BoveriT. Zur Frage der Entstehung maligner Tumoren. Gustav Fisher (Jena, Germany)., 1914; 4:1–64.
2.
VauxDL. In defense of the somatic mutation theory of cancer. BioEssays, 2011; 33:341–343.
3.
SotoAM, SonnenscheinC. The Society of Cells: Cancer and Control of Cell Proliferation. New York, NY: Springer Verlag, 1999.
4.
ReyaT, MorrisonSJ, ClarkeMF, WeissmanIL. Stem cells, cancer, and cancer stem cells. Nature, 2001; 414:105–111.
5.
BonnetD, DickJE. Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell. Nat Med., 1997; 3:730–737.
6.
GreenblattM, ShubiP. Tumor angiogenesis: Transfilter diffusion studies in the hamster by the transparent chamber technique. J Natl Cancer Inst., 1968; 41:111–124.
7.
FolkmanJ. Role of angiogenesis in tumor growth and metastasis. Semin Oncol., 2002; 29:15–18.
8.
BalkwillF, MantovaniA. Inflammation and cancer: Back to Virchow?Lancet, 2001; 357:539–545.
9.
CoussensLM, WerbZ. Inflammation and cancer. Nature, 2002; 420:860–867.
10.
UemuraNet al.Helicobacter pylori infection and the development of gastric cancer. N Engl J Med., 2001; 345:784–789.
11.
zur HausenH. The search for infectious causes of human cancers: Where and why (Nobel lecture)Angew Chem Int Ed Engl., 2009; 48:5798–5808.
12.
El-SeragHB. Epidemiology of viral hepatitis and hepatocellular carcinoma. Gastroenterology, 2012; 142:1264–1273.e1261.
13.
GrivennikovSI, GretenFR, KarinM. Immunity, inflammation, and cancer. Cell, 2010; 140:883–899.
14.
SotoAM, SonnenscheinC. The tissue organization field theory of cancer: A testable replacement for the somatic mutation theory. BioEssays, 2011; 33:332–340.
15.
VauxDL. Response to “The tissue organization field theory of cancer: A testable replacement for the somatic mutation theory”BioEssays, 2011; 33:660–661.
16.
KurzrockR, KantarjianHM, DrukerBJ, TalpazM. Philadelphia chromosome-positive leukemias: From basic mechanisms to molecular therapeutics. Ann Intern Med., 2003; 138:819–830.
17.
HeisterkampNet al.Acute leukaemia in bcr/abl transgenic mice. Nature, 1990; 344:251–253.
18.
DrukerBJet al.Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells. Nat Med., 1996; 2:561–566.
19.
DrukerBJet al.Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. N Engl J Med., 2001; 344:1031–1037.
20.
GrahamSMet al.Primitive, quiescent, Philadelphia-positive stem cells from patients with chronic myeloid leukemia are insensitive to STI571 in vitro. Blood, 2002; 99:319–325.
21.
CorbinASet al.Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity. J Clin Invest., 2011; 121:396–409.
22.
PerlA, CarrollM. BCR-ABL kinase is dead; long live the CML stem cell. J Clin Invest., 2011; 121:22–25.
23.
ShahNPet al.Overriding imatinib resistance with a novel ABL kinase inhibitor. Science (New York, NY), 2004; 305:399–401.
24.
ShahNPet al.Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia. Cancer Cell, 2002; 2:117–125.
25.
MuvarakN, NagariaP, RassoolFV. Genomic instability in chronic myeloid leukemia: Targets for therapy?Curr Hematol Malig Rep., 2012; 7:94–102.
26.
NowellPC. The clonal evolution of tumor cell populations. Science (New York, NY), 1976; 194:23–28.
27.
LengauerC, KinzlerKW, VogelsteinB. Genetic instabilities in human cancers. Nature, 1998; 396:643–649.
