Combination of Q-Switched Nd:YAG and Fractional Erbium:YAG Lasers in Treatment of Melasma: A Randomized Controlled Clinical Trial

Introduction: Ablative and nonablative lasers have been used to treat melasma. We aimed to assess and compare the combining Q-switched Nd:YAG laser (QSNYL) and fractional erbium:YAG laser (FEYL) with QSNYL alone in treatment of melasma.Methods: This randomized controlled clinical trial was performed in our Research Center during 2013-2014. Women with melasma and without a history of keloid formation, hypersensitivity to hydroquinone, or pigmentary changes due to laser therapy were randomly allocated to receive four sessions of either QSNYL-FEYL combination or QSNYL alone. All patients received topical treatment with Kligman’s formula. Before laser therapy and 4 weeks after the last treatment session, patients’ skin was assessed for changes in skin color, melanin content, and erythema intensity of melasma lesions quantitatively.Results: Finally, 21 patients in QSNYL-FEYL and 20 in QSNYL group (mean age, 38.57 [5.60] and 42.60 [8.44] years, respectively) completed study. The skin color had become lighter in both groups (mean [SD] percentage change of 56.95 [40.29] and 29.25 [13.20] in QSNYL-FEYL and QSNYL groups, respectively) with significantly better results in QSNYL-FEYL group (P = 0.006). Percentage of decrease of melanin content was significantly higher in QSNYL-FEYL group (22.01 [10.67] vs. 7.69 [4.75]; P < 0.001). After adjustment for baseline values, the post treatment intensity of erythema was significantly lower in QSNYL-FEYL group (P < 0.001). The patients reported no adverse events.Conclusion: QSNYL-FEYL was significantly more effective in decreasing melanin content of lesions than QSNYL and led to a lighter skin.

The molecular biology and therapeutic potential of Nrf2 in leukemia

NF-E2-related factor 2 (Nrf2) transcription factor has contradictory roles in cancer, which can act as a tumor suppressor or a proto-oncogene in different cell conditions (depending on the cell type and the conditions of the cell environment). Nrf2 pathway regulates several cellular processes, including signaling, energy metabolism, autophagy, inflammation, redox homeostasis, and antioxidant regulation. As a result, it plays a crucial role in cell survival. Conversely, Nrf2 protects cancerous cells from apoptosis and increases proliferation, angiogenesis, and metastasis. It promotes resistance to chemotherapy and radiotherapy in various solid tumors and hematological malignancies, so we want to elucidate the role of Nrf2 in cancer and the positive point of its targeting. Also, in the past few years, many studies have shown that Nrf2 protects cancer cells, especially leukemic cells, from the effects of chemotherapeutic drugs. The present paper summarizes these studies to scrutinize whether targeting Nrf2 combined with chemotherapy would be a therapeutic approach for leukemia treatment. Also, we discussed how Nrf2 and NF-κB work together to control the cellular redox pathway. The role of these two factors in inflammation (antagonistic) and leukemia (synergistic) is also summarized

The role of SF3B1 and NOTCH1 in the pathogenesis of leukemia

The discovery of new genes/pathways improves our knowledge of cancer pathogenesis and presents novel potential therapeutic options. For instance, splicing factor 3b subunit 1 (SF3B1) and NOTCH1 genetic alterations have been identified at a high frequency in hematological malignancies, such as leukemia, and may be related to the prognosis of involved patients because they change the nature of malignancies in different ways like mediating therapeutic resistance; therefore, studying these gene/pathways is essential. This review aims to discuss SF3B1 and NOTCH1 roles in the pathogenesis of various types of leukemia and the therapeutic potential of targeting these genes or their mutations to provide a foundation for leukemia treatment