Precancers are lesions that precede the appearance of invasive cancers. The successful prevention or treatment of precancers has the potential to eliminate deaths due to cancer.
A National Cancer Institute-sponsored Conference on Precancer was convened on November 8-9, 2004, at The George Washington University Medical Center, Washington, DC. A definition of precancers was developed over 2 days of Conference discussions.
The following five criteria define a precancer: (1) evidence must exist that the precancer is associated with an increased risk of cancer; (2) when a precancer progresses to cancer, the resulting cancer arises from cells within the precancer; (3) a precancer differs from the normal tissue from which it arises; (4) a precancer differs from the cancer into which it develops, although it has some, but not all, of the molecular and phenotypic properties that characterize the cancer; (5) there is a method by which the precancer can be diagnosed.
The Conference participants developed a general definition for precancers that would provide a consistent and clinically useful way of distinguishing precancers from all other types of lesions. It was recognized that many precancerous lesions may not meet this strict definition, but the group felt it was necessary to define criteria that will help standardize clinical and biological studies. Furthermore, a set of defining criteria for putative precancer lesions will permit pathologists to build a diagnostically useful taxonomy of precancers based on specified clinical and biological properties. Precancers thus characterized can be classified into clinically relevant sub-groups based on shared properties (i.e. biomarkers, oncogenes, common metabolic pathways, responses to therapy, etc.). Publications that introduce newly described precancer entities should describe how each of the five defining criteria apply. This manuscript reviews the proposed definition of precancers and suggests how pathologists, oncologists and cancer researchers may determine when these criteria are satisfied.
"We have recently outlined the evidentiary basis for the consideration of EmGD as the precancerous lesion for ESC in a recent authoritative review article . EmGD fulfils the National Cancer Institute criteria for a precancerous lesion , as briefly summarized below. The first criterion calls for the putative precancerous lesion to be distinct from the normal tissue from which it arose. "
[Show abstract][Hide abstract] ABSTRACT: Die exakte Kenntnis der Inzidenz und Prävalenz von Vorläuferläsionen maligner Erkrankungen wäre von entscheidender Bedeutung für die präzise Bewertung des klinisch-pathologischen Progressionspotenzials und damit für die individuelle Beratung und Intervention, aber auch für die Planung und Bewertung von Präventions- und Früherkennungsstrategien. Angesichts dieser hohen Erwartung ist es erstaunlich, dass präzise Daten über Inzidenz, Prävalenz und das exakte Progressionsrisiko für viele Tumorvorstufen fehlen. Die Datenquellen (Krebsregister, spezifische Vorstufenregister, Früherkennungsprogramme und spezifische Studien) werden auf ihre Aussagekraft und Verlässlichkeit hin geprüft. Ein wesentlicher Grund für die mangelhafte Datenlage ist die unpräzise und redundante Terminologie.
Der Pathologe 11/2011; 32(2). DOI:10.1007/s00292-011-1510-7 · 0.39 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The identification as well as the molecular characterization of breast precancerous lesions in terms of increased risk of progression and/or recurrence is becoming a critical issue today as improved non-surgical procedures are detecting cancer at an earlier stage. The strategy we have been pursuing to identify early apocrine breast lesions is based on the postulate that invasive apocrine carcinomas evolve from epithelial cells in terminal duct lobular units (TDLUs) in a stepwise manner that involves apocrine metaplasia of normal breast epithelia, hyperplasia, atypia, and apocrine carcinoma in situ. First, we identify specific protein biomarkers for benign apocrine metaplasia and thereafter we search for biomarkers that are highly overexpressed by pure invasive apocrine carcinomas. Here we present studies in which we have used antibodies against components of a benign apocrine signature that includes 15-prostaglandin dehydrogenase (15-PGDH), a protein that is expressed by all benign apocrine lesions, and markers that are highly overexpressed by pure invasive apocrine carcinomas such as MRP14 (S100A9), psoriasin (S100A7), and p53 to identify precancerous lesions in sclerosing adenosis (SA) with apocrine metaplasia. The latter is a benign proliferative lesion of the breast that exhibits an increase in the size of the TDLUs and characterized by retained two-cell lining, and myoepithelial (ME) and stromal hyperplasia. SA with apocrine metaplasia, i.e. apocrine adenosis (AA), presents with a higher degree of atypical apocrine hyperplasia, and these lesions are believed to be precursors of apocrine carcinoma, in situ and invasive. Analysis of 24 selected SA samples with apocrine metaplasia revealed non-obligate putative apocrine precancerous lesions that displayed some, or in same cases all the three markers associated with pure invasive apocrine carcinomas. These studies also revealed p53 positive, non-apocrine putative precancerous lesions as well as novel phenotypes for ME and some luminal cells characterized by the expression of cytokeratin 15.
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