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INTRODUCTION

Cell growth and maturation are normal events in organ development during embryogenesis, growth, and tissue repair, and in remodeling after injury. Disordered regulation of these processes can result in loss of control over cell growth, differentiation, and spatial confinement. Human neoplasia collectively represents a spectrum of diseases characterized by abnormal cell growth, loss of tissue homeostasis, and distorted architecture. Such new growth is called a neoplasm or tumor and can sometimes be a proliferative process confined to one specific tissue site with little systemic manifestations and no threat to the overall state of health. The term “benign” is often used to describe such low-impact tumors, which include many common growths such as dermal nevi, warts, and uterine fibroids. The term “cancer” or “malignant tumor” is used to describe a more advanced form of neoplasia that involves tissue invasion and destruction and defines an inherently progressive biologic process that can culminate in systemic disease and host death. The process of tumorigenesis involves a series of stochastic events in a proliferative context that can generate unlimited diversity in the molecular and phenotypic attributes of tumor cells, both among affected individuals and within a single affected individual. Classification schemes have been devised to provide a framework to reduce this complexity and capture many of the shared attributes of cancers, which are largely based on tissue type and organ of origin. Each type of cancer can exhibit a diversity of biologic behaviors among different patients, and molecular or histologic attributes are used to further sub-classify cancers and identify patterns of behavior.

The recognition of overt malignancy by symptoms or physical examination findings defines the clinical phase of disease. The clinical phase is preceded by a preclinical phase, which is usually unknown to the patient but may sometimes be identified by screening interventions. Preclinical signs and potential precursors of colon cancer and breast cancer may consist of polyps in the colon and proliferative abnormalities of the breast, respectively. Such precursor lesions usually harbor molecular genetic abnormalities and exhibit features of abnormal cell proliferation without demonstrating invasiveness and may precede the development of an invasive cancer by months to years; or they may not progress to an invasive cancer within the individual’s lifetime. More commonly, the preclinical phase goes undetected until an invasive cancer is present, occasionally with regional or distant metastases. Our understanding of the pathophysiology of various neoplasma is based on clinical and pathologic observations of large series of patients, along with a more recently gained understanding of the cellular and molecular underpinnings of these disorders.

THE CELLULAR & MOLECULAR BASIS OF NEOPLASIA

Neoplasia is a result of stepwise alterations in cellular function. These phenotypic alterations produce morphologic changes that are readily evident by microscopy and may predate tumor development by many years. Morphologic abnormalities may include enlargement of the cell, called cell hypertrophy, reflecting too much protein and ...

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