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Books on the topic 'Cell Line, Tumor'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Brail, Leslie Harris. Heterogeneity of plasminogen activator activity produced by two murine tumour cell lines. National Library of Canada, 1994.

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2

Weinstein, Ellen Michele. Inhibition of CA 125, a novel high molecular weight glycoprotein expressed by an ovarian carcinoma cell line: 0VCA 433, is related to glucocorticoid effects of altered cell growth, morphology, and growth pattern. s.n.], 1988.

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3

Turnbull, Heather. Biochemical and physiological characterization of newly established drug-resistant MCF-7 breast tumour cell lines. Laurentian University, 2000.

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4

Al-Hakim, Abdallah. A role for the type 4 adenylyl cyclase isoform in forskolin-response pathway of Y1 mouse adrencortical tumor cell lines. National Library of Canada, 2003.

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5

service), SpringerLink (Online, ed. Insulin-like Growth Factors and Cancer: From Basic Biology to Therapeutics. Springer Science+Business Media, LLC, 2012.

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6

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

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7

Drexler, Hans G. The Leukemia-Lymphoma Cell Line Factsbook. Academic Press, 2000.

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8

Drexler, Hans G. The Leukemia-Lymphoma Cell Line Factsbook. Academic Press, 2000.

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9

B, Roninson Igor, ed. Molecular and cellular biology of multidrug resistance in tumor cells. Plenum Press, 1991.

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10

Moerdler, Scott, and 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 r

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11

Isaacs, John D., and Philip M. Brown. Rituximab and abatacept. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0083.

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Two biologics that target cells have been licensed to treat rheumatoid arthritis (RA). Rituximab is a chimeric monoclonal antibody (mAb) against CD20 that depletes B cells; abatacept is a soluble form of CTLA-4 that blocks costimulation and interferes with T-cell function. Both drugs alleviate signs and symptoms of RA and have been shown to retard radiographic progression. Rituximab is licensed for use following failure of tumour necrosis factor (TNF) blockade whereas abatacept's licence permits it use as a first-line biologic. In the United Kingdom, however, the National Institute for Health

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12

Grant, Warren, and Martin Scott-Brown. Principles of oncogenesis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0322.

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It is obvious that the process of developing cancer—oncogenesis—is a multistep process. We know that smoking, obesity, and a family history are strong independent predictors of developing malignancy; yet, in clinics, we often see that some heavy smokers live into their nineties and that some people with close relatives affected by cancer spend many years worrying about a disease that, in the end, they never contract. For many centuries scientists have struggled to understand the process that make cancer cells different from normal cells. There were those in ancient times who believed that tumo

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13

Powell, Craig M. PTEN and Autism With Macrocepaly. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199744312.003.0010.

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Phosphatase and Tensin homolog deleted on chromosome 10 (PTEN) is a gene encoding an intracellular signaling molecule. PTEN was originally discovered as the gene responsible for a subset of familial hamartoma (tumor) syndromes associated with increased risk for certain cancers (Nelen et al., 1997) and as a gene often mutated in human cancers and tumor cell lines (Li et al., 1997; Steck et al., 1997). More recently, mutations in PTEN have been linked genetically to the clinical phenotype of autism or developmental delay with macrocephaly (Boccone et al., 2006; Butler et al., 2005; Buxbaum et al

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14

Weiner, Howard, and Peter B. Crino. Familial tumour syndromes: tuberous sclerosis complex. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0017.

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Tuberous sclerosis complex (TSC) is a multisystem, genetic disorder that results from mutations in TSC1 or TSC2 genes. Neurological and neuropsychiatric disabilities include epilepsy, intellectual disability, autism, attention deficit disorder, and generalized anxiety. Cortical dysplasias (also known as tubers) are developmental abnormalities of the cerebral cortex that are believed to be responsible for seizures, cognitive disability, and autism. Subependymal giant cell astrocytomas (SEGAs) are intraventricular tumours that can cause hydrocephalus, increased intracranial pressure, and death.

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15

O'Brien, Donalee. DNA-mediated transfer of a neomycin resistance gene into the Y r mouse adrenocortical tumour cell line. 1987.

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16

Haymann, Jean-Philippe, and Francois Lionnet. The patient with sickle cell anaemia. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0167.

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In sickle cell anaemia (SCA) a single mutation in the haemoglobin beta-globin gene is responsible for a pleomorphic phenotype leading to acute and chronic life-threatening complications. Healthcare management programmes, patient and family education, infection prophylaxis (especially in childhood), and long-term treatment for some patients (such as hydroxyurea) have significantly improved survival, giving rise to some new long-term issues.Sickle cell-associated nephropathy (SCAN) leads in some cases to chronic renal failure with a significant impact on survival. SCAN is characterized by an inc

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17

Kempermann, MD, Gerd. Adult Neurogenesis 2. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199729692.001.0001.

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This resource is aimed at those interested in adult neurogenesis and stem cell biology of the adult brain, and covers the historical background and describes in detail adult neurogenesis in the hippocampus as well as the subventricular zone and olfactory bulb. It then discusses the regulatory mechanisms, and the subject of neurogenesis outside the "canonical" neurogenic regions of rodents and primates, as well as how adult neurogenesis in different species. It concludes with coverage of the provocative hypotheses that link failing adult neurogenesis with diseases such as temporal lobe epilepsy

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18

Fang, Xianjun. Immortalization and transformation of rat hepatocytes by oncogenes: phenotypic analysis of tumors produced in nude mice by cell lines. 1994.

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19

Quantification of the p53 tumor suppressor gene product in cell lines and serum of cancer patients: Development of new methodology and clinical studies. National Library of Canada = Bibliothèque nationale du Canada, 1993.

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20

Andrejeva, Liva, Jaime L. Geisel, and Malini Harigopal. Spiculated Masses. Edited by Christoph I. Lee, Constance D. Lehman, and Lawrence W. Bassett. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190270261.003.0025.

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A spiculated mass is a centrally dense lesion seen on mammography with sharp lines radiating from its margin. The spicules can vary greatly in length, from a few millimeters to several centimeters. In malignant lesions, spicules represent a mixture of tumor cells and fibrosis invading the normal tissue surrounding the lesion. Although a spiculated mass is thought of as a classic finding of malignancy on mammography, ultrasound, and MRI, its differential diagnosis includes benign lesions. However, unless clinical history strongly supports a benign diagnosis, a spiculated mass on any modality ty

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21

1932-, Macieira-Coelho Alvaro, ed. Developmental biology of neoplastic growth. Springer, 2005.

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22

LeRoith, Derek. Insulin-like Growth Factors and Cancer: From Basic Biology to Therapeutics. Springer, 2011.

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