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Ondruš, D; Pribylincová, V; Breza, J; Bujdák, Peter; Miklosi, M; Reznícek, J; Zvara, V

doi:10.1023/a:1007194607496

Cited by 49 publications

(6 citation statements)

References 3 publications

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“…This concept is supported by the observation that chronically immunosuppressed patients living in regions of intense sun exposure experience a higher rate of cutaneous malignancies 4 . The incidence of skin cancers is also high among organ transplant recipients who receive continuous immunosuppressive therapy 5 . Considerable experimental data indicate that UVB radiation-induced suppression of the immune system contributes to the development of skin tumors 6, 7 .…”

Section: Introductionmentioning

confidence: 99%

Honokiol inhibits ultraviolet radiation-induced immunosuppression through inhibition of ultraviolet-induced inflammation and DNA hypermethylation in mouse skin

Prasad

Singh

Katiyar

2017

Sci Rep

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Ultraviolet (UV) radiation exposure induces immunosuppression, which contributes to the development of cutaneous malignancies. We investigated the effects of honokiol, a phytochemical found in plants of the genus Magnolia, on UVB-induced immunosuppression using contact hypersensitivity (CHS) as a model in C3H/HeN mice. Topical application of honokiol (0.5 and 1.0 mg/cm 2 skin area) had a significant preventive effect on UVB-induced suppression of the CHS response. The inflammatory mediators, COX-2 and PGE 2 , played a key role in this effect, as indicated by honokiol inhibition of cyclooxygenase-2 (COX-2) expression and PGE 2 production in the UVB-exposed skin. Honokiol application also inhibited UVB-induced DNA hypermethylation and its elevation of the levels of TET enzyme, which is responsible for DNA demethylation in UVB-exposed skin. This was consistent with the restoration of the CHS response in mice treated with the DNA demethylating agent, 5-aza-2′-deoxycytidine, after UVB exposure. There was no significant difference in the levels of inhibition of UVB-induced immunosuppression amongst mice that were treated topically with available anti-cancer drugs (imiquimod and 5-fluorouracil). This study is the first to show that honokiol has the ability to inhibit UVB-induced immunosuppression in preclinical model and, thus, has potential for use as a chemopreventive strategy for UVB radiation-induced malignancies.Constant exposure of the skin to solar ultraviolet (UV) radiation induces a variety of harmful effects, including premature aging or photoaging of the skin as well as a heightened risk of skin cancers (both melanoma and non-melanoma) [1][2][3] . The immunosuppressive effects of UV radiation, particularly in the UVB spectrum (290-320 nm wavelengths), are considered to represent one of the most important environmental risk factors for development of skin cancers in humans 1-3 . This concept is supported by the observation that chronically immunosuppressed patients living in regions of intense sun exposure experience a higher rate of cutaneous malignancies 4 . The incidence of skin cancers is also high among organ transplant recipients who receive continuous immunosuppressive therapy 5. Considerable experimental data indicate that UVB radiation-induced suppression of the immune system contributes to the development of skin tumors 6, 7 . UV-induced inflammation is considered to be an early event in skin tumor promotion and progression. UV-induced inflammatory responses result in the development of erythema, edema, and hyperplastic responses, as well as increases in the levels of cyclooxygenase-2 (COX-2) and prostaglandin (PG) metabolites. The UV-induced PG metabolites (PGE 2 , PGD2 and PGF 2α ) have been implicated in UVB-induced

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Section: Introductionmentioning

confidence: 99%

Honokiol inhibits ultraviolet radiation-induced immunosuppression through inhibition of ultraviolet-induced inflammation and DNA hypermethylation in mouse skin

Prasad

Singh

Katiyar

2017

Sci Rep

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“…Malignant cancers following long-term treatment with prednisone and prednisone-like immunosuppressant drugs have been reported [ 6 , 7 , 8 , 9 , 10 ]. This is the first report of multiple cancers following long-term treatment of TA with prednisone.…”

Section: Introductionmentioning

confidence: 99%

Multiple Tumor Induction after Treatment of Temporal Arteritis with Prednisone

Piraino¹

2017

Case Rep Oncol

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A 74-year-old female was diagnosed with the autoimmune inflammatory disease temporal arteritis and treated with high and low doses of prednisone over a period of 6 years. During that time, she developed cancers of the lung and colon as well as a soft tumor mass on lumbar vertebrate L3. She also experienced a series of debilitating and disabling symptoms while on prednisone treatment. A temporal analysis of the association of prednisone therapy and immune markers to the successive appearance of the malignant tumors strongly suggests that in the absence of a functioning natural immune and surveillance system by treatment with the immune knockout drug prednisone, spontaneous, multiple independent mutations occurred in several sites in the organ systems of this patient. Over a period of time, these developed into malignant cancers, including a lung nodule which became cancerous 256 days later, as well as the cancers of the colon and a soft tumor mass on lumbar vertebrate L3.

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“…Probably, the best studied scenario in this setting is the association of EBV and posttransplantation lymphoproliferative diseases [ 1 ]. But also squamous cell carcinomas and Kaposi sarcomas as well as specific myeloid malignancies, notably myelodysplastic syndromes and acute myeloid leukemia, have been observed more frequently in patients following solid organ transplantation [ 2 , 3 ]. In addition, after the first report by Battin et al (1976), a remarkable number of case reports describing cases of chronic myeloid leukemia (CML) following solid organ transplantation and immunosuppression were published over the past decades ([ 4 – 27 ], Table 1 ).…”

Section: Introductionmentioning

confidence: 99%

Clinical Lessons to Be Learned from Patients Developing Chronic Myeloid Leukemia While on Immunosuppressive Therapy after Solid Organ Transplantation: Yet Another Case after Orthotopic Heart Transplantation

Oberender

Kleeberg

Nienhues

et al. 2014

Case Reports in Hematology

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Chronic myeloid leukemia developing after transplantation of solid organs and concomitant immunosuppression is a rare but still significant clinical phenomenon. We here describe an additional case of a 62-year-old male patient developing CML after orthotopic heart transplantation and medication with cyclosporine A, mofetil-mycophenolate, and steroids. Initial antileukemic therapy was imatinib at a standard dose and within 15 months of therapy a complete cytogenetic response was noted. In this report we discuss the clinical implications of these rare but biologically important cases.

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Cited by 49 publications

References 3 publications

Honokiol inhibits ultraviolet radiation-induced immunosuppression through inhibition of ultraviolet-induced inflammation and DNA hypermethylation in mouse skin

Honokiol inhibits ultraviolet radiation-induced immunosuppression through inhibition of ultraviolet-induced inflammation and DNA hypermethylation in mouse skin

Multiple Tumor Induction after Treatment of Temporal Arteritis with Prednisone

Clinical Lessons to Be Learned from Patients Developing Chronic Myeloid Leukemia While on Immunosuppressive Therapy after Solid Organ Transplantation: Yet Another Case after Orthotopic Heart Transplantation

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