Correlation between <i>Bcl‐2</i> and <i>Bax</i> in atrophic and hypertrophic type of actinic keratosis

Tomas, Davor; Krušlin, Božo; Čupić, Hrvoje; Stanimirović, Andrija; Bošnjak, Berislav; Lovričević, Ivo; Belicza, Mladen

doi:10.1111/j.1468-3083.2005.01364.x

Cited by 7 publications

(8 citation statements)

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“…Treatment‐resistant AKs were present for a longer period of time before definitive treatment than were lesions in both control groups. Tomas and colleagues theorized that duration of lesion contributes to potential for malignant transformation, stating that, if AKs “lived longer,” they had longer to develop further mutations and transform into invasive SCC . Fuchs and colleagues analyzed the time to progression from AK to SCC and found that 10% of AKs progress to SCC in 24.6 months, suggesting that at least 10% of lesions continue to transform over time .…”

Section: Discussionmentioning

confidence: 99%

“…Tomas and colleagues examined the expression of apoptosis‐related proteins in atrophic and hypertrophic AKs. They found that hypertrophic AKs resisted apoptotic stimuli more than atrophic AKs and concluded that hypertrophic AKs “lived longer” and may therefore have a higher likelihood for further mutations and transformation into invasive SCC . Fukamizu and colleagues reported on four cases of metastasis arising from a cutaneous primary SCC.…”

Section: Discussionmentioning

confidence: 99%

“…Tomas and colleagues theorized that duration of lesion contributes to potential for malignant transformation, stating that, if AKs "lived longer," they had longer to develop further mutations and transform into invasive SCC. 10 Fuchs and colleagues analyzed the time to progression from AK to SCC and found that 10% of AKs progress to SCC in 24.6 months, suggesting that at least 10% of lesions continue to transform over time. 2 It follows that the other 90% of AKs persist as AKs or spontaneously resolve, although the actual range for conversion to SCC in that study spanned 2.0 to 75.6 months, indicating that some AKs transform to SCC well after 24 months, and some of our patients with treatment-resistant AKs might have fallen into this category if left untreated (range of duration 3-85 months).…”

Section: O N D O E T a Lmentioning

confidence: 99%

“…They found that hypertrophic AKs resisted apoptotic stimuli more than atrophic AKs and concluded that hypertrophic AKs "lived longer" and may therefore have a higher likelihood for further mutations and transformation into invasive SCC. 10 Fukamizu and colleagues reported on four cases of metastasis arising from a cutaneous primary SCC. Their histologic analysis revealed that one of the lesions arose in a hypertrophic AK.…”

Section: O N D O E T a Lmentioning

confidence: 99%

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Treatment-Refractory Actinic Keratoses Successfully Treated Using Simultaneous Combination Topical 5-Fluorouracil Cream and Imiquimod Cream: A Case–Control Study

Ondo¹,

Padilla²,

Miedler³

et al. 2012

Dermatologic Surgery

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: O N D O E T a Lmentioning

confidence: 99%

Section: O N D O E T a Lmentioning

confidence: 99%

See 2 more Smart Citations

Treatment-Refractory Actinic Keratoses Successfully Treated Using Simultaneous Combination Topical 5-Fluorouracil Cream and Imiquimod Cream: A Case–Control Study

Ondo¹,

Padilla²,

Miedler³

et al. 2012

Dermatologic Surgery

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“…There are many studies showing Bcl-2 expression among AK cases (23,24). A study by Thomas et al showed that typically AK cases had 35-41% weak positive Bcl-2 expression (25). Contrary to this, Hussein et al showed high Bcl-2 expression in 73% of AK cases.…”

Section: Discussionmentioning

confidence: 98%

Assessment of BCL-2 expression in actinic keratosis, keratoacanthoma and seborrheic keratosis cases

Önder¹,

Erdem²,

Haktanır³

et al. 2019

Ann Med Res

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Aim: One of the main functions of apoptosis is the elimination of cells with damaged DNA, including premalignant cells in skin. Apoptosis is regulated by the balance between antiapoptotic and proapoptotic proteins. The bcl-2 protein has been shown antiapoptotic effect. It protects cell against apoptosis induced by different death-inducing signals. Material and Methods: In this study the authors have analyzed imunohistochemically the expression of bcl-2 protein in the histopathological variants of the precancerous lesion [actinic keratosis (AK) (28 cases) and keratoacanthomas (KA) (12 cases) and seborrheic keratosis (SK) (22 cases) in skin. Results: In cases of AK, bcl-2 expression was confined to basal cell layer, as well as in two cases of thorough epidermis. SK expression of bcl-2 protein was in areas of basaloid proliferation.KA expression of bcl-2 protein was not dome-shaped keratin-filled crater areas but bcl-2 expression was confined of non crater areas. Conclusion: In conclusion, bcl-2 expression supports the observation that tumor cells are derived from basal keratinocytes in AK and SK and not support the observation that tumor cells are derived from basal keratinocytes in KA.

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Clinical, dermoscopic and immunohistochemical assessment of actinic keratoses and evaluation of the effectiveness of diclofenac therapy with immunohistochemical analysis

Çayirli¹,

Köse

Demiriz

2013

Arch Dermatol Res

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Actinic keratoses (AKs) is a keratinocytic neoplasm that typically develops on the face of elderly patients. Little is known regarding the clinical, dermatoscopic and immunohistochemical assessments of AK using topical diclofenac therapy. We sought to determine these assessments and evaluate the efficacy of topical diclofenac gel in AK. In this prospective, open-label study, 44 patients with 66 AKs were treated for 12 weeks with topically applied diclofenac (3% gel in 2.5% hyaluronic acid). Immunohistopathologic analyses were performed before and after diclofenac treatment using epidermal stem cell markers such as Cytokeratin 15 (CK15), Cytokeratin 19 (CK19) and p63, in addition to proliferation markers (Bcl-2, Ki-67). Diclofenac gel was found to be effective in AK, including the hyperkeratotic type. Surprisingly, complete remission was observed at a significantly higher rate in Grade 3 lesions (p = 0.017). However, imunohistochemical and histopathologic examinations revealed that 12-week treatment periods may not be sufficient to fully cure AK. The immunohistochemical analyses revealed no change in the expression levels of CK15, CK19 and Bcl-2 following diclofenac therapy. However, the expression of Ki-67 (p = 0.042) and p63 (p = 0.030) exhibited a significant decrease after therapy. Dermatoscopy is an effective method for diagnosis of AK, and topical diclofenac sodium gel was found as an effective additional treatment modality. Since positive histopathological findings were detected in some patients even with significant remission, a 12-week treatment period should be extended even in patients presenting with positive clinical response. Importantly, anti-proliferative effects of diclofenac were demonstrated by decreased Ki-67 and p63 expression levels.

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Correlation between Bcl‐2 and Bax in atrophic and hypertrophic type of actinic keratosis

Cited by 7 publications

References 50 publications

Treatment-Refractory Actinic Keratoses Successfully Treated Using Simultaneous Combination Topical 5-Fluorouracil Cream and Imiquimod Cream: A Case–Control Study

Treatment-Refractory Actinic Keratoses Successfully Treated Using Simultaneous Combination Topical 5-Fluorouracil Cream and Imiquimod Cream: A Case–Control Study

Assessment of BCL-2 expression in actinic keratosis, keratoacanthoma and seborrheic keratosis cases

Clinical, dermoscopic and immunohistochemical assessment of actinic keratoses and evaluation of the effectiveness of diclofenac therapy with immunohistochemical analysis

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