This document provides a comprehensive summary of the Neoplasia chapter from Robbins Pathology. It covers the key concepts, definitions, and characteristics of neoplasia, including benign and malignant tumors, carcinogenesis, and tumor markers.
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Summary Robbins and Cotran Chapter7 Neoplasia
Arbeid, leefstijl en gezondheid (OUD) (Vrije Universiteit Amsterdam)
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Chapter 7: Neoplasia
Nomenclature
Neoplasm: abnormal mass or tissue, abnormal and uncoordinated growth, which
persist after cessation of the stimuli which evoked the change.
2 basic components: (1) proliferating neoplastic cells that constitute their
parenchyma; (2) supportive stroma made up of connective tissue and blood vessels.
Benign tumors. In general, benign tumors are designated by attaching the suffix –
oma to the cell of origin fibroma, chondroma, and osteoma
Adenoma: benign epithelial neoplasm that forms glandular patterns and tumors
derived from glands.
Papilloma: benign epithelial neoplasms producing microscopically or
macroscopically visible finer-like or warty projections from epithelial surfaces.
Cystadenoma: benign neoplasms that form large cystic masses.
Polyp: a, benign or malignant, neoplasm that produces a macroscopically visible
projection above a mucosal surface into a lumen.
Malignant tumors. Malignant tumors arising in mesenchymal tissue are usually
called sarcomas because they have little connective stroma and are so fleshy.
Malignant neoplasms of epithelial origin, derived from any of the 3 germ layers, are
called carcinomas.
In benign and in differentiated malignant neoplasms, the parenchymal cells bear a
close resemblance to each other. Infrequently, divergent differentiation of a single
line of parenchymal cells into another tissue creates mixed tumors. The great
majority of neoplasms, even mixed tumors, are composed of cells representative of
a single germ layer (the exception is a teratoma).
Hamartoma: a mass of disorganized but mature specialized cells or tissue
indigenous to the particular site, produced by aberrant differentiation.
Biology of tumor growth
Anaplasia: lack of differentiation.
In general, benign tumors are well differentiated. Malignant neoplasms range from
well differentiated to undifferentiated. Malignant neoplasms composed of
undifferentiated cells are said to be anaplastic. The well-differentiated cancer
evolves from maturation or specialization of undifferentiated cells as they
proliferate. The undifferentiated malignant tumor derives from proliferation
without complete maturation of the transformed cells.
Anaplasia is marked by:
- pleomorphism is both cells and nuclei (variation in size and shape)
- abundance of DNA and extremely dark staining (hyperchromatic) nuclei
- large number of mitoses
- loss of polarity anarchic, disorganized tissue
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- other changes: formation of tumor giant cells, vascular stroma is scant, large
central areas undergo ischemic necrosis.
Dysplasia is encountered principally in eptithelia, is characterized by loss in
uniformity of the individual cells as well as a loss in their architectural orientation.
Also pleomorphism, hyperchromatic nuclei, abnormally lagre cells and mora
abundant mitotic figures are present.
Preinvasive tumor: when dysplastic changes are marked and involve the entire
thickness of the epithelium, but the lesion remains confined to the normal tissue.
A tumor becomes invasive when the tumor cells move beyond the normal confines.
Dysplasia does not necessarily progress to cancer.
In general, the more rapidly growing and the more anaplastic a tumor, the less
likely it is that there will be specialized functional activity. The cells in benign
tumors are almost always well differentiated and resemble their normal cells of
origin; the cells in cancer are more or less differentiated, but some loss of
differentiation is always present.
By the time a solid tumor is clinically detected, it has already completed a major
portion of its life cycle. The rate of growth of a tumor is determined by 3 main
factors:
- the doubling time of tumor cells
- the fraction of tumors cells that are in the replicative pool
- the rate at which cells are shed and lost in the growing lesion
Growth of tumors is not commonly associated with a shortening of cell-cycle time.
During the early, submicroscopic phase of tumor growth, the vast majority of
transformed cells are in the proliferative pool. As tumors continue to grow, cells
leave the proliferative pool in ever-increasing numbers owing to shedding, lack of
nutrients, or apoptosis; by differentiating, and by reversion to G0.
Tumor cell kinetics:
- fast-growing tumors may have a high cell turnover, implying that rates of
both proliferation and apoptosis are high;
- the growth fraction of tumour cells has a profound effect on their
susceptibility to cancer therapy.
In general, the growth rate of tumors correlates with their level of differentiation,
an thus most malignant tumors grow more rapidly than benign lesions.
It has been difficult to identify cancer stem cells.
Apparently, cancer stem cells, similar to their normal counterparts, have a low
rate of replication. If this is the case, cancer therapies that may efficiently kill the
replicating progeny of cancer stem cells would leave in place the cells capable of
generating the tumor.
Nearly all benign tumors grow as cohesive expansile masses that remain localized
to their site of origin and do not have the capacity to infiltrate, invade or
metastasise to distant sites fibrous capsule.
The growth of cancers is accompanied by progressive infiltration, invasion, and
destruction of the surrounding tissue.
The invasiveness of cancers permits them to penetrate into blood vessels,
lymphatics and body cavities, to spread. With few exceptions(gliomas and basal
cell carcinomas of the skin), all cancers can metastasise.
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