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(Ana)plasia - dedifferentiation
(Hyper)plasia - physiological proliferation
(Neo)plasia - abnormal proliferation
(Dys)plasia - maturation abnormality
(Meta)plasia - cell type conversion
(Desmo)plasia - connective tissue growth

Anaplasia refers to a reversion of differentiation in cells and is characteristic of malignant neoplasms (tumors). Sometimes, the term also includes an increased capacity for multiplication.[1] Lack of differentiation is considered a hallmark of malignancy. The term anaplasia literally means "to form backward". It implies dedifferentiation, or loss of structural and functional differentiation of normal cells. It is now known, however, that at least some cancers arise from stem cells in tissues; in these tumors failure of differentiation, rather than dedifferentiation of specialized cells, account for undifferentiated tumors.

Anaplastic cells display marked pleomorphism. The nuclei are characteristically extremely hyperchromatic (darkly stained) and large. The nuclear-cytoplasmic ratio may approach 1:1 instead of the normal 1:4 or 1:6. Giant cells that are considerably larger than their neighbors may be formed and possess either one enormous nucleus or several nuclei (syncytia). Anaplastic nuclei are variable and bizarre in size and shape. The chromatin is coarse and clumped, and nucleoli may be of astounding size. More important, mitoses are often numerous and distinctly atypical; anarchic multiple spindles may be seen and sometimes appear as tripolar or quadripolar forms. Also, anaplastic cells usually fail to develop recognizable patterns of orientation to one another (i.e. they lose normal polarity). They may grow in sheets, with total loss of communal structures, such as gland formation or stratified squamous architecture. Anaplasia is the most extreme disturbance in cell growth encountered in the spectrum of cellular proliferations. [2]


  1. ^ biology-online dictionary
  2. ^ Kumar, Vinay, Abul Abbas, Nelson Fausto, and Richard Mitchell. Robbins Basic Pathology. 8th ed. Philadelphia: Saunders Elsevier, 2007. 176-177.

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