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Libros sobre el tema "Tumoral cell"

Autor: Grafiati
Publicado: 10 de marzo de 2023
Última modificación: 24 de agosto de 2024

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1

1938-, Hay Robert, Park Jae-Gahb y Gazdar Adi F, eds. Atlas of human tumor cell lines. San Diego: Academic Press, 1994.

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2

Derek, Raghavan, ed. Germ cell tumors. Hamilton, [Ont.]: BC Decker, 2003.

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3

Raghavan, Derek. Germ cell tumors. Hamilton [Ont.]: BC Decker, 2003.

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4

Aarbakke, Jarle, Peter K. Chiang y H. Phillip Koeffler, eds. Tumor Cell Differentiation. Totowa, NJ: Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4594-0.

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5

Mazurek, Sybille y Maria Shoshan, eds. Tumor Cell Metabolism. Vienna: Springer Vienna, 2015. http://dx.doi.org/10.1007/978-3-7091-1824-5.

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6

Frazier, A. Lindsay y James F. Amatruda, eds. Pediatric Germ Cell Tumors. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-38971-9.

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7

Bagrodia, Aditya y James F. Amatruda, eds. Testicular Germ Cell Tumors. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-0860-9.

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8

Sawamura, Yutaka, Hiroki Shirato y Nicolas de Tribolet, eds. Intracranial Germ Cell Tumors. Vienna: Springer Vienna, 1998. http://dx.doi.org/10.1007/978-3-7091-6821-9.

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9

Yutaka, Sawamura, Shirato Hiroki y Tribolet Nicolas de, eds. Intracranial germ cell tumors. Wien: Springer, 1998.

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10

Fan, Z. Hugh. Circulating tumor cells: Isolation and analysis. Hoboken, New Jersey: John Wiley & Sons, Inc., 2016.

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11

1939-, Levine Arnold J., ed. Tumor suppressor genes, the cell cycle, and cancer. Plainview, N.Y: Cold Spring Harbor Laboratory Press, 1992.

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12

1940-, Dexter Daniel L., ed. Mammalian tumor cell heterogeneity. Boca Raton, Fla: CRC Press, 1986.

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13

Smoller, Bruce R. y Kim M. Hiatt. Epidermal Cell Tumors: The Basics. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-7704-5.

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14

M, Hiatt Kim y SpringerLink (Online service), eds. Epidermal Cell Tumors: The Basics. Boston, MA: Springer Science+Business Media, LLC, 2011.

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15

Yaqoob, Nausheen. Desmoplastic small round cell tumor. New York: Nova Biomedical Books, 2012.

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16

Britta, Wahren, Karolinska institutet Nobel Assembly y Karolinska Institute Nobel Conference (8th : 1984 : Lidingö, Sweden), eds. Molecular biology of tumor cells. New York: Raven Press, 1985.

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17

Bonavida, Benjamin. Chemo-immunosensitization of resistant tumor cells to cell death by apoptosis, 2006. Trivandrum: Transworld Research Network, 2006.

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18

Nicholaus, Zavazava, ed. T-cell, tolerance, transplantation, tumor. Lengerich: Pabst Science Publishers, 1995.

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19

Zhang, Huang-Ge, ed. Emerging Concepts of Tumor Exosome–Mediated Cell-Cell Communication. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-3697-3.

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20

United States. Environmental Protection Agency. Risk Assessment Forum, ed. Assessment of thyroid follicular cell tumors. Washington, DC: U.S. Environmental Protection Agency, Office of Research and Development, 1998.

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21

United States. Environmental Protection Agency. Risk Assessment Forum., ed. Assessment of thyroid follicular cell tumors. Washington, DC: U.S. Environmental Protection Agency, Office of Research and Development, 1998.

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22

United States. Environmental Protection Agency. Risk Assessment Forum., ed. Assessment of thyroid follicular cell tumors. Washington, DC: U.S. Environmental Protection Agency, Office of Research and Development, 1998.

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23

Melchers, F. Mechanisms of B cell neoplasia 1991: Workshop at the Basel Institute for Immunology, April 14-16, 1991. Basel, Switzerland: Editiones Roche, 1991.

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24

1940-, Herberman Ronald B., ed. Influence of the host on tumor development. Dordrecht: Kluwer Academic Publishers, 1989.

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25

Fan, Z. Hugh, ed. Circulating Tumor Cells. Hoboken, NJ, USA: John Wiley & Sons, Inc, 2016. http://dx.doi.org/10.1002/9781119244554.

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26

Cote, Richard J. y Ram H. Datar, eds. Circulating Tumor Cells. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3363-1.

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27

M. Magbanua, Mark Jesus y John W. Park, eds. Circulating Tumor Cells. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7144-2.

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28

Cote, Richard J. y Evi Lianidou, eds. Circulating Tumor Cells. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-22903-9.

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29

Kawakami, Toshiyuki. Cell differentiation of neoplastic cells originating in the oral and craniofacial regions. New York: Nova Science, 2008.

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30

1942-, Niemtzow Richard C., ed. Transmembrane potentials and characteristics of immune and tumor cells. Boca Raton, Fla: CRC Press, 1985.

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31

Kolenik, Steven Andrew. The effects of interleukin-1, granulocyte macrophage colony-stimulating factor, and tumor necrosis factor-α on cultured human langerhans cells and cortical thymocytes. [New Haven: s.n.], 1990.

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32

Jarle, Aarbakke, Chiang Peter K, Koeffler H. Phillip y International Symposium on the Biology and Pharmacology of Tumor Cell Differentiation (1986 : University of Tromsö), eds. Tumor cell differentiation: Biology and pharmacology. Clifton, N.J: Humana Press, 1987.

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33

Sybert, Virginia P. Tumors/Hamartomas. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780195397666.003.0010.

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Basal Cell Nevus Syndrome – Bathing Trunk Nevus – Cowden Disease – Cylindromatosis – Dysplastic Nevus Syndrome – Epidermal Nevus – Gardner Syndrome – Hereditary Keratoacanthomas – Infantile Myofibromatosis – Multiple Endocrine Neoplasia Types 1, 2A, and 2B/3 – Multiple Leiomyomatosis – Pilomatricoma – Proteus Syndrome – Sebaceous Nevus Syndrome – Tumoral Calcinosis
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34

Sybert, Virginia P. Tumors/Hamartomas. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190276478.003.0010.

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Chapter 10 covers Basal Cell Nevus Syndrome, Cowden Syndrome, Cylindromatosis, Dysplastic Nevus Syndrome, Epidermal Nevus, Gardner Syndrome, Giant congenital nevocytic nevus, Hereditary Keratoacanthomas, Hereditary Leiomyomatosis and renal cell cancer, Infantile Myofibromatosis, Multiple Endocrine Neoplasia Types 1, 2A, and 2B/3, Pilomatricoma, Proteus Syndrome, Sebaceous Nevus Syndrome, and Tumoral Calcinosis. Each condition is discussed in detail, including dermatologic features, associated anomalies, histopathology, basic defect, treatment, mode of inheritance, prenatal diagnosis, and differential diagnosis.
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35

Cattaneo, Giuditta Filippini. A new flow cytometric P53 detection method as start point to study the effects of classical anti-tumor agents and of two endogenous substances (norepinephrine and lysophosphatidylcholine) on tumoral cell growth. 1997.

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36

Josephs, Debra H., Heather J. Bax, Giulia Pellizzari, James F. Spicer, Ana Montes y Sophia N. Karagiannis. Antibody Therapeutics for Ovarian Carcinoma and Translation to the Clinic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0001.

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Despite improvements over the past decade in the treatment of ovarian cancer, many patients are at risk of recurrent disease and emerging drug resistance. The increased selectivity and reduced toxicity of molecularly targeted anti-cancer agents renders them attractive for development in ovarian cancer, and monoclonal antibodies targeting ovarian cancer-specific tumor antigens represent the largest such group investigated in this clinical setting. This chapter describes examples of monoclonal antibodies clinically evaluated for efficacy in ovarian cancer. These agents recognize molecular targets expressed on tumors or within tumor microenvironments that may be essential for tumor cell survival and proliferation. Recently, antibodies targeting checkpoint molecules on immune cells have shown efficacy in modulating anti-tumor immunity, and applications in ovarian carcinomas are evaluated. The chapter focuses on therapeutic agents’ attributes on targeting key cancer growth and progression pathways, and propensity to engender effector functions by activating immune effector cells in tumors and the circulation.
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37

Chiang, Peter K., Jarle Aarbakke y H. Phillip Koeffler. Tumor Cell Differentiation: Biology and Pharmacology. Humana Press, 2012.

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38

Chiang, Peter K., Jarle Aarbakke y H. Phillip Koeffler. Tumor Cell Differentiation: Biology and Pharmacology. Humana Press, 2011.

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39

Hargadon, Kristian Michael y Timothy Bullock, eds. Tumor Cell/Dendritic Cell Interactions and the Influence of Tumors on Dendritic Cell-mediated Anti-Tumor Immune Responses and Dendritic Cell-Based Tumor Immunotherapies. Frontiers Media SA, 2014. http://dx.doi.org/10.3389/978-2-88919-245-8.

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40

Siemann, Dietmar W. Tumor Microenvironment. Wiley & Sons, Incorporated, John, 2011.

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41

Siemann, Dietmar W. Tumor Microenvironment. Wiley & Sons, Incorporated, John, 2011.

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42

Siemann, Dietmar W. Tumor Microenvironment. Wiley & Sons, Incorporated, John, 2010.

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43

Tumor microenvironment. Hoboken: Wiley, 2011.

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44

Moerdler, Scott y Xingxing Zang. PD-1/PDL-1 Inhibitors as Immunotherapy for Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0010.

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Programmed death 1 (PD-1), a member of the B7-CD28 immunoglobulin superfamily, and its ligands PD-L1/PD-L2 inhibit T-cell activation. They also play a key role in the tumor microenvironment, allowing for cancer immune escape. PD-1 is induced on a variety of immune cells, including tumor-infiltrating lymphocytes (TILs), while PD-L1 is found on many types of solid tumors including ovarian cancer and some TILs. The use of immunocheckpoint inhibitors like anti-PD-1 and anti-PD-L1 therapies has been shown to reactivate the immune system to attack tumor cells. Ovarian cancers have been shown to be responsive to anti-PD-1 and anti-PD-L1 therapies, though immunocheckpoint inhibitors are not enough. Current research is evaluating combination therapies to improve response rates.
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45

Shandling, Relif J. Neuronal Cell Apoptosis Research. Nova Science Publishers, 2007.

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46

Felbaum, Daniel R., Jonathan H. Sherman y Walter C. Jean. Pineal Tumors. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190696696.003.0003.

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Pineal region tumors can include a variety of histologies including pineal parenchymal tumor, germ cell tumor, glial tumor, metastasis and meningioma. The workup for pineal region tumors includes standard magnetic resonance imaging for anatomic imaging, as well as cerebrospinal fluid markers to assess for certain germ cell tumors. Cerebrospinal fluid diversion may be necessary if patients present with hydrocephalus. If surgical resection is indicated based on the suspected diagnosis, magnetic resonance venogram is an important study that influences the surgical trajectory. This chapter reviews common pineal region tumors in the setting of a case presentation. Management strategies and surgical approaches are also discussed in this chapter. Pearls for how to select the surgical approach and complication avoidance are also presented.
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47

Shandling, Relif J. Neuronal Cell Apoptosis Research. Nova Science Publishers Inc, 2006.

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48

Shandling, Relif J. Neuronal Cell Apoptosis Research. Nova Science Publishers Inc, 2006.

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49

Mazurek, Sybille y Maria Shoshan. Tumor Cell Metabolism: Pathways, Regulation and Biology. Mazurek Sybille, 2016.

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50

Mazurek, Sybille y Maria Shoshan. Tumor Cell Metabolism: Pathways, Regulation and Biology. Mazurek Sybille, 2015.

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