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Dr.

Suha Saleh, HSC 4555



Copyright 2010, 2005 by Saunders, an imprint of Elsevier Inc.
Copstead-Kirkhorn: Pathophysiology, 4
th
Edition

Chapter 7: Neoplasia

KEY POINTS

BENIGN VERSUS MALIGNANT GROWTH
Malignant tumors have the potential to kill the host, whereas benign tumors generally do not.
The primary difference between malignant and benign tumors is the propensity of malignant
tumors to invade adjacent tissue and spread to distant sites (metastasize).
The suffix -oma is used to indicate a benign tumor (e.g., fibroma). Carcinoma and sarcoma
are used to indicate malignancy (e.g., fibrosarcoma). Exceptions include melanomas,
lymphomas, hepatomas, and leukemia, all of which are malignant.
Malignant cells exhibit antisocial properties that allow them to ignore growth-controlling
signals from the environment. Cancer cells proliferate excessively, become immortal, invade
locally, and may travel to distant sites where they establish new colonies.

EPIDEMIOLOGY AND CANCER RISK FACTORS
The risk of developing cancer increases with age. It is estimated that men have almost a 1 in
2 lifetime chance of developing cancer, whereas women have a little more than a 1 in 3
chance.
The development of many cancers is related to lifestyle, particularly tobacco use and
nutrition. Smoking cessation is considered important in reducing cancer risk. Guidelines
regarding nutrition are less clear. Limiting excessive fat, carbohydrate, and alcohol intake
while increasing dietary fiber, fruit, and vegetables may be of benefit.

GENETIC MECHANISMS OF CANCER
Cancer is thought to develop when proto-oncogenes become inappropriately activated in a
cell or when tumor suppressor genes become inactivated. This change in gene function is
usually due to mutations in the cells DNA.
Mutant proto-oncogenes disrupt the intercellular communication pathway that normally
regulates cell proliferation. This disruption may occur through abnormal production of
growth factors, receptors, cytoplasmic signaling molecules, or nuclear transcription factors.
Both copies of a tumor suppressor gene usually must be inactivated to eliminate its function.
Tumor suppressor genes inhibit cellular proliferation in various ways. The Rb protein serves
as a master brake on cell proliferation by inhibiting transcription factors. P53 inhibits cell
cycling when the cell is damaged to allow time for DNA repair. P53 is also important in
initiating apoptosis of damaged or unwanted cells.

MULTISTEP NATURE OF CARCINOGENESIS
Full expression of cancer in a host is a multistep process. These steps have been described as
initiation, promotion, and progression. The initiating event is usually from genetic mutations.
Promotion refers to the stage in which the mutant cell is induced to proliferate. Progression is
the stage during which the mutant, proliferating cells acquire properties that allow malignant
behavior.
Dr. Suha Saleh, HSC 4555
Copyright 2010, 2005 by Saunders, an imprint of Elsevier Inc.
Malignant cells commonly produce telomerase, an enzyme that repairs the telomeres and
may be a key for attaining immortality. The majority also have insufficient p53, which allows
the tumor cells to escape apoptosis despite DNA damage.

METASTASIS
Malignant cells produce specialized enzymes and receptors to enable them to escape their
tissue of origin and metastasize.
The spread of tumors generally occurs by way of the bloodstream or lymphatics. Tumor cells
often lodge in the capillary beds of the organs that drain them, such as liver and lung. Some
tumors appear to home to certain tissues.
Grading and staging are done to predict tumor behavior and guide therapy. Grading is the
histologic characterization of tumor cells, whereas staging describes the location and pattern
of tumor spread within the host.
The TNM staging system is used to describe the tumor size, lymph nodes affected, and
degree of metastasis.

EFFECTS OF CANCER ON THE BODY
Regardless of the type of malignancy, affected individuals exhibit characteristic signs and
symptoms, including pain, cachexia, bone marrow suppression, and infection.
Bone marrow suppression is manifested as anemia, leukopenia, and thrombocytopenia.
Immunosuppression with consequent infection is a primary cause of cancer-associated death.

CANCER THERAPY
Early detection of cancer while it remains localized is associated with the best prognosis for
cure. The overall 5-year survival rate for patients with cancer is about 66%.
The mainstays of cancer therapy are surgery, radiation therapy, and chemotherapy. Surgery
and radiation therapy are effective for cancers that are localized. Chemotherapy is usually the
treatment of choice for cancers known or suspected to be disseminated in the body.
Cells that divide rapidly are the most susceptible to damage from radiation therapy or
chemotherapy. However, in addition to cancer cells, rapidly dividing normal cells may be
killed. Cells of the bone marrow, hair follicles, and gastrointestinal mucosa are particularly
susceptible.
Immunotherapy has the potential to specifically target cancer cells. At present, interferon, IL-
2, and monoclonal antibodies are being used to boost the immune systems ability to locate
and destroy cancer cells.
Gene and molecular therapy may be used to alter cancer cells to suppress oncogenes,
enhance tumor suppressor genes, make tumor cells more susceptible to cytotoxic agents, or
interfere with the function of cancer gene products.
Transplantation of hematopoietic stem cells is an important adjunct to cancer therapy that
provides a method to restore bone marrow function after high-dose irradiation or
chemotherapy.

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