p53 expression related to the aggressive infiltrative histopathological feature of basal cell carcinoma

Auepemkiate, Sauvarat; Boonyaphiphat, Pleumjit; Thongsuksai, Paramee

doi:10.1046/j.1365-2559.2002.01393.x

Cited by 45 publications

(48 citation statements)

References 35 publications

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“…Surprisingly, there was no correlation between expression level and tumor aggressiveness because the pattern of p53 staining was similar in nodular and infiltrative BCC-like tumors. This contrasts with a study of relation of p53 expression to the aggressive infiltrative histopathological feature of human BCC (24).…”

Section: Discussionmentioning

confidence: 64%

Basal Cell Carcinoma and Its Development

Mancuso¹,

Pazzaglia²,

Tanori³

et al. 2004

Cancer Research

110

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Loss-of-function mutations in Patched (Ptch1) are implicated in constitutive activation of the Sonic hedgehog pathway in human basal cell carcinomas (BCCs), and inherited Ptch1 mutations underlie basal cell nevus syndrome in which a typical feature is multiple BCC occurring with greater incidence in portals of radiotherapy. Mice in which one copy of Ptch1 is inactivated show increased susceptibility to spontaneous tumor development and hypersensitivity to radiation-induced tumorigenesis, providing an ideal in vivo model to study the typical pathologies associated with basal cell nevus syndrome. We therefore examined BCC development in control and irradiated Ptch1 neo67/؉ mice. We show that unirradiated mice develop putative BCC precursor lesions, i.e., basaloid hyperproliferation areas arising from both follicular and interfollicular epithelium, and that these lesions progress to nodular and infiltrative BCCs only in irradiated mice. Data of BCC incidence, multiplicity, and latency support the notion of epidermal hyperproliferations, nodular and infiltrative BCC-like tumors representing different stages of tumor development. This is additionally supported by the pattern of p53 protein expression observed in BCC subtypes and by the finding of retention of the normal remaining Ptch1 allele in all nodular, circumscribed BCCs analyzed compared with its constant loss in infiltrative BCCs. Our data suggest chronological tumor progression from basaloid hyperproliferations to nodular and then infiltrative BCC occurring in a stepwise fashion through the accumulation of sequential genetic alterations.

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Section: Discussionmentioning

confidence: 64%

Basal Cell Carcinoma and Its Development

Mancuso¹,

Pazzaglia²,

Tanori³

et al. 2004

Cancer Research

110

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“…In those studies over-expression of p53 ranges from 40 to 90% [17][18][19][20][21][22][23][24][25][26]. The above variations could be attributed to the use of different antibodies and/or staining procedures applied for the detection of p53 protein expression as well as to differences in the assessment of the results.…”

Section: Discussionmentioning

confidence: 99%

B-Raf Mutations, Microsatellite Instability and p53 Protein Expression in Sporadic Basal Cell Carcinomas

Stamatelli

Saetta

Bei

et al. 2011

Pathol. Oncol. Res.

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Basal Cell Carcinoma (BCC) is the most common skin malignancy. Genes related to the Ras/Raf signalling pathway have been implicated in the pathogenesis of skin cancer. The objective of this study was to investigate the presence of B-Raf mutations in sporadic BCCs as well as its correlation with the phenotype of microsatellite instability (MSI), the clinicopathological parameters of the tumours and p53 protein expression. 83 BCC specimens were screened for B-Raf mutations, applying polymerase chain reaction, single-stranded conformation polymorphism (PCR-SSCP) and DNA sequencing. MSI status was examined using mononucleotide microsatellite markers and p53 protein expression was demonstrated by immunohistochemical staining. A C to T transition at 1790 nucleotide leading to a silent mutation L597L; and a T to A transversion causing an amino acid change (F610I) have been found. MSI was detected in 5% of the cases and p53 accumulation was present in 37/83 samples studied. Although rare B-Raf alterations have been observed in BCC, none of them harboured the hot-spot mutation T1799A commonly present in melanomas and colon carcinomas. Consequently, no correlation could be determined between B-Raf alterations, MSI status, the clinicopathological features and p53 protein expression. Our results are in favour of a secondary importance for Ras signalling cascade genes in BCC pathogenesis.

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“…Non-melanoma skin cancer is the most common type of skin cancer in the world. 77% of skin cancer is basal cell carcinoma (BCC), 20% of is squamous cell carcinoma (SCC), and melanoma and other rare skin cancers include remaining 3% [25]. Malignant tumors of the epidermis containing BCC and SCC constituting about 90% of all cutaneous malignancies [26][27][28][29].…”

Section: Autophagy and Basal Cell Carcinomamentioning

confidence: 99%

The Role of Autophagy in Stress and Cancer

Bostancıklıoğlu¹

2015

Single Cell Biol

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Programmed cell death plays an important role in development and disease. There are three main types of programmed cell death: apoptosis, autophagy, and necrosis. Apoptosis works on the two basic pathways called extrinsic and intrinsic; when there is a stress factor in a cell, apoptosis starts. Autophagy is critical for the continuation of normal human physiology such as the cellular homeostasis, energy balance, development and cellular defense. In addition to these, it may play a role in the pathogenesis of cancer, neurodegenerative diseases, aging, muscular diseases, infectious diseases, and immune system diseases.While some autophagy genes showed tumor suppressive effect during the development of cancer, some other genes contributes to the survival of cancer cells during cancer progression. Therefore, the relationship between autophagy and cancer is quite complex. The role of autophagy in cancer varies depending on the stage of the cancer, the metabolic status of cell and the presence of stress. Also, it was reported that the expression of certain molecules associated with autophagy vary in different types of cancer. Autophagy is activated and allows the continuation of the viability of tumor cells in hypoxia. In case of nutrient deficiency, autophagy allows tumor tissue to gain time until nutrient, oxygen and growth factors become eligible again. Therefore, autophagy is seen as a necessary mechanism for tumor continuity. Autophagy increases both in cancer cells and normal cells during the cancer treatment. But, due to cancer cells use autophagy to survive more than normal cells; this case may generate new therapeutic opportunities. The studies needed to conduct to find new ways for using the genes play role in autophagy in cancer treatment.In the present study, we aimed to throw light on the interaction of autophagy mechanism and some stresses such as ischemia and reperfusion and cancer development.

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p53 expression related to the aggressive infiltrative histopathological feature of basal cell carcinoma

Cited by 45 publications

References 35 publications

Basal Cell Carcinoma and Its Development

Basal Cell Carcinoma and Its Development

B-Raf Mutations, Microsatellite Instability and p53 Protein Expression in Sporadic Basal Cell Carcinomas

The Role of Autophagy in Stress and Cancer

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