Expression of p53, bcl-2 and growth hormone receptor in actinic keratosis, hypertrophic type

Abstract

According to novel investigations, actinic keratosis (AK) is not a premalignant lesion but is a malignant lesion in the evolution to invasive squamous cell carcinoma (SCC). Thus, we analyzed p53, bcl-2 and growth hormone receptor (GHR) expression in hypertrophic-type AK (HAK) to determine the relative importance of these protooncogenes in the biological behavior of HAK. Expression of p53, bcl-2 and GHR was determined by immunohistochemistry in 33 HAK specimens and surrounding perilesional normal skin (PNS). The relative proportions of immunoreactive cells were determined. Of the 33 HAK specimens, 30 (91%) showed immunopositive staining for p53, 33 (100%) for bcl-2, and 12 (36%) for GHR. Highly positive p53 expression in HAK lesions could indicate that p53 mutation is an early and crucial event in lesion development. The detected pattern of the p53/ bcl-2 ratio in HAK suggests an important role for another gene: the proapoptotic gene bax. Our findings indicate that GHR expression could be a biological marker of progression of HAK to SCC.

Expression of p53, bcl-2 and growth hormone receptor in atrophic type of actinic keratosis

“…In spite of pathohistological differences, only few studies confined investigation on specific types of AK [3][4][5][6]. Our earlier investigation of tumor suppressor gene p53, oncogene bcl-2 and growth hormone receptor (GHR) expression was focused on hypertrophic actinic keratosis (HAK) [6]. We had restricted present investigation only on atrophic AK (AAK) and compared results with investigation conducted on HAK [6] to determine if differences on molecular level reflect pathohistological discrepancy and could serve as possible marker of distinct biological properties.…”

“…Although all types of AK share similar clinical features, their pathohistological properties are somewhat divergent. In spite of pathohistological differences, only few studies confined investigation on specific types of AK [3][4][5][6]. Our earlier investigation of tumor suppressor gene p53, oncogene bcl-2 and growth hormone receptor (GHR) expression was focused on hypertrophic actinic keratosis (HAK) [6].…”

“…Clinical information about the patients was obtained from the files of the Ljudevit Jurak University, Department of Pathology, Sisters of Charity, University Hospital, Zagreb, Croatia. Immunohistochemical (IHC) procedure was done as described previously [6,7]. Expression of immunohistochemical staining was represented as a percent of immunoreactive cells on 1000 analyzed cells.…”

“…1A, C and E). Investigated genes were expressed in NS skin layers as previously described [3][4][5][6][7][8][9][10].…”

Erbb2 Regulates Inflammation and Proliferation in the Skin after Ultraviolet Irradiation

“…66 Ghr expression, suppressed on inhibition of Erbb2, is a marker for the progression from actinic keratosis to squamous cell carcinoma. 67 Significant correlations have been shown between Mmp9, reduced by the Erbb2 inhibitor, and Erbb2 expression with respect to clinico-pathological parameters in head and neck squamous cell carcinoma, 68 and oral squamous cell carcinomas have higher expression of Mmp9. 69 These data support a multifaceted role for Erbb2 in skin cancer development and progression.…”