P53 Expression In Squamous Cell Carcinoma Research Articles

Prognostic impact of p53, c-erbB-2 and epidermal growth factor receptor on head and neck carcinoma

p53, c-erbB-2 and epidermal growth factor receptor (EGFR) are cancer-related proteins that are usually expressed in head and neck squamous cell carcinoma (SCC). Their prognostic value remains controversial. To evaluate the prognostic impact of p53, c-erbB-2 and EGFR expression in head and neck SCC. Prospective. Head and Neck Surgery Department, Hospital AC Camargo, São Paulo. Fifty-four patients were studied for p53, c-erbB-2 and EGFR expression in head and neck SCC and adjacent mucosa, via immunohistochemistry. These data were correlated with histoclinical data and survival. There was a direct association of p53 expression in SCC and mucosa (p = 0.001); loss of c-erbB-2 expression (-) from normal mucosa to SCC (p = 0.04); lower frequency of association of c-erbB-2 (+) with EGFR (-) in SCC (p = 0.02); and a direct association of EGFR (+) expression in SCC and mitotic index (p = 0.03). The 60-month actuarial survival rates for patients presenting lymph node metastasis were higher when there was no capsule rupture by SCC (48.3%; p = 0.02), no more than one positive lymph node (52.3%; p = 0.004) or clear surgical margins (47.0%; p = 0.01), in comparison with patients presenting capsule rupture (20.2%), two or more positive lymph nodes (18.7%) or compromised surgical margins (0.0%), respectively. Patients presenting SCC p53 (+) and EGFR (-) demonstrated greater survival (75.0%; p = 0.03) than for the remaining group (33.1%). Multivariate analysis confirmed the positive impact of p53 (+) and EGFR (-) on survival (p = 0.02). Associations were found for p53, c-erbB-2 and EGFR expression with histoclinical data and prognosis. Interestingly, these results suggest that loss of mucosal c-erbB-2 expression could be involved in SCC carcinogenesis; EGFR expression in SCC is related to tumor mitotic index; and presence of p53 with absence of EGFR expression in head and neck SCC may be a prognostic factor for survival. Further prospective studies should be conducted to confirm the influence of p53, c-erbB-2 and EGFR on histoclinical data and prognosis.

P16 and p53 Expression in (Pre)Malignant Epidermal Tumors of Renal Transplant Recipients and Immunocompetent Individuals

Ultraviolet (UV) radiation is a prevailing factor implicated in the etiology of keratinocytic intraepidermal neoplasia (KIN) and squamous cell carcinomas (SCCs), as evidenced by the high frequency of UV-related mutations in the p53 and p16 tumor suppressor genes. In renal transplant recipients (RTRs), immunosuppression is considered another important risk factor in the enhanced carcinogenesis in these patients. So far, effects of UV and immune status on p53 and p16 immunoexpression in SCCs and precursors have not been studied. The aims of this study were to assess (1) the relation between risk factors for carcinogenesis, sun exposure and immune status, and p16 or p53 expression, and (2) to assess differences in p16 and p53 expression between KINs and SCCs. Immunostaining for p16 and p53 was performed on paraffin-embedded sections of 23 low-grade KIN (LKIN) lesions, 28 high-grade KINs (HKINs), and 35 SCCs from 44 RTRs and 42 immunocompetent controls (ICIs). In 74/86 lesions (86%), p53 was expressed, and in 63/86 (76%) lesions, p16 expression was present. Negativity for both p16 and p53 was found in 4/86 (5%) cases, whereas combined p53/p16 staining was most prevalent (55/86 lesions, 64%). P16 staining proved independent of p53 expression (P = .8), and immune status, sun exposure, and histological diagnosis (LKIN-HKIN-SCC) had no influence on this independence. Transplantation was associated with p53 expression in SCCs (P = .02; power = 34%) caused by higher prevalence of p53-negative SCCs in RTRs than in ICIs (30% versus 0). In HKINs, p16 was more frequently positive than in LKINs (P = .003; power = 49%) and SCCs (P = .03; power = 53%). HKINs showed more frequent transepidermal p16 and p53 staining than LKIN lesions (P < .001; power ≥ 99%). This study demonstrates that in KIN lesions and cutaneous SCCs, p16 expression is independent of p53 expression, and immune status, sun exposure, and histological diagnosis have no influence on this independence. Furthermore, HKIN lesions express significantly more p16 than LKINs and SCCs.