Model examinatioï¿½n of chemoprevention with retinoids in squamous cell carcinomas of the head and neck region and suitable biomarkers for chemoprevention

Fabricius, Eva‐Maria; Kruse-Boitschenko, Ute; Schneeweiss, U; Wildner, Gustav‐Paul; Hoffmeister, Bodo; Raguse, Jan-Dirk

doi:10.3892/ijo.2011.1139

Cited by 4 publications

(3 citation statements)

References 101 publications

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“…It should be emphasized that most breast carcinomas and breast cancer cell lines show loss or down-regulation of RARβ receptor expression, whereas RARα and γ, as well as RXRs, appear to be variably expressed in both normal and tumor cells [220]. Expression of RARβ could be modulated by chemopreventive intervention [221,222] and may therefore serve as an intermediate biomarker in chemoprevention trials for some cancers [223]. Provitamin A carotenoids, such as β-carotene and its excentric cleavage metabolites, can serve as direct precursors for (all- trans )-retinoic acid and (9- cis )-retinoic acid which are ligands for RAR and RXR, respectively.…”

Section: Mechanisms Of Cancer Chemoprevention By Carotenoidsmentioning

confidence: 99%

Cancer Chemoprevention by Carotenoids

2012

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Carotenoids are natural fat-soluble pigments that provide bright coloration to plants and animals. Dietary intake of carotenoids is inversely associated with the risk of a variety of cancers in different tissues. Preclinical studies have shown that some carotenoids have potent antitumor effects both in vitro and in vivo, suggesting potential preventive and/or therapeutic roles for the compounds. Since chemoprevention is one of the most important strategies in the control of cancer development, molecular mechanism-based cancer chemoprevention using carotenoids seems to be an attractive approach. Various carotenoids, such as β-carotene, a-carotene, lycopene, lutein, zeaxanthin, β-cryptoxanthin, fucoxanthin, canthaxanthin and astaxanthin, have been proven to have anti-carcinogenic activity in several tissues, although high doses of β-carotene failed to exhibit chemopreventive activity in clinical trials. In this review, cancer prevention using carotenoids are reviewed and the possible mechanisms of action are described.

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Section: Mechanisms Of Cancer Chemoprevention By Carotenoidsmentioning

confidence: 99%

Cancer Chemoprevention by Carotenoids

2012

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“…All-trans retinoic acid (ATRA) therapy has been successfully used for chemoprevention of SCCs in several studies. [21][22][23] In a recent trial, Cheepala and colleagues compared the gene expression profiles of control skin to skin exposed to ATRA and concluded that ATRA's mechanism involves targeting the BRAF signaling pathway. 22 This patient's lesions improved after starting isotretinoin and 5-fluorouracil 5% cream.…”

Section: Discussionmentioning

confidence: 99%

Eruptive Squamous Cell Carcinomas after Vemurafenib Therapy

Mays

Curry²,

Kim

et al. 2013

J Cutan Med Surg

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Background: Vemurafenib is an oral BRAF inhibitor recently approved for the treatment of metastatic melanoma. Patients treated with this medication have been reported to have the occurrence of squamous cell carcinoma (SCC) and/or actinic keratosis (AK).Objective: We report the case of a patient treated with vemurafenib for papillary thyroid carcinoma who subsequently developed multiple SCCs and AK of the skin. The lesions were deemed related to the medication and treated with excision. In addition, subsequent development of SCCs and AK was successfully prevented with a combination of isotretinoin and 5-fluorouracil in this patient. We discuss postulated mechanisms for these findings, as well as potential preventive therapy with the aforementioned combination regimen in patients undergoing treatment with vemurafenib.Contexte: Le vé murafé nib est un inhibiteur oral de la proté ine BRAF, approuvé derniè rement dans le traitement du mé lanome mé tastatique. L'apparition de lé sions de carcinome à cellules squameuses (CS) et/ou de ké ratose actinique (KA) a dé jà é té signalé e chez des patients traité s par ce mé dicament.Objectif: Sera dé crit ici le cas d'un patient traité par le vé murafé nib pour un carcinome papillaire de la thyroïde, chez qui sont apparues plus tard de nombreuses lé sions de CS de la peau et de KA. On a jugé que ces lé sions é taient lié es au mé dicament, et elles ont é té traité es par exé rè se. Par ailleurs, l'association d'isotré tinoïne et de 5-fluoro-uracile a permis de pré venir efficacement l'apparition ulté rieure d'autres lé sions de CS et de KA chez ce patient. Il sera question des mé canismes mis de l'avant pour expliquer l'apparition de ces lé sions ainsi que de la thé rapie potentiellement pré ventive, composé e des mé dicaments mentionné s plus haut, chez les patients devant ê tre traité s par le vé murafé nib.

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“…Various approaches have been reported to address these issues associated with retinoid therapy of PMOLs, including the use of newer synthetic retinoid analogues (for example, fenretinide: [9] and studies focussed on the identification of biomarkers, which may predict retinoid sensitivity [9,[19][20][21][22]. A further possible approach has been used in other cancers: the addition of de-methylating agents to retinoids treatment.…”

Section: Introductionmentioning

confidence: 99%

RARβ Expression in Keratinocytes from Potentially Malignant Oral Lesions: The Functional Consequences of Re-Expression by De-Methylating Agents

Radhakrishnan

Crane

Daigneault

et al. 2021

Cancers

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Loss of RARβ2 expression by promoter methylation is an early event in oral carcinogenesis. Understanding the mechanisms and consequences of RARβ loss may aid in understanding the disappointing results of retinoid chemoprevention trials. This study aimed to describe the effects of all-trans retinoic acid (ATRA) and the de-methylating agent 5-Aza-2′ deoxycytidine (5-AZA-CdR) on a panel of immortal potentially malignant oral lesion (PMOL) cell cultures. RARβ expression was assessed in PMOL tissues by immunohistochemistry. Cells were treated with ATRA ± 5-AZA-CdR, and the effects on the cell cycle and senescence were assessed. In PMOL tissues, RARβ expression was variable, but lower in biopsies which gave rise to immortal cell cultures. Treatment of iPMOL cells with ATRA resulted in little change in RARβ expression, but the addition of 5-AZA-CdR resulted in significant increases. The effects on the cell cycle and senescence were variable and may be related to 5-AZA-CdR, as this has wider effects on the cell cycle. Overall, the response of iPMOL cells to ATRA and 5-AZA-CdR treatment was variable and is dependent on several factors, including RARβ-promoter methylation. These findings may help to explain the lack of consistent effect of retinoids in PMOLs seen in chemoprevention trials.

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Model examinatioï¿½n of chemoprevention with retinoids in squamous cell carcinomas of the head and neck region and suitable biomarkers for chemoprevention

Cited by 4 publications

References 101 publications

Cancer Chemoprevention by Carotenoids

Cancer Chemoprevention by Carotenoids

Eruptive Squamous Cell Carcinomas after Vemurafenib Therapy

RARβ Expression in Keratinocytes from Potentially Malignant Oral Lesions: The Functional Consequences of Re-Expression by De-Methylating Agents

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