Chapter 8 reviewed the range of methods in use for tumour detection and radiation therapy together with the continuing search for biomarkers to detect the presence of tumours and monitor their progression in response to therapies. In this chapter, we reach what has in many ways become the central goal of cancer research, namely chemotherapy – the notion that it is possible to bring cancers under control through the use of drugs without the requirement for surgical intervention or radiotherapy. The science of treating cancer with specific chemicals was initiated in the second half of the twentieth century as an adjunct to surgery and radiotherapy. Starting from the use of single agents and advancing to the administration of drug cocktails, they gave spectacular results for some types of cancer. By the beginning of the next millennium, these anti-cancer drugs had been joined by the first ‘targeted’ agents, namely kinase inhibitors and the first monoclonal antibodies. The astonishing success of vaccines that prevent infection by human papillomaviruses (HPVs) has had a major impact on the incidence of cervical carcinoma and other types of cancer caused by oncogenic forms of these viruses.

Epidemiology is the study of the distribution and determinants (causes and risk factors) of health-related states and events. This chapter focuses on the distribution of cancers across the world; the next chapter deals with causes. We begin by looking at global patterns. These are of interest because they show marked variations in the forms of the disease that afflict different populations. These differences indicate the importance of environmental factors that include lifestyle – for example, what we eat and tobacco use – in determining both the type of cancer and the frequency of occurrence.

Chapter 1 surveyed the global picture of cancer incidence and mortality, revealing that across nations there is an almost sixfold range in new cases per year. The mortality variation is somewhat smaller at just over threefold, but, taken together, these figures indicate that multiple factors give rise to cancers and that there are considerable differences in the efficacy of treatment. The current figures of 18 million diagnoses and 10 million deaths each year are predicted to increase by over 60% in the next 20 years. The human implications of these figures are beyond comprehension, but the economic costs are also staggering. In the USA alone, cancer research funding runs to billions of dollars a year and the annual cost of caring for cancer patients to hundreds of billions.

Chapter 7 led us through the maze of signalling pathways in cancer cells to a core network that lies at the heart of tumour development and, predictably, features the most prominent oncogenes and tumour suppressors. This established a solid molecular base upon which to review the critical cancer questions: (1) how to detect them, (2) once detected, whether the course of their progression can be predicted, and (3) where we are in terms of treatment by drugs (chemotherapy). The first two are considered in this chapter before we turn to the current chemotherapy situation in Chapter 9 and future prospects in Chapter 10.

Chapter 6 described the phenotypic features that characterise tumour cells and the underlying molecular changes that subvert normal signalling pathways (Chapter 4) through the mutations acquired in the cancer cell genome (Chapter 5). As we’ve seen, the major ‘drivers’ of cancer development arise in pathways from receptor tyrosine kinases (RTKs) that ultimately control cell division. Thus, for example, aberrant activity of the RAS–mitogen-activated protein kinase (MAPK) pathway occurs frequently across a broad spectrum of cancer types. However, cancer-promoting mutations occur in other signalling pathways and ultimately they can affect all aspects of cellular behaviour. The molecular details of most of these pathways and how they can be subverted in cancers are now well established. The integration between diverse pathways creates a picture of a complex ‘information network’ rather than of discrete, linear systems. Despite the multiplicity of signalling pathways that can be involved, the tumour cells that emerge as the result of appropriate groups of mutations are phenotypically similar in that they share the characteristics discussed in the previous chapter. This suggests that the diverse pathways converge on a ‘central axis’, and in this chapter we’ll look first at the central defenders that do indeed constitute the heart of our protection mechanisms against cancer. We’ll then overlay the major pathways from receptor to nucleus to show how they impact on the central axis and dissect from this complex map each of the pathways in turn to introduce the key players. The intention is not show all known detail but to convey the principle features of the pathways with particular emphasis on identified proto-oncogenes and tumour suppressors.

Overview of cardiac complicationsincluding arrhythimias, heart failure, acute coronary syndrome, disseminated intravascular coagulation, hyperviscosity syndrome, and pulmonary embolism

Overview of cardiac complicationsincluding arrhythimias, heart failure, acute coronary syndrome, disseminated intravascular coagulation, hyperviscosity syndrome, and pulmonary embolism

Overview of cardiac complicationsincluding arrhythimias, heart failure, acute coronary syndrome, disseminated intravascular coagulation, hyperviscosity syndrome, and pulmonary embolism

Overview of toxicities related to immunotherapy agents, and other complications in the lymphatic system such as tumor lysis, hyperviscosity syndrome, graft vs host disease, and neutropenic fever

Overview of gastrointestinal complications including constipation, diarrhea, nausea, and vomiting, feeding tube complications, bowel perforation and obstruction, and neutropenic enterocolitis

Overview of respiratory complications such as hemoptysis, hiccups, laryngectomy and tracheostomy troubleshooting, airway obstruction, pneumonitis, and pleural effusion management

Tumor: a mass of tissue formed via disruption of the normal cell cycle resulting in abnormal cell growth.

Defines terminology, an overview of cancer types, modes and locations of metastasis, cancer statistics, and treatment modalities.

Overview of genitourinary complications such as obstructive uropathy, percutaneous nephrostomy tube trouble shooting, electrolyte abnormalities, and gynecological surgical complications

Defines terminology, an overview of cancer types, modes and locations of metastasis, cancer statistics, and treatment modalities.

Overview of cardiac complicationsincluding arrhythimias, heart failure, acute coronary syndrome, disseminated intravascular coagulation, hyperviscosity syndrome, and pulmonary embolism

Overview of gastrointestinal complications including constipation, diarrhea, nausea, and vomiting, feeding tube complications, bowel perforation and obstruction, and neutropenic enterocolitis