This chapter explores recent insights from preclinical and clinical studies of cancer induced bone pain (CIBP). There are various neuropathic, nociceptive, and inflammatory pain mechanisms that contribute to CIBP. Neuropathic pain can be induced as tumor cell growth injures distal nerve fibers that innervate bone and pathological sprouting of both sensory and sympathetic nerve fibers. These changes in the peripheral sensory neurons result in the generation and maintenance of tumor induced pain. CIBP is usually described as dull in character, constant in presentation, and gradually increasing in intensity with time. A component of bone cancer pain appears to be neuropathic in origin as tumor cells induce injury or remodeling of the primary afferent nerve fibers that normally innervate the tumor bearing bone. The treatment of pain from bone metastases involves the use of multiple complementary approaches including radiotherapy, chemotherapy, surgery, bisphosphonates, and analgesics.

Cancer can affect the autonomic nervous system in a variety of ways: direct tumor compression or infiltration, treatment effects (irradiation, chemotherapy), indirect effects (e.g., malabsorption, malnutrition, organ failure, and metabolic abnormalities), and paraneoplastic/autoimmune effects. This chapter focuses on a diagnostic approach and treatment of cancer patients with dysautonomia, with an emphasis on immune-mediated autonomic dysfunction, a rare but potentially highly treatable cause of dysautonomia. Autonomic dysfunction can be divided into nonneurogenic (medical) and neurogenic (primary or secondary) causes. Orthostatic hypotension is a cardinal symptom of dysautonomia. The autonomic testing battery includes sudomotor, vasomotor, and cardiovagal function testing and defines the severity and extent of dysautonomia. Conditions encountered in the cancer setting that are associated with autonomic dysfunction include Lambert-Eaton Myasthenic Syndrome, anti-Hu antibody syndrome, collapsin response-mediator protein 5, subacute autonomic neuropathy, neuromyotonia (Isaacs’ syndrome), and intestinal pseudo-obstruction. The chapter describes various pharmacologic and nonpharmacologic therapies for treatment of orthostatic hypotension.

Despite treatment advances in the world of oncology, problems with sexuality, intimacy, and fertility persist for many women and men treated for cancer. Life expectancy of cancer patients, both young and old, has significantly increased due to advances in treatments of malignant diseases. Consequently, medical attention has expanded its focus to improving the quality of life of patients who have undergone cancer treatment. Sexual function and feeling healthy enough to be a parent represent two of the strongest predictors of emotional well-being in cancer survivors, and parenthood can represent a return to normalcy, contributing happiness and life-fulfillment. Often, cancer survivors fear that their disease or treatment history may adversely affect offspring conceived posttreatment, contributing risk for congenital anomalies, impaired growth and development, or even for malignancy. This chapter provides physical psychosocial spiritual dimensions of the fertility issues or symptom followed by its nonpharmacological and pharmacological treatment.

In human cancer, the role of genetic mutations, epigenetic alterations, and cellular repair mechanisms are becoming increasingly apparent. Recent studies have elucidated significant variations of the genetic codes that underpin cancer development in a variety of cancer subtypes. Genetic variations provide a backbone upon which cancer cells can adapt to overcome both intrinsic and extrinsic mechanisms designed to limit the growth of abnormal cells. This chapter provides an overview of the types of mutations, various epigenetic modifications, DNA repair mechanisms, and their relationship to the development of cancer, as well as various techniques utilized for the detection of these genetic alterations in cancer. With the development of new, advanced, and sensitive molecular techniques like next-generation sequencing and digital droplet polymerase chain reaction, our understanding of cancer biology is rapidly developing, and a critical appreciation and knowledge of these cancer-associated changes will likely lead to continued development of more effective therapies.

The vast majority of cervical cancer cases are human papillomavirus -mediated. Incidence and mortality significantly declined with introduction of screening with Pap smears. Adenocarcinoma often presents with larger tumors (“barrel cervix”) with higher risk of local failure. Cervical cancers are often asymptomatic and detected on screening, or can present with abnormal vaginal discharge, post-coital bleeding, dyspareunia, or pelvic pain. Three Food and Drug Administration approved vaccines are available that prevent the development of cervical cancer. Imaging includes positron emission tomography/computed tomography (nodal staging), pelvic magnetic resonance imaging (to delineate local disease extent and guide decisions on fertility vs. non-fertility sparing approaches). Treatment at early stages is often surgical, while Radiation therapy (RT)+/− Chemotherapy (CHT) is employed in later stages. When treating definitively, External beam radiation therapy is followed by an intracavitary or interstitial brachytherapy boost. Post-operative RT +/− CHT is occasionally indicated for adverse pathologic features.

World Health Organization grade III gliomas are referred to as anaplastic gliomas. The general treatment paradigm includes maximal safe surgical resection followed by adjuvant radiation therapy and chemotherapy (CHT). The randomized trials that established a survival benefit from chemotherapy used Procarbazine, Lomustine, and Vincristine (PCV). Concurrent and adjuvant temozolomide (TMZ) is given more often and is still subject to ongoing study. An improved understanding of genomics is rapidly informing the clinical behavior and treatment. Histologic subtypes of anaplastic gliomas include anaplastic astrocytoma and anaplastic oligodendroglioma (AO). Headache and seizures are the most common symptoms of anaplastic gliomas. Adjuvant radiation improves overall survival after surgery compared to observation or CHT alone and is indicated for all high-grade gliomas. Despite the survival advantage demonstrated with PCV in patients with AOs and AOs, many substitute TMZ as it is easier to administer and generally better tolerated.

This chapter discusses treatment planning for gastrointestinal radiotherapy. It describes patient setup, immobilization, and planning technique for esophageal cancer external beam radiation therapy (EBRT). The chapter provides patient setup and immobilization, motion management techniques, target delineation, and planning technique for pancreas fractionated EBRT. It explains patient setup and immobilization, motion management techniques, and planning technique for pancreas stereotactic body radiation therapy (SBRT). The chapter presents patient setup and immobilization, motion management techniques and planning technique for rectal cancer EBRT. It describes patient setup and immobilization, and planning technique for anal cancer EBRT. Finally the chapter explores patient setup and immobilization, motion management techniques and planning technique for liver SBRT.

This chapter discusses strategies for radiation therapy treatment planning for thoracic cancer. It provides a brief description of immobilization on 3D and modulated radiation therapy (intensity modulated radiation therapy [IMRT], volumetric modulated arc therapy [VMAT]), and stereotactic body radiation therapy (SBRT). It describes the image acquisition for 3D and modulated radiation therapy (IMRT or VMAT) and SBRT. The chapter discusses the localization for 3D and modulated radiation therapy (IMRT or VMAT) and SBRT. It presents the beam energy requirements for 3D plans, IMRT and VMAT, and SBRT. The chapter also provides treatment planning volumes for beam energy. Finally it describes treatment planning for 3D, IMRT and VMAT, and SBRT.

Intracranial imaging is vital to the initial evaluation, staging and treatment planning, and posttreatment follow-up of brain tumor patients. The modalities used to evaluate the brain are CT and MRI. A familiarity with basic radiologic concepts can enable a provider to better translate the intracranial process to clinical care. This chapter is intended to give the clinician a baseline for interpreting images independently in either the acute or chronic setting. Imaging of the brain using CT and MRI techniques is essential to the evaluation of patients with intracranial malignancy, both in the acute and chronic setting. Knowledge of basic imaging principles related to the presence of an intracranial mass and familiarity with findings unique to certain malignancies are useful tools for the clinician. These skills can be built over time by reviewing patient images independently, utilizing the kinds of fundamentals discussed in this chapter.