes héréditaires de cancer a largement contribué au développement des connaissances concernant la pathogenèse des cancers rénaux. Le travail décrit dans cette thèse porte sur deux maladies héréditaires prédisposant au développement de tumeurs rénales soit la maladie de Von Hippel-Lindau (VHL) et le syndrome de Birt-Hogg-Dubé (BHD) ainsi que les gènes associés à ces dernières, VHL et FLCN respectivement. Premièrement, nous avons étudié le rôle de la régulation de l'assemblage de la matrice extracellulaire (MEC) par VHL durant la tumorigénèse et nous avons démontré que l'assemblage inadéquat de la MEC corrèle avec une croissance tumorale accrue et induit la formation de tumeurs fort vascularisées. Nous avons conclu que la perte de l'intégrité de la MEC favorise l'angiogénèse tumorale en fournissant une voie permettant aux vaisseaux sanguins d'infiltrer la tumeur. Deuxièmement, nous avons développé un modèle murin pour étudier la coopération potentielle entre VHL et p53 durant le développement tumoral. Nous avons observé que l'inactivation simultanée de VHL et p53 accélère la progression d'hémangiomes du foie et d'hémangiosarcomes de la rate. De plus, la perte concomitante de VHL et p53 inhibe le développement de lymphomes normalement associés à l'inactivation de p53. Nos résultats indiquent que les phénotypes apparaissant suite à l'inactivation de VHL et p53 varient selon l'organe étudié. Finalement, nous avons développé un modèle murin pour étudier de la pathologie associée au syndrome BHD et à avons observé la formation d'un continuum de lésions rénales allant de l'hyperprolifération des tubules rénaux à de rares adénomes. Finalement, nous avons conf
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Sandström, Karl. "Radioimmunodiagnosis of Head and Neck Squamous Cell Carcinomas : Preclinical Studies." Doctoral thesis, Uppsala universitet, Öron-, näs- och halssjukdomar, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-156523.

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Despite improvements in treatment, the prognosis for patients with advanced head and neck squamous cell carcinomas (HNSCC) has only improved to a minor degree. To raise the success rate and minimize morbidity further developments in diagnostics are highly desired. Radioimmunodiagnosis could offer a more specific and sensitive diagnostic method. Herein, we have evaluated different radioimmunoconjugates directed against CD44v6 and epidermal growth factor receptor (EGFR) for imaging of HNSCC. The studies were performed in a murine HNSCC xenograft model. Initially, the 111In-labeled anti CD44v6 chimeric monoclonal antibody U36 (cMAb U36) was evaluated. The novel radioimmunoconjugate showed high and accumulating tumor uptake. Since small molecules might be advantageous for imaging, due mainly to their shorter circulation half-life in the bloodstream, we then investigated antibody fragments F(ab’)2 and Fab’ derived from cMAb U36. The highest tumor-to-blood ratio was achieved with the dimeric antibody fragment F(ab’)2, compared with both the intact anti-body and monomeric Fab’. Furthermore, the possibility of improving EGFR-targeted imaging was explored by pre-blocking EGFR. The liver uptake of injected labeled human epidermal growth factor (hEGF) was significantly reduced when an excess of unlabeled hEGF was injected 30 minutes in advance. However, as hEGF stimulates cell proliferation it may be inadvisable to treat cancer patients with large amounts. Alternatively, pre-blocking with an anti-EGFR Affibody molecule (ZEGFR:955)2 demonstrated similar decrease in liver uptake as unlabeled hEGF. Finally, (ZEGFR:955)2 was compared with other Affibody molecules with higher affinity to EGFR, ZEGFR:1907 and (ZEGFR:1907)2, as pre-blocking agents. In addition, a novel hEGF radioimmunoconjugate, [67Ga]Ga-NOTA-Bn-NCS-hEGF was used for EGFR targeting. The dimeric (ZEGFR:1907)2 showed greatest reduction in non-tumor uptake, and highest tumor-to-organ ratio in EGFR expressing organs, when injected in advance of the radioimmunoconjugate. To summarize, the results presented here demonstrate how different radioimmunoconjugates as well as pre-blocking EGFR can improve the radioimmunodiagnosis of head and neck squamous cell carcinomas.
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Ekberg, Tomas. "Diagnosis and Radioimmunotherapy of Head and Neck Squamous Cell Carcinomas." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Universitetsbiblioteket [distributör], 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8395.

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Santos, Harim Tavares dos 1989. "Gotas lipídicas intracitoplasmáticas em carcinomas de glândulas salivares = estudo imunohistoquímico." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/289546.

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Orientadores: Albina Messias de Almeida Milani Altemani, Fernanda Viviane Mariano
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba
Made available in DSpace on 2018-08-24T17:05:31Z (GMT). No. of bitstreams: 1 Santos_HarimTavaresdos_M.pdf: 2437979 bytes, checksum: 15b0ad672ced32a375d9670dcdeb69ad (MD5) Previous issue date: 2014
Resumo: Introdução: Gotas lipídicas (GL) são organelas altamente reguladas envolvidas na ativação e metabolismo celular assim como em processos inflamatórios e neoplásicos. O aumento da lipogênese levando a um aumento no número de GL é um fenótipo comum a numerosos carcinomas humanos e tem sido associado com: diferenciação, proliferação e agressividade tumoral. Objetivo: Avaliarem carcinomas salivares: a) a frequência e quantidade das GLs citoplasmáticas, correlacionando-as com a morfologia tumoral, grau de diferenciação e proliferação celular e b) a expressão de proteínas relacionadas ao processo secretório celular (STAT5a e mamoglobina). Material e métodos:em 79 casos de carcinomas de glândulas salivares foram utilizados os anticorpos Ki-67, adipophilin, STAT 5a e mamoglobina. A quantificação da imunoreatividade ao adipophilin, STAT 5a e mamoglobina foi através de uma escala semi-quantitativa. A intensidade de marcação do STAT 5a e mamoglobina foi subjetivamente avaliada como fraca/moderada ou intensa. A positividade ao Ki-67 foi calculada através da relação entre o número de células positivas e o número total de células tumorais em três áreas selecionadas da amostra. Resultados:os subtipos histopatológicos que apresentaram positividade ao adipophilin em 50% ou mais das células, foram os casos: MASC (100%), CCA (85,64%), CM (83%), CDS (75%) e CSeb (50%). Índice de proliferação maior que 10% das células tumorais foi observado no CSeb (Ki-67 = 29%), seguido do CDS (Ki-67 = 23,11%) e do CM (Ki-67 = 12,15%). Nos casos de CAC com transformação para alto grau a área transformadaapresentou maior proliferação e lipogênese quando comparada à área convencional. Somente os casos de MASC apresentaram imunorreatividade acentuada para STAT5a e mamoglobina. Conclusões: Embora exista correlação entre o acúmulo de gotas lipídicas e o índice proliferativo do tumor, em alguns tipos de carcinomas salivares tal depósito está possivelmente relacionado à diferenciação celular (CSeb e MASC) ou alteração metabólica (CCA). O acúmulo de Gl refletindo diferenciação celular se apresenta como gotas maiores em contraste com as microgotas frequentemente detectadas nos carcinomas com alto índice proliferativo. No MASC a forte expressão de STAT5a e mamoglobina sugere que a que o acúmulo de GL possivelmente reflete diferenciação do tipo lactacional.Mais estudos são necessários para entender o papel das gotas lipídicas citoplasmáticas em carcinomas de glândulas salivares. (Apoio FAPESP: 2012/18104-4 e 2012/18086-6)
Abstract: Introduction: Lipid droplets (LD) are highly regulated organelles involved in cell activation and metabolism as well as in inflammatory and neoplastic processes Upregulated lipogenesis leading to an increased number of cytoplasmic LD is a common phenotype to numerous human carcinomas and has been associated with: differentiation, proliferation and aggressiveness of the tumor. Objective: to evaluate in salivary carcinomas: a) the frequency and quantity of cytoplasmics LDs, correlating it with tumoral morphology, differentiation grade e cellular proliferation and b) the expression of proteins associated with cellular secretor process (STAT5a and mammaglobin). Material and Methods:in 79 cases of salivary gland carcinomas, an immunohistochemical study was performed with the antibodies Ki-67, adipophilin, STAT 5a and mammaglobin. The positive neoplastic cells were assessed regarding quantity using a semi-quantitative scale. The intensity of expression for each antibody was subjectively evaluated as weak/ moderate or intense.The positivity for Ki-67 was calculated based on the relation between the number of positive cells and the total number of the tumoral cells in three selected areas. Results: the histopatologic subtypes that presented positivity for adipophilin in 50% or more of cells were: AciCC (85,64%), MASC (100%), MC (83%), SDC (75%), SebC (50%). Proliferation index higher than 10% of tumoral cells was observed in SebC (Ki-67 = 29%), SDC (Ki-67 = 23,11%) and MC (Ki-67 = 12,15%). In ACC with high grade transformation the, the transformed area presented both higher proliferation and lipogenesis when compared to the convencional area. Only the cases of MASC presented accentuated immunoreactivity for STAT5a and mammaglobin. Conclusions: Although in salivary carcinomas there is correlation between the accumulation of lipid droplets and the proliferative index of the tumor, in some types of carcinomas such deposit is possibly related to cellular differentiation (SebC and MASC) or metabolic alteration (AciCC). The accumulation of LD that reflects cellular differentiationpresents features of macro droplets in contrast to micro-droplets frequently detected in carcinomas with high proliferative index. In MASC, the strong expression of STAT5a and mammaglobin suggests that LD accumulation is probably due to lactational-like differentiation. More studies are necessary to understand the role of cytoplasmic lipid droplets in salivary gland carcinomas (Supported by FAPESP: 2012/18104-4and2012/18086-6)
Mestrado
Patologia
Mestre em Estomatopatologia
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Kass, Youssef Khalil. "Identification of cellular origin and molecular mechanism in basal and squamous cell carcinomas." Doctoral thesis, Universite Libre de Bruxelles, 2012. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209771.

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Skin cancers are very common in humans. The two most frequent epithelial skin cancers are the basal cell carcinoma (BCC) and the squamous cell carcinoma (SCC). For the vast majority of cancers, the cell at the origin of tumour initiation is still unknown and assumptions concerning their origin rely mainly on morphological and immunohistochemical studies. Recently, adult stem cells (SCs) have been suggested to be at the origin of tumour initiation based on their long term self-renewing capacities. According to these, two important questions arise; do epithelial skin cancers arise from mutations in a specific cell lineage of the epidermis? And are the stem cells more competent to initiate tumors than committed cells?

BCCs result from aberrant activation of HH signaling and several mouse models carrying mutations in HH signaling genes are capable to form tumors resembling to human BCCs.

To identify the cell lineage at the origin of BCC and to investigate the role of stem cells in tumor initiation, we followed a genetic approach where we conditionally expressed SmoM2 oncogene (a constitutively active Smoothened mutant) in distinct skin epidermal compartments including SCs. Targeting basal epidermis cells, showed that only SmoM2-clones in the inter follicular epidermis (IFE) and the infundibulum can progress into BCC, whereas SmoM2 expression in Bulge SCs or in matrix transit amplifying progenitor cells never leads to BCC formation. Progressively after SmoM2 expression, tumor-initiating cells lose their normal differentiation to adopt a hair placode-like shape and markers, demonstrating that biochemical and morphological tumour features can be misleading in extrapolating their cellular origin.

The molecular changes occurring in tumor initiating cells and the mechanisms regulating the early steps of cancer development are poorly characterized for the majority of tumors. To address these questions in BCC, we took advantage of our ability to isolate SmoM2 expressing cells at different stages of tumor initiation and progression. Transcriptional profiling of SmoM2-basal IFE cells isolated one week (normal histology) and 4 weeks (dysplastic lesion), suggests that adult IFE cells undergo a reprogramming into embryonic hair follicle (EHFP) like fate. In addition, we showed that Wnt/β-catenin signaling is essential for BCC initiating cell reprogramming into EHFP like fate and for tumor initiation in a cell autonomous manner. Finally, we show that EHFP reprogramming occurs also in human BCCs in addition to the presence of a similar canonical Wnt activation signature to the one revealed in the SmoM2-BCC mouse model.

SCC is the second most frequent skin cancers after BCC and mutations in p53 and Ras genes has been suggested to be potentially the primary events in this tumour. SCCs present signs of squamous differentiation, suggesting that SCCs may originate from the inter follicular epidermis (IFE). To identify the cell lineage at the origin of SCC and the role of the hair follicle SCs in tumor initiation, we use a genetic tools driving oncogenic KRas (KRasG12D) expression at physiological levels in different epidermal compartments.

Targeting KRasG12D expression in bulge SCs and their progeny or in IFE results in benign tumor development with no sign of malignant transformation. In contrast, KRasG12D expression in HF Transit amplifying (TA) matrix cells do not promotes any macroscopic tumors or microscopic defects in the epidermis. Interestingly, papillomas arising from the IFE express follicular markers such as CD34 and K17, indicating that the expression of HF markers by tumor cells does not necessarily reflect their cellular origin. Using a combination of deletion of both p53 alleles together with KRasG12D expression, we showed that bulge SCs and/or their progeny but not HF matrix TA cells, promote SCC formation, suggesting that additional genetic hits such as p53 are required to promote full-blown invasive skin SCC.

In summary, our work demonstrated the non-follicular origin of BCC resulting from Smo mutation, as well as the implication of the IFE progenitors in tumor initiation. We also revealed the progressive reprogramming of BCC initiating cells towards an EHFP-like fate and the key role of Wnt/β-catenin pathway in this process. In contrast, we showed the competence of several epidermal lineages to initiate benign tumors upon expression of KRasG12D oncogene at physiological levels. We also demonstrated that lineage -specific markers expression within tumor cells does not necessarily reflect their cellular origin. Finally, we demonstrated the requirement of additional hits, such as P53 loss, to promote malignant progression in the context of oncogenic Ras.


Doctorat en Sciences biomédicales et pharmaceutiques
info:eu-repo/semantics/nonPublished

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Blat, Irene Catherine. "Functional miRNA regulation of metastatic genes promotes tumor cell dissemination in non-small cell and small cell lung carcinomas." Thesis, Massachusetts Institute of Technology, 2013. http://hdl.handle.net/1721.1/80982.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2013.
Cataloged from PDF version of thesis. Vita.
Includes bibliographical references.
Tumor progression, from initiation to advanced metastatic disease, requires the orchestration of a diverse group of cell-intrinsic and extrinsic factors. This multifactorial disease is promoted by an accumulation of genetic and epigenetic changes that confer selective advantage to cells and enable unrestrained proliferation, survival, motility, and self-renewal. While much emphasis over the last 35 years has been dedicated to understanding the regulators of tumor initiation, the number of cancer-related deaths worldwide continues to rise, of which the majority are attributed to metastasis. The lengthy progression to metastasis requires invasion out of the primary tumor site and into the bloodstream, survival in and exit from circulation, and colonization and expansion in a foreign environment. Developmental pathways such as the Transforming Growth Factor [beta] (TGF[beta]) signaling network are frequently dysregulated during metastatic progression due to the similarities between early embryogenesis and tumor progression. Furthermore, the TGF[beta] pathway highlights how cell-intrinsic and extrinsic signals help coordinate the complex interactions required between tumor cells, as well as those of the tumor microenvironment to achieve metastasis. Facilitating alterations to pathways such as TGF[beta] and many others are modulators of gene expression that can target multiple nodes of the signaling cascade instead of requiring genetic alterations to single genes. Moreover, in the last decade, emphasis on the role of noncoding RNAs in post-transcriptional modifications has revealed their important contribution in the regulation of developmental programs across metazoan species. More recently, the role of alterations in expression of small noncoding RNAs, microRNAs (miRNAs) has emerged as a significant contributor to disease states, including each stage of tumor progression from initiation to metastatic colonization. miRNAs hold great promise not only as biomarkers but also as potential therapeutics. For these reasons, we have characterized the role of two important examples of miRNA families - the miRNA-200 family and the miRNA-1 7~92 cluster - that regulate early stages of tumor initiation in addition to later steps of cell migration, invasion, survival, and colonization. Examination of their contribution to tumor progression in relevant in vitro and in vivo cellular contexts using genetic tools reveals they are functional contributors to tumor cell dissemination. Furthermore, modulation of their expression in the appropriate tumor microenvironments elucidates a network of targets underlying the molecular mechanisms of metastasis.
by Irene Catherine Blat.
Ph.D.
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Books on the topic "Cell carcinomas"

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Small cell carcinomas: Causes, diagnosis and treatment. New York: Nova Biomedical Books, 2009.

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Maldonado, Jonathon G. Small cell carcinomas: Causes, diagnosis and treatment. New York: Nova Biomedical Books, 2009.

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Maldonado, Jonathon G., and Mikayla K. Cervantes. Small cell carcinomas: Causes, diagnosis and treatment. New York: Nova Biomedical Books, 2009.

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Hastie, G. Michael. Ribonucleic acid isolation from small cell lung carcinomas. Sudbury, Ont: Laurentian University, 1992.

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El-Salam, Mahmoud Abd. The prevalence of different human papillomavirus types and p53 mutations in laryngeal squamous cell carcinomas. [s.l.]: typescript, 1994.

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Kuo, Michael Jeo-Ming. Aberrations of chromosome arms 5q and 8p in squamous cell carcinomas of the head and neck. Birmingham: University of Birmingham, 1998.

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Burton, Jean. A study of cellular proliferation rates in squamous cell carcinomas of the lung, with relation to p53 status. [S.l: The Author], 1994.

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Renal cell carcinoma. Shelton, Conn: People's Medical Pub. House, 2009.

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Mortensen, Daniel V. Squamous cell carcinoma. Hauppauge, N.Y: Nova Science Publishers, 2011.

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Bukowski, Ronald M., and Andrew Novick. Renal Cell Carcinoma. New Jersey: Humana Press, 2000. http://dx.doi.org/10.1385/1592592295.

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Book chapters on the topic "Cell carcinomas"

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Knowlton, Christin A., Michelle Kolton Mackay, Tod W. Speer, Robyn B. Vera, Douglas W. Arthur, David E. Wazer, Rachelle Lanciano, et al. "Carcinomas: Basal Cell Carcinoma." In Encyclopedia of Radiation Oncology, 96. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_1059.

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Meyer-Breiting, Erhard, and Arne Burkhardt. "Squamous Cell Carcinomas." In Tumours of the Larynx, 79–113. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-71100-8_5.

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Corrin, B. "Small Cell Carcinomas Versus (Atypical) Carcinoids." In Clinical and Experimental Pathology of Lung Cancer, 47–52. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-5036-8_5.

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Chahoud, Jad, Gabriel G. Malouf, and Nizar M. Tannir. "Translocation Renal Cell Carcinomas." In Rare Genitourinary Tumors, 41–52. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30046-7_3.

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Weissferdt, Annikka, and Cesar A. Moran. "Non-Small Cell Carcinomas." In Diagnostic Pathology of Pleuropulmonary Neoplasia, 53–120. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0787-5_3.

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Jonasch, Eric, and Patrick G. Pilie. "Hereditary Renal Cell Carcinomas." In Rare Kidney Tumors, 1–10. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-96989-3_1.

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Liu, Dongyou. "Basal Cell and Squamous Cell Carcinomas." In Tumors and Cancers, 9–14. Boca Raton : Taylor & Francis, 2018. | Series: Pocket guides to biomedical sciences | “A CRC title, part of the Taylor & Francis imprint, a member of the Taylor & Francis Group, the academic division of T&F Informa plc.”: CRC Press, 2017. http://dx.doi.org/10.1201/9781315120553-3.

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Stöppler, H., M. Conrad Stöppler, M. Kisiela, A. Holzbach, I. Moll, P. Houdek, and R. Moll. "Merkel Cell Carcinomas Possess Telomerase Activity." In The Merkel Cell, 237–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-10358-6_35.

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Schwartz, Robert A. "Appendageal Carcinomas, Merkel Cell Carcinoma, and Cutaneous Sarcomas." In Skin Cancer, 71–79. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3790-7_8.

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Compton, Carolyn C., David R. Byrd, Julio Garcia-Aguilar, Scott H. Kurtzman, Alexander Olawaiye, and Mary Kay Washington. "Cutaneous Squamous Cell Carcinoma and Other Cutaneous Carcinomas." In AJCC Cancer Staging Atlas, 357–70. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-2080-4_29.

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Conference papers on the topic "Cell carcinomas"

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Mishra, Amita, Archit Pandit, Namit Kalra, and Bhawna Narula. "Primary signet ring cell mucinous carcinoma ovary: A very rare neoplasm." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685405.

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Introduction: Mucinous ovarian carcinomas are less common than serous and endometriod type, and are more frequently confined to the ovary at the time of diagnosis. But primary signet ring cell mucinous carcinomas of the ovary are extremely rare. Case Presentation: A 40 yr old patient presented with extremely rare primary signet cell mucinous carcinoma of ovary. She presented with abdominal distension and frequency of urination for one month. She was evaluated and CECT whole abdomen was s/o large left ovarian mass. All the tumor markers were with in normal range. Laparotomy frozen section of left adnexal mass was done and was reported as malignant with sheets of signet ring cells seen. Hence complete staging laparotomy including TAH with RSO with bilateral pelvic lymph node dissection with total omentectomy with para aortic lymph node dissection. Final histopathology with IHC markers were S/O primary signet ring cell carcinoma of ovary with no extracapsular invasion, no lymph nodal involvement & no metastatic spread. Conclusion: We present a very rare case of primary signet ring cell of ovary, confined to ovary itself. On literature review only 14 cases have been reported and of them very few are malignant.
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Stravinskaite, Kristina, and Raimundas Sakalauskas. "Multiple Primary Carcinomas: Kidney Clear Cell Carcinoma, Rectum Adenocarcinoma, Recessus Piriformis Squamose Cell Carcinoma And Non Small Cell Lung Carcinoma." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5876.

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Linka, RM, Q. Zhu, C. Wiek, J. Schipper, W. Birchmeier, and K. Scheckenbach. "Stem Cell Therapies of Head and Neck Squamous Cell Carcinomas." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1686023.

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Feil, L., J. Senz, M. Ta, J. Huvila, K. Greif, B. Krämer, S. Brucker, et al. "Molecular stratification of clear cell ovarian carcinomas." In Kongressabstracts zur Tagung 2020 der Deutschen Gesellschaft für Gynäkologie und Geburtshilfe (DGGG). © 2020. Thieme. All rights reserved., 2020. http://dx.doi.org/10.1055/s-0040-1718135.

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Rollison, Dana E., Anna R. Giuliano, Jane L. Messina, Neil A. Fenske, Basil S. Cherpelis, Vernon K. Sondak, Richard G. Roetzheim, et al. "Abstract 950: Merkel cell polyomavirus infection in cutaneous squamous cell carcinomas." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-950.

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He, Qingli, Harvey Lui, David Zloty, Bryce Cowan, Larry Warshawski, David I. McLean, and Haishan Zeng. "Microscopic fluorescence spectral analysis of basal cell carcinomas." In SPIE Proceedings, edited by Qingming Luo, Lihong V. Wang, Valery V. Tuchin, and Min Gu. SPIE, 2007. http://dx.doi.org/10.1117/12.741593.

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Soni, Abhishek, Nupur Bansal, A. K. Dhull, Vivek Kaushal, Rajeev Atri, and Monica Verma. "Diagnostic dilemma of mesonephric adenocarcinoma cervix." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685283.

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Introduction: Mesonephric carcinoma is a rare type of epithelial tumor of the uterine cervix which derive from the remnants of the paired mesonephric (Wolff’s) ducts. The incidence of such neoplasms is difficult to determine due to rarity, previous misclassification of clear cell carcinomas and yolk sac tumours as mesonephric carcinomas and potential underreporting due to misclassification of mesonephric carcinoma as Mullerian tumours or mesonephric hyperplasia. The evidence regarding the clinical course, prognosis and optimal treatment is limited. Materials and Methods: Searches were performed on MEDLINE, EMBASE and Google Scholarly articles. All the relevant articles were included in the study. Only approximate 40 cases have been reported till now. Discussion: Mesonephric adenocarcinoma cervix has different morphologies like ductal, tubular, solid, retiform, sex-cord like pattern, clear cell and serous papillary structures. IHC assessment is helpful in differentiating it from Mullerian counterpart, as it is negative for CEA, CK20, p16, PAX2, ER/PR and vimentin and positive for CD10, calretinin, CK7, CAM5.2 and EMA. It has no relation with HPV infection. Unlike squamous epithelial carcinoma, it is rarely presenting with the abnormal cervical smear result, has more advanced age at presentation and its incidence does not appear to decline with age. The diagnosis has been supported by endometrial curettings, directed/cone cervical biopsies and hysterectomy specimens. The majority of patients are diagnosed at stage IB with mean DFS of 48.6 months. Recurrence rate is 23%, with a mean interval of 40 months. Hysterectomy is the primary treatment. Advanced stage disease of adenocarcinoma seemed to respond to radiotherapy, but for the MMMTs the combination of chemotherapy with radiotherapy appears to be preferable. Conclusion: Rarity of the neoplasm, varied morphology, mix presentation and very low number of cases leads to difficulty in correct diagnosis in a small biopsy specimen. IHC helpful in differentiating it from other lesions.
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Salmanzadeh, Alireza, Harsha Kittur, Michael B. Sano, Mark A. Stremler, P. Christopher Roberts, Eva M. Schmelz, and Rafael V. Davalos. "Investigating Dielectrophoretic Signature of Mouse Ovarian Surface Epithelial Cells, Macrophages and Fibroblasts." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80872.

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Epithelial ovarian carcinomas are the fourth leading cause of death in women in the United States among all cancers and the leading cause of death from gynecological malignancies1. The main reason for this high rate of mortality is the inability to properly detect these carcinomas early. Investigations for diagnosing ovarian cancer in early stages have been hindered by two major obstacles: lack of adequate cell models to study different cancer stages and lack of a reliable technique to isolate these cancer cells from peritoneal fluid. In trying to solve the first challenge, Dr. Schmelz and collaborators presented a transformed mouse ovarian surface epithelial (MOSE) cell model by isolating different transitional stages of ovarian cancer as cells progressed from a premalignant nontumorigenic phenotype to a highly aggressive malignant phenotype2, 3. In this model four stages of transformed cells, namely early (MOSE-E), early-intermediate (MOSE-E/I), intermediate (MOSE-I) and late (MOSE-L) cells, were distinguishable3. In the current study, we attempt to solve the second challenge of isolating cancer cells from macrophages and fibroblasts, which are found in the peritoneal fluid. Based on differences in cells’ intrinsic electrical properties, a new cell manipulation technique, contactless dielectrophoresis (cDEP), was implemented.
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Lal, Anita, Rebecca Panos, Mira Marjanovic, Michael Walker, Eloisa Fuentes, W. David Henner, Ljubomir Buturovic, and Meredith Halks-Miller. "Abstract 1724: A gene expression profile test to resolve squamous cell carcinomas of head & neck from squamous cell carcinomas of the lung." In 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.am2012-1724.

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Salas-García, I., F. Fanjul-Vélez, N. Ortega-Quijano, and J. L. Arce-Diego. "Photodynamic diagnosis model for depth evaluation of basal cell carcinomas." In Biomedical Optics. Washington, D.C.: OSA, 2012. http://dx.doi.org/10.1364/biomed.2012.bsu3a.6.

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Reports on the topic "Cell carcinomas"

1

Mahoney, My G., Ulrich Rodeck, and Jouni Uitto. Molecular Characterization of Squamous Cell Carcinomas From Recessive Dystrophic Epidermolysis Bullosa. Fort Belvoir, VA: Defense Technical Information Center, September 2006. http://dx.doi.org/10.21236/ada463709.

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Mahoney, My G., Ulrich Rodeck, and Jouni Uitto. Molecular Characterization of Squamous Cell Carcinomas Derived from Recessive Dystrophic Epidermolysis Bullosa. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada446877.

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Mahoney, My G., Ulrich Rodeck, and Jouni Uitto. Molecular Characterization of Squamous Cell Carcinomas Derived from Recessive Dystropic Epidermolysis Bullosa. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada427184.

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Mahoney, My G., Ulrich Rodeck, and Jouni Uitto. Molecular Characterization of Squamous Cell Carcinomas Derived From Recessive Dystrophic Epidermolysis Bullosa. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada419358.

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Alessa, Mohammed, Tayba Wahedi, Jumanah Alsairafi, Nouf Almatrafi, Wisal Shuaib, Johara Alnafie, Fatimah Alzubaidi, and Soha Elmorsy. Prevalence of Thyroid cancer in Saudi Arabis: Systematic review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0088.

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Review question / Objective: What is the prevalence of Thyroid cancer among population in kingdom of Saudi Arabia?. The aim of this systematic review is to scrutinize the prevalence of thyroid cancer (TC) in Saudi Arabia and assess the relative frequency of subgroups related to types of thyroid cancer, age, and gender. Condition being studied: Thyroid cancer is an abnormal growth of cells that starts in the thyroid gland. There is four types of differentiated thyroid cancer, three of these cancer develop from the follicular cells, the papillary thyroid cancer, follicular thyroid cancer, Hürthle cell carcinoma, and one rare type develops from the thyroid’s C cells called medullary thyroid cancer. There is one undifferentiated thyroid cancer called anaplastic thyroid cancer.
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Jones, Richard. Ovarian Carcinoma Stem Cells. Fort Belvoir, VA: Defense Technical Information Center, May 2009. http://dx.doi.org/10.21236/ada508216.

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Freire, Mariana, Diana Martins, Maria Filomena Botelho, and Fernando Mendes. Biomarkers of resistance mechanisms in innovative lung cancer treatments - A systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0011.

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Review question / Objective: This systematic review aims to provide an overview of the immunotherapy resistance mechanisms and identify potential biomarkers associated with immunotherapy response in NSCLC, as well as examine new treatment options to overcome this hurdle. Condition being studied: Lung Cancer (LC) remains one of the leading cancers worldwide. In 2020, were globally estimated 2 206 771 new cases and 1 796 144 deaths, representing the uttermost frequent cause of cancer death. LC is classified histologically into small cell lung cancer (SCLC) or non-small cell lung cancer (NSCLC), being the last one the most common, representing 80 to 85% of all LC. The three predominantly subtypes of NSCLC are lung adenocarcinoma (LUAD), lung squamous cell carcinoma (LUSC) and large cell carcinoma (LCLC). NSCLC is usually diagnosed in advanced-staged disease due to ambiguous and delayed severe symptoms.
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8

Giancotti, Filippo G. Cell-Matrix Interactions in Breast Carcinoma Invasion. Fort Belvoir, VA: Defense Technical Information Center, January 1996. http://dx.doi.org/10.21236/ada305438.

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Curatola, Anna M. Cell-Matrix Interactions in Breast Carcinoma Invasion. Fort Belvoir, VA: Defense Technical Information Center, January 2000. http://dx.doi.org/10.21236/ada391446.

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Drucker, Aaron, Gaelen P. Adam, Valerie Langberg, Abhilash Gazula, Bryant Smith, Farah Moustafa, Martin A. Weinstock, and Thomas A. Trikalinos. Treatments for Basal Cell and Squamous Cell Carcinoma of the Skin. Agency for Healthcare Research and Quality, 2017. http://dx.doi.org/10.23970/ahrqepccer199.

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