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Results for “retinoid resistance”

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PubMed2025

Targeting PRAME directly or via EZH2 inhibition overcomes retinoid resistance and represents a novel therapy for keratinocyte carcinoma.

Retinoids have demonstrated efficacy as preventative/treatment agents for keratinocyte carcinomas (KCs): basal cell carcinoma (BCC) and cutaneous squamous cell carcinoma (SCC). However, retinoid resistance mechanisms limit the efficacy of these compounds. A subset of KCs expresses Preferentially Expressed Antigen in Melanoma (PRAME): a retinoid signaling corepressor. PRAME is proposed to repress retinoid signaling by guiding enhancer of zeste homolog 2 (EZH2) to retinoic acid response elements (RARE) in promoters. We investigated the effects of PRAME on KC pathogenesis and retinoid response. High-PRAME expression in tumors was negatively correlated with epidermal differentiation gene signatures. PRAME overexpression downregulated epidermal differentiation gene signatures and impaired differentiation in 3D culture. PRAME overexpression attenuated retinoid-induced RARE activation, growth suppression, and differentiation responses. Conversely, low-PRAME tumors and PRAME-depleted KC cells demonstrated enriched epidermal differentiation gene signatures. PRAME downregulation restored retinoid-induced RARE activation, growth suppression, keratinization in SCC, and cell death signaling in BCC. Furthermore, combined retinoid and EZH2 inhibitor treatment augmented RARE activation and suppressed PRAME-expressing KC cell growth. Hence, PRAME confers retinoid resistance in KC, which may be overcome by EZH2 inhibition.

Enhancer of Zeste Homolog 2 Protein↗

PubMedDate not supplied

Stimulation of cell-mediated resistance in mice to infection with Listeria monocytogenes by vitamin A.

Vitamin A given as retinol-acetate, retinol-palmitate as well as the derivates retinoic acid and a retinoid, strongly fortified the resistance of mice to infection with virulent cells of Listeria monocytogenes. However, strong enhancement of resistance was only achieved when high toxic doses of vitamin A were given. Apparently, this effect was due to a stimulation of the function of the mononuclear phagocytic system rather than of the T lymphocyte.

Animals↗

PubMed1978

[Retinoid PUVA (RePUVA): systemic combination therapy in psoriasis].

RePUVA is a new therapeutic approach in psoriasis, consisting in oral administration of a retinoid derivative and systemic PUVA treatment. The retinoid (Ro 10-9359) was given daily (50--75 mg) before, simultaneously and, before and simultaneously with PUVA. The overall response was 73%; however, 14 patients resistant to previous standard PUVA treatment also responded surprisingly well to RePUVA. If PUVA-resistent patients were excluded, the overall response was 82.6%. The mean number of treatments required for clearing was 19.4 +/- 6.1, the mean total UVA-dose 57.9 +/- 32.3 J/cm2 and the mean duration of treatment was 55.4 +/- 14.1 days, including pretreatment with retinoid. It seems that RePUVA may be most successful if the retinoid is given before and with PUVA: 33.7 +/- 8.7 J/cm2 in 17.0 +/- 4.7 sessions were then required for clearing. Compared with previous results of our group and recent publications these findings indicate that the RePUVA schedule may reduce the duration of treatment and the total UVA-dose and, therefore, the possible long-term hazards of PUVA management. In addition, RePUVA can be successfully applied in patients resistant to standard PUVA.

Coumarins↗

PubMed1979

Oral treatment of pustulosis palmo-plantaris with a new retinoid, Ro 10-9359.

Ro 10-9359 is a retinoic acid derivative, selected for study because of a better tolerance than retinoic acid, shown in animal experiments. Earlier clinical experience has proved Ro 10-9359 to be an extremely potent antipsoriatic drug. The well-known association between psoriasis and pustulosis palmoplantaris was a motivation to evaluate Ro 10-9359 also in the last-mentioned disease, which is notoriously known to be resistant to treatment. In this study 30 patients were given either 75 mg/day of Ro 10-9359 or 200 mg twice every week according to a randomized pattern. All patients had suffered from the disease for at least 2 years without any spontaneous remission during the year preceding the trial. After a treatment period of about 2 weeks with Ro 10-9359 hyperkeratotic scales had usually disappeared, and 2 weeks later there were in general significantly less pustular lesions. The treatment continued for 8 weeks, and at this time the average reduction of the number of pustules was 80%. The daily dosage seemed to give better results and was also better tolerated than was the twice-weekly dosage. Side effects were common, but generally mild. On average, the remission lasted 1 month after cessation of therapy.

Administration, Oral↗

PubMed2026

Therapeutic Potential of Terpenes in Lung Cancer: Modulation of 4-Oxo- Retinoic Acid, TNF-α, NF-κB, and HDAC2 Pathways.

Non-small cell lung cancer (NSCLC) includes various epithelial malignancies, such as squamous cell carcinoma, large cell carcinoma, and adenocarcinoma. Despite advancements in surgical resection, chemoradiotherapy, and multimodal therapies, NSCLC prognosis remains challenging due to its complex molecular landscape, drug resistance, and high treatment costs. Recent research highlights the potential of natural compounds, particularly terpenes and terpenoids, derived from essential oils (EOs), to enhance NSCLC treatment. These compounds exhibit anticancer properties and modulate key pathways like the 4-oxo-retinoic acid pathway, TNF-α signaling, NF-κB activation, and histone deacetylases (HDACs). Retinoids, a subclass of terpenes, show both chemopreventive and therapeutic benefits, especially when combined with other agents, though challenges in dosing and delivery methods limit their clinical application. Terpenes may also synergize with emerging therapies, such as antiangiogenic treatments and immunotherapy, to improve outcomes. Biomarkers, including genomic, epigenomic, and proteomic markers, play a critical role in predicting responses to terpene-based treatments, supporting personalized medicine. The integration of terpenes into existing regimens, in combination with conventional therapies, holds promise in overcoming clinical challenges, improving patient outcomes, and advancing natural compound use in modern oncology. Future research should focus on optimizing terpene therapies and addressing clinical hurdles.

Humans↗