Majority Of Basal Cell Carcinomas Research Articles

Immunolocalization of PTCH protein in odontogenic cysts and tumors.

The human patched gene (PTCH) functions in both embryologic development and tumor suppression. PTCH mutations have been found in odontogenic keratocysts. However, the expression and localization of the protein product of the gene have not been determined in odontogenic tumors and cysts. We investigated 68 odontogenic lesions by immunohistochemistry, and compared their PTCH expression with that in basal cell carcinomas. All odontogenic lesions, including two keratocysts with truncating mutations, were positive for PTCH. Different types of lesions had different amounts of staining. Lack of staining was noted in the majority of basal cell carcinomas. Taken together, these data suggest that odontogenic keratocysts arise with heterozygous mutations of the PTCH gene.

A study of secondary cutaneous amyloidosis in basal cell carcinoma in Chinese patients: lack of correlation with bcl-2 or p53 protein expression.

Pigmented basal cell carcinoma (BCC) is an uncommon form of BCC among Caucasians. In contrast, the majority of BCC in Orientals are pigmented BCC. To assess the occurrence of secondary amyloid deposits in BCC among Chinese patients, a retrospective study was conducted on 53 BCC specimens. We used a terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling method for detecting the apoptotic cells. In addition, immunohistochemical staining was performed to examine the expression of the B-cell leukemia/lymphoma-2 gene (bcl-2) and p53 protein. Of the 53 BCC specimens, 37 (69.8%) were pigmented BCC and 31 (58.5%) showed amyloid deposits in the stroma of the tumor cells. The mean percentage of apoptotic tumor cells was 0.29%. Immunostaining of bcl-2 and p53 was detected in 33 BCCs (62.3%) and 19 BCCs (35.8%), respectively. No relationship between amyloid deposition and the number of apoptotic cells was found. In addition, there was no correlation between amyloid deposition and bcl-2 protein expression or between amyloid deposition and p53 protein expression. Our results indicate that the frequency of secondary amyloidosis in BCC among Chinese patients is not higher than that reported in the West. Although no correlation could be detected between amyloid deposition and bcl-2/p53 protein expression, the possible role of apoptosis in the pathogenesis of amyloid deposition in BCC still needs further investigation.

Immunohistochemical nuclear staining for p53, PCNA, and Ki-67 in different histologic variants of basal cell carcinoma

Background: Increased expression of p53 has been found in the majority of basal cell carcinomas (BCCs); however, UV-light–induced signature mutations are present in only about 50% of cases. Increased nuclear staining with an immunohistochemical marker of proliferation, proliferating cell nuclear antigen (PCNA), has been correlated with aggressive behavior in BCC. Objective: Our purpose was to determine whether there is any relationship between different histologic variants of BCC and their expression of p53, PCNA, and Ki-67. Methods: We used immunohistochemical stains for p53, PCNA, and Ki-67, in superficial-multicentric, nodular-noduloulcerative, sclerosing, infiltrative, and metatypical BCC, to determine whether the staining patterns differ in these different histologic variants of BCC. Results: Superficial-multicentric BCCs were negative for p53 in four of eight tumors. Nodular BCC showed moderately intense p53 nuclear staining with some peripheral accentuation. PCNA nuclear staining was greater than Ki-67, and PCNA-positive cells were fewer than 10% in nodular BCC. Sclerosing and infiltrative BCC showed intense p53 nuclear staining with peripheral accentuation. PCNA nuclear staining was greater than Ki-67, and PCNA-positive cells were greater than 30% in the majority of these tumors. Metatypical BCCs showed diffuse intense p53 staining. PCNA nuclear staining was greater than Ki-67, and PCNA-positive cells were greater than 30% in all tumors studied. When overlying actinic keratoses showed p53 staining, the staining did not necessarily correlate with the intensity or even the presence of positive staining in the subjacent BCC. Conclusion: There are at least four distinctive patterns for staining of p53, PCNA, and Ki-67 that correlate with different histologic variants of BCC. (J Am Acad Dermatol 1997;37:430-7.)

Immunohistochemical nuclear staining for p53, PCNA, and Ki-67 in different histologic variants of basal cell carcinoma

<h2>Background</h2> Increased expression of p53 has been found in the majority of basal cell carcinomas (BCCs); however, UV-light–induced signature mutations are present in only about 50% of cases. Increased nuclear staining with an immunohistochemical marker of proliferation, proliferating cell nuclear antigen (PCNA), has been correlated with aggressive behavior in BCC. <h3>Objective</h3> Our purpose was to determine whether there is any relationship between different histologic variants of BCC and their expression of p53, PCNA, and Ki-67. <h3>Methods</h3> We used immunohistochemical stains for p53, PCNA, and Ki-67, in superficial-multicentric, nodular-noduloulcerative, sclerosing, infiltrative, and metatypical BCC, to determine whether the staining patterns differ in these different histologic variants of BCC. <h3>Results</h3> Superficial-multicentric BCCs were negative for p53 in four of eight tumors. Nodular BCC showed moderately intense p53 nuclear staining with some peripheral accentuation. PCNA nuclear staining was greater than Ki-67, and PCNA-positive cells were fewer than 10% in nodular BCC. Sclerosing and infiltrative BCC showed intense p53 nuclear staining with peripheral accentuation. PCNA nuclear staining was greater than Ki-67, and PCNA-positive cells were greater than 30% in the majority of these tumors. Metatypical BCCs showed diffuse intense p53 staining. PCNA nuclear staining was greater than Ki-67, and PCNA-positive cells were greater than 30% in all tumors studied. When overlying actinic keratoses showed p53 staining, the staining did not necessarily correlate with the intensity or even the presence of positive staining in the subjacent BCC. <h3>Conclusion</h3> There are at least four distinctive patterns for staining of p53, PCNA, and Ki-67 that correlate with different histologic variants of BCC.

Micronodular basal cell carcinoma. A deceptive histologic subtype with frequent clinically undetected tumor extension.

Micronodular basal cell carcinoma (BCC) is thought to have a greater potential for clinically surreptitious tumor spread compared with the majority of BCCs that are nodular. However, most supporting data are anecdotal. This study gives objective evidence that micronodular BCCs have wider and deeper tumor extensions than nodular BCCs of similar clinical size. In this retrospective study, 69 cases of micronodular BCC excised by Mohs' micrographic surgery (MMS) were matched to a control group of 69 cases of nodular BCC that were similarly excised. They were paired by site, size, number of recurrences, age, gender, and previous treatment type. The cases were selected and paired by computer from 1070 consecutive BCCs (primary and recurrent) referred for MMS over a 4-year period. The MMS technique allowed us to quantitate and compare the extent of tumor spread using three measurements: the number of surgical stages required for complete removal of the tumor, the width of tissue required to remove subclinical extension of tumor, and the depth of defect at completion of MMS. Analysis showed the micronodular BCC to have significantly more covert tumor extension, making it more difficult to detect and to eradicate than the nodular BCC. The number of surgical stages required for complete removal of tumor, the width of tissue required to remove subclinical extension of tumor, and the depth of defect at completion of MMS were all greater with micronodular BCCs when compared with nodular BCCs regardless of whether cases were primary or recurrent. These differences were all statistically significant. Micronodular BCCs can be significantly more destructive than nodular BCCs because tumor extension is difficult to detect clinically. When treating micronodular BCC, clinicians should keep in mind its potential for clandestine invasion.

Recalling basal cell carcinoma patients. A regional survey.

Patients with a basal cell carcinoma (BCC) are at increased risk for developing further BCCs, and long-term follow-up has been recommended to detect new cancers at an earlier, more easily treatable stage. The majority of BCCs are treated by dermatologists in their offices; we do not know to what extent they perform long-term follow up on their patients. To determine how practicing dermatologists follow up their BCC patients. A mailed questionnaire survey of 166 practicing members of a regional dermatologic society (the San Francisco Dermatological Society), to which 142 (85%) replied. Two thirds of the respondents recalled BCC patients for screening examinations; of these, 58% followed up non-responders. Recall efforts were hampered by inefficient, unwieldy, and time-consuming techniques. Practicing dermatologists are motivated to recall BCC patients for examination, but guidelines and techniques for effective and efficient computerized recalling of skin cancer patients are needed. It is suggested that the American Academy of Dermatology set up a task force to develop guidelines and criteria for effective recall software.

Trends in the presentation and treatment of basal cell carcinomas.

Analysis of 1,620 basal cell carcinomas treated at the Cleveland Clinic Foundation from 1981 to 1983 confirms that the majority of basal cell carcinomas occur on the face and that the relative risk for recurrent tumor is high in certain locations, especially the nose. Alternately, tumors found on the neck/scalp, trunk, and arms have a low relative risk of recurrence when compared to all other anatomic locations. More primary and fewer recurrent tumors now presenting to our unit have been referred for Mohs surgery as primary therapy. This results in higher cure rates for treatment of all basal cell carcinoma.