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Dysplasia and carcinoma in situ !

  • Lesion

Dysplasia is disordered growth in a lining; when it fills the whole thickness without crossing the basement membrane, it is carcinoma in situ.

Updated 2026-11-01

What it is

Dysplasia is disordered growth of an epithelium: cells lose uniformity and orientation and show atypia, usually beginning in the basal layers. It is graded as low or high grade (mild, moderate, severe) and may regress, persist or progress. When the atypia involves the full thickness but the basement membrane is intact, the lesion is carcinoma in situ, a preinvasive neoplasm that cannot metastasise; once it breaks through, it is invasive carcinoma.

Structure

  • Loss of the normal maturation from basal cells to flat surface cells.
  • Pleomorphic, hyperchromatic nuclei with a high nuclear-to-cytoplasmic ratio.
  • Mitoses above the basal layer, sometimes up to the surface.
  • Architectural disarray: cells crowd and lose their orientation.
  • In carcinoma in situ, these changes span the full thickness, but the basement membrane under the epithelium remains continuous.

Step by step

  1. A carcinogen or persistent infection (for example high-risk HPV) damages the DNA of basal epithelial cells.
  2. Mutated cells proliferate and fail to mature: low-grade dysplasia in the lower third of the epithelium.
  3. More mutations accumulate and atypia climbs toward the surface: high-grade dysplasia.
  4. Atypia spans the whole thickness with an intact basement membrane: carcinoma in situ.
  5. Tumour cells degrade the basement membrane and enter the stroma: invasive carcinoma, now able to metastasise.

Classic precursor lesions and the cancer they lead to

PrecursorTypical causeResulting cancer
Cervical intraepithelial neoplasiaPersistent high-risk HPVSquamous cell carcinoma of the cervix
Barrett oesophagus with dysplasiaChronic gastro-oesophageal refluxOesophageal adenocarcinoma
Colorectal adenomaAPC pathway, age, dietColorectal adenocarcinoma
Actinic keratosisChronic ultraviolet exposureCutaneous squamous cell carcinoma
Ductal carcinoma in situHormonal and genetic factorsInvasive ductal carcinoma of the breast

Clinical notes

  • Cervical screening (HPV testing and cytology) exists to find and treat high-grade lesions before they invade; in Colombia and Latin America cervical cancer is still a leading cancer in women.
  • HPV vaccination in childhood prevents most of the precursor lesions.
  • In Barrett oesophagus, the grade of dysplasia guides surveillance and endoscopic treatment.

Test yourself

Think of the answer, then tap the question to see it.

What distinguishes carcinoma in situ from invasive carcinoma?

In carcinoma in situ the basement membrane is intact, so the lesion cannot metastasise; invasive carcinoma has crossed it into the stroma.

How does dysplasia differ from metaplasia?

Metaplasia replaces one mature cell type with another normal-looking type; dysplasia is disordered growth with cellular atypia and loss of maturation.

Which agent causes most cervical intraepithelial neoplasia?

Persistent infection with high-risk human papillomavirus (especially types 16 and 18).

Can low-grade dysplasia regress?

Yes. Low-grade lesions, such as many CIN 1 lesions, often regress when the cause is removed or the infection clears.

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Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Sources: HPV and Cancer (National Cancer Institute (NCI), 2026); Cervical cancer (World Health Organization, 2026); Cervical Cancer (StatPearls (NCBI Bookshelf), 2026).

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