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1

The oncogene and tumour suppressor gene factsbook. 2nd ed. San Diego, Calif: Academic Press, 1997.

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2

Phillips, Stewart Mark Anthony. The loss of tumour suppressor genes in prostate cancer. Birmingham: University of Birmingham, 1995.

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3

Lecane, Philip Sidney. A study of the p53 tumour suppressor gene in adenovirus transformed human cells. Birmingham: University of Birmingham, 1995.

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4

Tammemagi, Martin Carl. Tobacco smoking, p53 tumour suppressor gene alterations, and clinicopathologic features and prognosis in non-small cell lung cancer. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1998.

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5

El-Deiry, Wafik S. Tumor Suppressor Genes. New Jersey: Humana Press, 2003. http://dx.doi.org/10.1385/1592593283.

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6

El-Deiry, Wafik S. Tumor Suppressor Genes. New Jersey: Humana Press, 2003. http://dx.doi.org/10.1385/1592593291.

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7

S, El-Deiry Wafik, ed. Tumor suppressor genes. Totowa, N.J: Humana Press, 2003.

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8

Rangnekar, Vivek M., ed. Tumor Suppressor Par-4. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-80558-6.

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9

Rangnekar, Vivek M., ed. Tumor Suppressor Par-4. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-73572-2.

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10

Macdonald, F. Oncogenes and tumor suppressor genes. Oxford: Bios Scientific Publishers, 1991.

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11

Macdonald, F. Oncogenes and tumor suppressor genes. Oxford: BIOS, 1990.

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12

Gregory, Bock, Marsh Joan, and Ciba Foundation, eds. Genetic analysis of tumour suppression. Chichester: Wiley, 1989.

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13

Fisher, David E. Tumor Suppressor Genes in Human Cancer. New Jersey: Humana Press, 2000. http://dx.doi.org/10.1385/1592592309.

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14

Tumor suppressor genes in breast cancer. Hauppauge (NY), USA: Nova Publishers, 2008.

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15

Gabrilovich, Dmitry I., and Arthur A. Hurwitz, eds. Tumor-Induced Immune Suppression. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-69118-3.

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16

Gabrilovich, Dmitry I., and Arthur Andrew Hurwitz, eds. Tumor-Induced Immune Suppression. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4899-8056-4.

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17

Chow, Nang-Ly. Tumor suppressor genes and reversion of tumorigenicity. Bethesda, MD: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute, International Cancer Research Data Bank, 1988.

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18

The p53 tumor suppressor pathway and cancer. New York: Springer, 2005.

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19

Zambetti, Gerard P., ed. The p53 Tumor Suppressor Pathway and Cancer. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/0-387-30127-5.

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20

1951-, Cavennee Webster, Hastie Nicholas, Stanbridge Eric J, and Banbury Center, eds. Recessive oncogenes and tumor suppression. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 1989.

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21

Adams, Peter D., and John M. Sedivy, eds. Cellular Senescence and Tumor Suppression. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1075-2.

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22

Adams, Peter D. Cellular senescence and tumor suppression. New York: Springer, 2009.

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23

Benz, Christopher C., and Edison T. Liu, eds. Oncogenes and Tumor Suppressor Genes in Human Malignancies. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3088-6.

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24

Christopher, Benz, and Liu Edison T, eds. Oncogenes and tumor suppressor genes in human malignancies. Boston: Kluwer Academic Publishers, 1993.

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25

Bock, Greg, and Joan Marsh, eds. Ciba Foundation Symposium 142 - Genetic Analysis of Tumour Suppression. Chichester, UK: John Wiley & Sons, Ltd., 1989. http://dx.doi.org/10.1002/9780470513750.

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26

Oncogenes. 2nd ed. Boston: Jones and Bartlett Publishers, 1995.

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27

Oncogenes. Boston: Jones and Bartlett Publishers, 1990.

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28

name, No. Tumor suppressor genes ; v. 2: Regulation, function, and medicinal applications. Totowa, NJ: Humana Press, 2003.

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29

service), SpringerLink (Online, ed. Tetramer Stability and Functional Regulation of Tumor Suppressor Protein p53. Tokyo: Springer Japan, 2012.

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30

Kamada, Rui. Tetramer Stability and Functional Regulation of Tumor Suppressor Protein p53. Tokyo: Springer Japan, 2012. http://dx.doi.org/10.1007/978-4-431-54135-6.

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31

I, Gabrilovich Dmitry, and Hurwitz Arthur A, eds. Tumor-induced immune suppression: Mechanisms and therapeutic reversal. New York, NY: Springer, 2008.

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32

1943-, Harris Curtis C., ed. Multistage carcinogenesis: Proceedings of the 22nd International Symposium of the Princess Takamatsu Cancer Research Fund, Tokyo, ₉91. Tokyo: Japan Scientific Societies Press, 1993.

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33

Tucker, J. Devin. Suppression of pancreatic glucagon production in mice carrying proglucagon-expressing tumours, and elucidation of the tumoural patterns of proglucagon processing. Ottawa: National Library of Canada, 1994.

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34

Hesketh, Robin. Oncogene and Tumour Suppressor Gene Factsbook. Elsevier Science & Technology Books, 1997.

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35

The Oncogene & Tumour Suppressor Gene Factsbook. Elsevier, 1997. http://dx.doi.org/10.1016/b978-0-12-344548-3.x5000-6.

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36

Dr, Peters Gordon, and Vousden Karen H, eds. Oncogenes and tumour suppressors. Oxford: IRL Press at Oxford University Press, 1997.

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37

Ivanchuk, Stacey M. Identification and characterization of novel p14ARF tumour suppressor binding partners. 2005.

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38

Hoornaert, Inge. Identification & Evaluation of Candidate Tumour Suppressor Genes on Chromosome Region 12P12-13. Leuven Univ Pr, 2002.

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39

Fabre, Aurélie. Immunostaining and DNA analysis of Wilms' tumour (WT1) suppressor gene in ductal carcinoma in situ (DCIS) of the breast: Thesis. 1998.

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40

Hastie, Nick, and Eve Miller-Hodges. WT1 and its disorders. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0329_update_001.

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Mutations in the Wilms tumour suppressor gene, WT1, are associated with Wilms tumour in childhood. However, in addition WT1 has a key role in renal development, emerging roles in podocyte function, and a potential role in tissue regeneration. An understanding of WT1 is of increasing importance to clinical practice. WT1 is a complex gene with multiple isoforms. It is crucial for normal embryonic development, especially kidney development, where it is necessary for mesenchymal-to-epithelial transition to form the nephron. WT1 mutations lead to abnormalities in renal and genitourinary development, causing diseases such as Denys–Drash syndrome and Frasier syndrome as well as Wilms tumour. Recently, WT1 mutations have been recognized as a significant cause of isolated steroid-resistant nephrotic syndrome in children and young adults, without other associated syndromic features. WT1 continues to be expressed in adult podocytes, where it acts as a transcriptional activator of many podocyte genes. However, the specific role of WT1 in adult podocyte function remains poorly understood.
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41

Hodgkiss, Andrew. Introduction to cancer biology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0001.

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A brief introduction to cancer biology, aimed at psychiatrists, is offered. Selective DNA transcription, the cell cycle, receptor tyrosine kinases, and cell signalling pathways are introduced, using the EGFR/RAS/MAPK pathway as an exemplar. The molecular pathology of oncogenesis is summarized, including discussion of oncogenes, tumour suppressor genes, and examples of driver mutations. The exploitation of such mutations in stratified medicine, using molecularly targeted agents, is mentioned. Finally, Hanahan and Weinberg’s six hallmarks of cancer are listed, adding angiogenesis and metastasis to the picture of oncogenesis.
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42

Tumor Suppressors. Nova Science Pub Inc, 2011.

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43

Connor, Thomas, and Patrick H. Maxwell. Von Hippel–Lindau disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0332.

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Von Hippel–Lindau (VHL) disease is a dominantly inherited familial cancer syndrome caused by germline mutations in the VHL tumour suppressor gene. The most frequent manifestations of VHL disease are retinal and central nervous system haemangioblastomas, clear cell renal cell carcinomas, and phaeochromocytomas. Genetic testing and active screening for clinical manifestations is now started in childhood and has greatly improved the prognosis for patients with VHL disease. The VHL protein plays a critical role in regulating the cellular response to changes in oxygen tension. Loss of VHL function results in constitutive activation of a range of angiogenic and metabolic pathways. New drug therapies have been developed that reverse some of the cellular consequences of VHL loss of function in kidney cancer.
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44

Tumor suppressor genes. New York: Dekker, 1990.

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45

Cheng, Yue, ed. Tumor Suppressor Genes. InTech, 2012. http://dx.doi.org/10.5772/1337.

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46

Tumor Suppressor Genes. Nova Science Pub Inc, 2007.

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47

Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne, and Gareth Morris-Stiff. Spinal cord compression and bone marrow suppression. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0030.

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Childhood cancer in adults outlines the uncommon challenge presented by the occurrence of these pathologies in young adults, and the need for shared expertise in their successful management. The embryonal tumours, medulloblastoma, retinoblastoma, neuroblastoma, and Wilms’ tumour are considered first, emphasising similarities and differences in the pathology and management of each when adults are compared with children. The soft tissue sarcoma, rhabdomyosarcoma, is frequently best managed with chemotherapy and surgery. The important role of specialist cytogenetics in all these tumours is emphasised.
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48

Meyer, Harriet S. Oncogenes and Tumor Suppressor Genes. Oxford University Press, 2009. http://dx.doi.org/10.1093/jama/9780195176339.022.479.

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49

Marsh, Joan, and Gregory R. Bock. Genetic Analysis of Tumour Suppression. Wiley & Sons, Incorporated, John, 2008.

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50

Symposium, CIBA Foundation, Joan Marsh, and Gregory R. Bock. Genetic Analysis of Tumour Suppression. Wiley & Sons, Limited, John, 2007.

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