Guided Lecture Notes
Chapter 5: Neoplasia: A Disorder of Cell Proliferation and Differentiation
Learning Objective 1. Define neoplasm and explain how neoplastic growth differs from
the normal adaptive changes seen in atrophy, hypertrophy, and hyperplasia.

Define neoplasm (refer to PowerPoint Slide 2).

Discuss the characteristics of a neoplasm that make it different from other types
of cell growth, such as atrophy, hypertrophy, and hyperplasia.
Learning Objective 2. Distinguish between cell proliferation and differentiation.

Explain the differences between the proliferation and differentiation of cells.

List the factors that determine the size of a population of cells.
Learning Objective 3. Define and give examples of permanent cells, labile cells, and
stable cells in regard to their ability to divide and reproduce.

Using examples, describe the ability of permanent cells to proliferate (refer to
PowerPoint Slide 4).

Using examples, describe the ability of labile cells to proliferate (refer to
PowerPoint Slide 4)

Using examples, describe the ability of stable cells to proliferate (refer to
PowerPoint Slide 4).

Identify factors that increase cell proliferation.
Learning Objective 4. Describe the five phases of the cell cycle.

Explain what occurs during the synthesis phase, and explain its duration (refer to
PowerPoint Slide 3).

Explain what occurs during the mitosis phase, and explain its duration (refer to
PowerPoint Slide 3).

Discuss the purposes of gap phases in the cell cycle, and explain the difference
between gaps 1 and 2 (refer to PowerPoint Slide 3).

Describe what makes gap 0 unique, and discuss cell types and instances when
cells can or cannot enter this phase (refer to PowerPoint Slide 3).
Learning Objective 5. Explain the functions of cyclins, cyclin-dependent kinases, and
cyclin-dependent kinase inhibitors in terms of regulating the cell cycle.

Explain the purpose of cell checkpoints.

Describe the actions of the proteins that control the entry and progression of cells
through the cell cycle (cyclins, cyclin-dependent kinases, and cyclin-dependent
kinase inhibitors) (refer to PowerPoint Slide 15).
Learning Objective 6. Cite the method used for naming benign and malignant
neoplasms (refer to Table 5-1).

Identify the suffix that is added to the affected parenchymal tissue in order to
name a benign tumor (refer to PowerPoint Slide 24).

Describe the way in which malignant tumors are named (refer to PowerPoint
Slide 24).
Learning Objective 7. State at least four ways that benign and malignant neoplasms
differ in regard to their characteristics (refer to PowerPoint Slides 25–28 and Table 5-2).

Describe how the cells of benign and malignant neoplasms differ.

Discuss the difference in growth rates between benign and malignant neoplasms.

Compare growth methods between benign and malignant neoplasms.

Describe the typical rates of metastasis associated with benign and malignant
neoplasms.
Learning Objective 8. Relate the process of cell differentiation to the development of a
cancer cell line and the behavior of the tumor.

Define anaplasia.

Explain why mutations that occur in well-differentiated cells are more likely to
result in benign neoplasms (refer to Fig. 5-2).

Explain how tumor grade relates to cell differentiation and malignancy (refer to
PowerPoint Slide 21).
Learning Objective 9. Trace the pathway for hematologic spread of a metastatic cancer
cell.

Define metastasis (refer to PowerPoint Slide 31).

Identify neoplasms that are most likely to spread via the bloodstream (refer to Fig.
5-3).

Explain why cells of certain types of tumors metastasize to specific organs.

Describe the venous hematogenous movement of cancer cells.

Identify factors that affect metastasis once cells have reached target tissue.
Learning Objective 10. Use the concept of growth fraction and doubling time to explain
the growth of cancerous tissue.

List the three factors that determine the rate of tissue growth.

Identify which of those factors makes it appear that cancer cells grow rapidly.

Define growth fraction and doubling time, and explain the relationship between
them (refer to Fig. 5-4).

Using the terms above, explain when a tumor becomes detectable, and when it is
large enough to kill the host.
Learning Objective 11. Describe the role of proto-oncogenes, tumor suppressor genes,
apoptosis genes, and genes that control signal pathways in the development of a cancer
cell line.

Define proto-oncogene, oncogene, tumor suppressor gene, apoptosis gene, and
DNA repair gene.

Explain why proto-oncogenes, tumor suppressor genes, apoptosis genes, and
DNA repair genes are the principal targets of developing cancer cells (refer to
PowerPoint Slides 16 and 17).

Explain the role of oncogenes in cancer cell proliferation (refer to PowerPoint
Slide 18).
Learning Objective 12. State the importance of angiogenesis in cancer growth and
metastasis.

Define angiogenesis, and explain why tumors cannot survive without it.
Learning Objective 13. Explain how host factors such as heredity, levels of endogenous
hormones, and immune system function increase the risk for development of selected
cancers.

Using examples, discuss the incidence of inherited predispositions to cancer.

Explain the autosomal dominant inheritance pattern of certain types of cancer
(refer to Fig. 5-7).

Discuss the possibility of hormonal influence on cancers of the reproductive
system.

Explain the concept of the immune surveillance hypothesis, and describe how it
may be disrupted in certain types of cancer.

Describe the function of tumor antigens.
Learning Objective 14. Relate the effects of environmental factors such as chemical
carcinogens, radiation, and oncogenic viruses to the risk for cancer development.

Identify common chemical and environmental agents that are known carcinogens
(refer to Chart 5-1).

Identify common chemical carcinogens that are associated with behavior or are
present in the diet.

Describe the role of alcohol consumption in the incidence of certain types of
cancer.

Describe the dose-dependent effects of carcinogens.

Explain the effects of ionizing radiation in carcinogenesis.

List and describe the oncogenic viruses that have been linked to cancer.
Learning Objective 15. Define and describe cancer cachexia as a clinical manifestation
of cancer.

Describe the clinical manifestations that characterize cancer cachexia/wasting
syndrome (refer to PowerPoint Slide 39).

Identify possible causes of cancer cachexia.
Learning Objective 16. Define the term paraneoplastic syndrome and explain its
pathogenesis and manifestations.

Describe paraneoplastic syndrome, and identify with which types of cancer it is
most often associated (refer to Table 5-3).

List the most common paraneoplastic syndromes, and identify the associated
tumors and hormones that are produced (refer to PowerPoint Slide 38).
Learning Objective 17. Describe methods used in detection and diagnosis of cancer,
including the Papanicolaou test, tissue biopsy, and tumor markers.

List common diagnostic tests for cancer, including x-rays, endoscopies, urine and
stool tests, bone marrow aspirations, MRI, CAT, and PET scans.

Discuss the importance of the Pap test as a screening tool for cervical cancer.

Define biopsy, and describe how tissue biopsies are obtained.

Explain how tumor markers can serve as diagnostic tools, and discuss their
limitations.
Learning Objective 18. Compare methods used in grading and staging cancers.

Define the terms grading and staging, and explain how they are different.

Discuss the TNM system of staging tumors, explaining what each letter of the
acronym represents (refer to Chart 5-2).
Learning Objective 19. Explain the mechanism by which radiation exerts its beneficial
effects in the treatment of cancer.

Identify the instances in which radiation therapy for cancer is used.

Explain how ionizing radiation exerts its effects.

Discuss why cancer cells are more responsive to radiation than are normal cells.
Learning Objective 20. Describe the adverse effects of radiation therapy.

List the adverse effects of radiation therapy, and discuss ways to minimize them.
Learning Objective 21. Compare the action of cell cycle–specific and cell cycle–
nonspecific chemotherapeutic drugs.

Describe on which phases of the cell cycle cycle–specific and cycle–nonspecific
drugs work.

Explain why these two types of cancer drugs are often combined.

Discuss the relationship between chemotherapy and tumor cell survival (refer to
Fig. 5-8).
Learning Objective 22. Define biotherapy, and list the three mechanisms whereby
biotherapy exerts its effects.

Define biotherapy, immunotherapy, and biologic response modifiers, and explain
how they work to change the immune response of the cancer patient.

Explain immunotherapy techniques in the treatment of cancer.

List examples of biologic response modifiers, including cytokines, interferons,
and interleukins.
Learning Objective 23. Cite the early warning signs of cancer in children.

Rank childhood cancer as a cause of death in the U.S., and describe mortality
rates.

Identify the most common types of childhood cancer (refer to Chart 5-3).

List the most common signs and symptoms of childhood cancers.
Learning Objective 24. Discuss possible concerns of adult survivors of childhood
cancer.

List common sequelae that occur in adult survivors of childhood cancer.

Discuss the risk of developing the above sequelae.