Abstract
“When I was diagnosed with chronic myeloid leukemia cancer, my wife and I were both runners, training pretty high miles,” recalls Matt W., a 37-year-old physicist and father of three. “At the time I hadn’t noticed anything in particular was wrong. I had a few episodes of night sweats, but I didn’t put it all together.” But when Matt could barely finish a 5K race, it was clearly time to see a doctor. As a graduate student, he didn’t have a regular physician, so he went to a walk-in clinic. “The poor doctor, who had never seen me before, basically said ‘you’ve got white cells off the charts and your spleen is the size of a grapefruit.’” The diagnosis was leukemia. That was Friday. Matt was scheduled for the oncologist the following Monday, which “gave me and Elizabeth [Matt’s wife] all weekend to freak out about it.”
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Notes
- 1.
Shannon Greene and Ann Reid, “Moving Targets,” American Society of Microbiology, (Washington, DC, 2012), 37, http://academy.asm.org/images/stories/documents/MovingTargets.pdf.
- 2.
For more on cancer over the ages, see: George Johnson, “Unearthing Prehistoric Tumors, and Debate,” New York Times, December 27 2010, www.nytimes.com/2010/12/28/health/28cancer.html?_r=2&; for more about the evolutionary “mismatch” among lifestyle, diet, and health, see: Daniel Lieberman, The Story of the Human Body: Evolution, Health, and Disease (New York: Random House 2013); Barbara Dunn, “Solving an Age-Old Problem,” Nature 483 (March 2012): S1–S6.
- 3.
Jacques Robert, “Comparative Study of Tumorigenesis and Tumor Immunity in Invertebrates and Nonmammalian Vertebrates,” Developmental and Comparative Immunology 34 (2010): 915–25.
- 4.
Denys Wheatley, “Carcinogenesis: Is There a General Theorem?” BioEssays 5 (2010): 111; Carlos Sonnenschein and Ana M. Soto, “Theories of Carcinogenesis: An Emerging Perspective,” Seminars in Cancer Biology 18 (October 2009): 372–77. For more about cancer in humans, see: Mel Greaves, Cancer: The Evolutionary Legacy (Oxford: Oxford University Press 2000).
- 5.
Mark Vincent, “The Animal Within: Carcinogenesis and the Clonal Evolution of Cancer Cells Are Speciation Events Sensu stricto,” Evolution 64 (April 2010): 1173–83; Robert Sanders, “Are Cancers Newly Evolved Species?” UC Berkeley News Center, July 26, 2011, http://newscenter.berkeley.edu/2011/07/26/are-cancers-newly-evolved-species/.
- 6.
Michael R. Stratton, Peter J. Campbell, and P. Andrew Futreal, “The Cancer Genome,” Nature 458 (2009): 719–24.
- 7.
For an interesting discussion of cell suicide and cancer defense, see: Adam Mann, “Sponge Genome Goes Deep,” Nature 466 (2010): 673; for more technical information, see: Tomislav Domazet-Loso and Diethard Tautz, “Phylostratigraphic Tracking of Cancer Genes Suggests a Link to the Emergence of Multicellularity in Metazoa,” BMC Biology 8 (2010): 66; Francesca D. Ciccarelli, “The (R)evolution of Cancer Genetics,” BMC Biology 8 (2010): 74.
- 8.
Douglas Hanahan and Robert A. Weinberg, “The Hallmarks of Cancer,” Cell 100 (January 2000): 57.
- 9.
Bernard Crespi and Kyle Summers, “Evolutionary Biology of Cancer,” Trends in Ecology & Evolution 20 (2005): 545–52.
- 10.
Tina Hesman Saey, “Dangerous Digs: A Cell’s Surroundings May Be Instrumental to the Development of Cancer,” Science News (October 5, 2013), www.sciencenews.org/article/dangerous-digs?mode=magazine&context=187280, accessed March 2014.
- 11.
For more on infectious disease and cancer, see: Paul Ewald and Holly Swain, Controlling Cancer: A Powerful Plan for Taking on the World’s Most Daunting Disease (TED Books, 2012).
- 12.
For an interesting summary of cell life spans, see: “Life-Spans of Human Cells Defined: Most Cells Are Younger Than the Individual,” Times Higher Education, September 2005, www.timeshighereducation.co.uk/198208 .article, accessed March 2014.
- 13.
Guy Faguet, The War on Cancer (Houten, the Netherlands: Springer, 2008): 69; following the war, mustard gas and other chemical weapons were outlawed by the Geneva Protocol of 1925.
- 14.
Alfred Gilman, “The Initial Trial of Nitrogen Mustard,” American Journal of Surgery 105 (May 1963): 574–78. Gilman noted, however, that this degree of success was not to be repeated in follow-up studies (577).
- 15.
Ibid., 577.
- 16.
Ibid.
- 17.
For more about early chemotherapy treatment, see: Isaac Berenblum, Man Against Cancer (Baltimore: Johns Hopkins Press, 1952).
- 18.
For more about the development of aminopterin, the folic acid analog and other anticancer treatments, see: Siddhartha Mukherjee, The Emperor of All Maladies: A Biography of Cancer (New York: Scribner, 2010).
- 19.
Faguet, The War on Cancer, 79.
- 20.
Ibid., 72.
- 21.
Amir Fathi (Massachusetts General Hospital and Harvard Medical School) in discussion with the author, September 12, 2013.
- 22.
For statistics and information on CML, see: “What Are the Key Statistics About Chronic Myeloid Leukemia?” American Cancer Society, www.cancer.org/cancer/leukemia-chronicmyeloidcml/detailedguide/leukemia-chronic-myeloid-myelogenous-key-statistics, last modified February 2014.
- 23.
For more about treatment, see: “CML—A Short History of Treatment Since the Mid-20th Century,” International Chronic Myeloid Leukemia Foundation, www.cml-foundation.org/index.php/news/169-cml-a-short-history-of-treatment-since-the-mid-20th-century, last modified June 2012.
- 24.
R. Hehlmann et al., “Randomized Comparison of Interferon-Alpha with Busulfan and Hydroxyurea in Chronic Myelogenous Leukemia, German CML Study Group,” Blood 84 (1994): 4064.
- 25.
Hehlmann et al., “Randomized Comparison,” 4064–77.
- 26.
John Goldman, “Chronic Myeloid Leukemia: A Historical Perspective,” Seminars in Hematology 47 (October 2010): 302–11.
- 27.
Mukherjee, Emperor, 435.
- 28.
Doug Jenson, “Imatinib: A Patient Perspective,” in 50 Years in Hematology: Research that Revolutionized Patient Care, American Society of Hematology, 14, www.hematology.org/About/History/50-Years/1944.aspx, accessed March 2014.
- 29.
Ibid.; see also: E. J. Mundell, “Gleevac Continues to Beat Blood Cancer,” Washington Post, December 6, 2006, www.washingtonpost.com/wp-dyn/content/article/2006/12/06/AR2006120601494.html.
- 30.
Mukherjee, Emperor, 437.
- 31.
Massimo Breccia and Guiliana Alimena, “Resistance to Imatinib in Chronic Myeloid Leukemia and Therapeutic Approaches to Circumvent the Problem,” Cadiovascular & Haematological Disorders—Drug Targets 9 (2009): 21–28.
- 32.
Michael Mathisen, Hagop Kantarjian, and Elias Jabbour, “Mutant BCR-ABL Clones in Chronic Myeloid Leukemia,” Haematologica 96 (March 2011): 347–49.
- 33.
Marco Gerlinger (Institute of Cancer Research, Center for Evolution and Cancer) in e-mail discussion with the author, August 2013.
- 34.
C. Athena Aktipis, Virginia Kwan, Kathryn Johnson, Steven Neuberg, and Carlo Maley, “Overlooking Evolution: A Systematic Analysis of Cancer Relapse and Therapeutic Resistance Research,” PLoS ONE 6 (November 2011): e26100, doi:10 1371/journal.pone.0026100.
- 35.
C. Athena Aktipis (Director of Human and Social Evolution and cofounder of the Center for Evolution and Cancer at the University of California, San Francisco, and Research Professor in the Psychology Department at Arizona State University) in e-mail discussion with author, May 2014.
- 36.
Gerlinger, discussion with author. For more about the clonal evolution of cancer, see: Peter Nowell, “The Clonal Evolution of Tumor Cell Populations,” Science 194 (October 1976): 23–28.
- 37.
For information on local environment and mutation, see: Bert Vogelstein et al., “Cancer Genome Landscapes,” Science 339 (March 2013): 1546–58; for more on random mutations in tumors, see: Christoph Klein, “Random Mutations, Selected Mutations: A PIN Opens the Door to New Genetic Landscapes,” Proceedings of the National Academy of Sciences 103 (November 2006): 18033–34.
- 38.
Robert Gillies, Daniel Verduzco, and Robert Gatenby, “Evolutionary Dynamics of Carcinogenesis and Why Targeted Therapy Does Not Work,” Nature Reviews 12 (July 2012): 487.
- 39.
Gerlinger, discussion with author; in some cases, cancer stem cells may also contribute to resistance. Stem cells have yet to commit to a particular cell type (an embryonic stem cell, for example, might differentiate into a skin or muscle cell). Cancer stem cells retain the ability to differentiate into a number of different cell types within a particular tumor. Whether embryonic or cancerous, stem cells are well protected from their environment, equipped with protein pumps capable of ejecting toxic chemicals from natural metabolites to chemotherapy drugs like water from a leaky rowboat. Should a tumor be under chemical attack, stem cells may be standing by with chemically resistant recruits. The potential role of cancer stem cells is reviewed in: Darryl Shibata, “Molecular Tumor Clocks to Study the Evolution of Drug Resistance,” Molecular Pharmaceutics 8 (2011): 2050–54; and S. Raguz and E. Yague, “Resistance to Chemotherapy: New Treatments and Novel Insights into an Old Problem,” British Journal of Cancer 99 (2008): 387–91.
- 40.
Mathisen et al., “Mutant BCR-ABL.”
- 41.
Jessica Cunningham, Robert Gatenby, and Joel Brown, “Evolutionary Dynamics in Cancer Therapy,” Molecular Pharmaceutics 8 (2011): 2094–100.
- 42.
Gillies et al., “Evolutionary Dynamics,” 492.
- 43.
Ibid., 490.
- 44.
Robert A. Gatenby, “A Change of Strategy in the War on Cancer,” Nature 459 (May 28, 2009): 508–9.
- 45.
Ibid.
- 46.
Gerlinger, discussion with author.
- 47.
For more discussion and review about resistance in agriculture, antibiotics, and chemotherapy, see: Greene and Reid, “Moving Targets,” 17.
- 48.
Francois-Xavier Mahon, “Is Going for Cure in Chronic Myeloid Leukemia Possible and Justifiable?” American Society of Hematology Education, Book 1 (December 2012): 122–28, doi:10.1182/asheducation-2012.1.122.
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Monosson, E. (2015). Treatment: Beyond Chemotherapy. In: Unnatural Selection. Island Press, Washington, DC. https://doi.org/10.5822/978-1-61091-500-7_4
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