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NCI CANCERLIT® Search: Basal Cell Nevus Syndrome - July 2002
National Cancer Institute®
Ultima Vez Modificado: 1 de julio del 2002
- The aggressive nature of the odontogenic keratocyst: is it a benign cystic neoplasm? Part 2. Proliferation and genetic studies.
- Basal cell nevus syndrome: guidelines for early detection.
Table of Contents
1
UI - 12076694
AU - Shear M
TI -
The aggressive nature of the odontogenic keratocyst: is it a benign
cystic neoplasm? Part 2. Proliferation and genetic studies.
SO - Oral Oncol 2002 Jun;38(4):323-31
AD - Department of Oral Pathology, University of the Western Cape, South
Africa. shear@iafrica.com
Immunocytochemical studies of the expression of PCNA, Ki67 and p53
protein have been done by different groups on sporadic keratocysts
(OKCs) and OKCs associated with the naevoid basal cell carcinoma
syndrome (NBCCS). These 'markers' have in common that they are all
expressed in actively proliferating cells, particularly in neoplasms.
The findings were compared with their expression in dentigerous and
radicular cysts. While there was some variability in the reported
results, probably because of technical inconsistencies and the use of
different antibodies, a definite trend emerged. In general PCNA, Ki67
and p53 positivity occurred more frequently and more intensely in the
OKCs, and in the syndrome-related more than the solitary, compared with
the other cyst types. In the OKCs the positivity was expressed mostly in
the suprabasal layers of epithelium whereas in the other cysts types it
was mainly in the basal layer that positivity was observed. Other
studies showed that the gene for the NBCCS (PTCH), a tumour suppressor
gene, mapped to chromosome 9q22.3. PTCH gene mutation has been shown to
be an important step in the pathogenesis of the OKC and was thought to
have a role in the development of the sporadic as well as the
syndrome-related OKCs. The 'two-hits' hypothesis was invoked in support
of the view that syndrome-related basal cell carcinomas (BCCs) and OKCs
probably arise from precursor cells that contain an inherited 'first
hit'. Only a single mutation was then required in the somatic cell to
cause homozygous inactivation and neoplastic progression. Sporadic OKCs
might arise from susceptible cells in which two somatic mutations or
'hits' have occurred, one of which manifests as allelic loss. The loss
of tumour suppressor genes supports the view that the OKC is a benign
neoplasm.
2
UI - 12086239
AU - Bitar GJ; Herman CK; Dahman MI; Hoard MA
TI -
Basal cell nevus syndrome: guidelines for early detection.
SO - Am Fam Physician 2002 Jun 15;65(12):2501-4
AD - Department of Plastic Surgery, Albert Einstein College of Medicine,
Bronx, New York, USA. GBITAR007@aol.com
Basal cell nevus syndrome is an autosomal dominant condition with
complete penetrance and variable expressivity. It is characterized by
five major components, including multiple nevoid basal cell carcinomas,
jaw cysts, congenital skeletal abnormalities, ectopic calcifications,
and plantar or palmar pits. Other features include a host of benign
tumors, ocular defects, and cleft lip and palate. Guidelines for
diagnosis include a family history, careful oral and skin examinations,
chest and skull radiographs, panoramic radiographs of the jaw, magnetic
resonance imaging of the brain, and pelvic ultrasonography in women.
The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.
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