Jr. Melanoma

ArticleinNew England Journal of Medicine 355(1):51-65 · August 2006with16 Reads
DOI: 10.1056/NEJMra052166 · Source: PubMed
This review summarizes the molecular and genetic lesions underlying the progression from benign nevus to malignant melanoma.
    • "Increase of the incidence of malignant skin cancer is rising at an alarming rate.[1920] However, the main problem to treat melanoma is its resistance to radiation and conventional chemotherapeutic agents.[2021] Hence, novel therapies are needed to reduce the effects of the increasing incidence in human melanoma. "
    [Show abstract] [Hide abstract] ABSTRACT: Background: Plumbago rosea is used in traditional systems of medicine for the preparation of formulations used for treating inflammations, cough, bronchitis, and gastrointestinal disorders, and also in conjunction with cancer chemotherapy. In the present study, the cytotoxic and anti-proliferative effects of plumbagin, and the ethanolic root extract of P. rosea (ETPR) was evaluated on SK-MEL 28 melanoma cell lines and human lymphocytes. Materials and Methods: MTT and apoptotic assays were used for the evaluation of cytotoxic and anti-proliferative effects, respectively. In addition, the effect of Plumbagin and ETPR in down regulation of BCL-2 expression is investigated using RT-PCR analysis. Results: Both plumbagin and ETPR dose-dependently decreased the cell viability more potently in melanoma cell lines. P. rosea extract demonstrated significant synergy in inhibiting BCL-2 expression than plumbagin. Moreover plumbagin showed more toxicity in human lymphocytes. Conclusion: Plumbagin has anti-cancer potential, but the side effects limits its use; yet plumbagin, in combination with other ingredients in Plumbago rosea extract, displays significant synergy leading to a stronger anticancer effect with significantly less toxicity.
    Full-text · Article · Aug 2014
    • "Melanoma is the most aggressive type of skin cancer, characterized by a rapid progression, metastasis to regional lymph nodes and distant organs as well as a limited efficiency of therapeutics [1]. Although it accounts for only about 4% of all dermatological cancers, it contributes to more than 80% death of skin cancer patients [2]. Therefore, it is necessary to understand thoroughly which factors involved in the development and progression of melanoma. "
    [Show abstract] [Hide abstract] ABSTRACT: Long non-coding RNAs (lncRNAs) have been shown to be implicated in the complex network of cancer including malignant melanoma and play important roles in tumorigenesis and progression. However, their functions and downstream mechanisms are largely unknown. This study aimed to investigate whether BRAF-activated non-coding RNA (BANCR), a novel and potential regulator of melanoma cell, participates in the proliferation of malignant melanoma and elucidate the underlying mechanism in this process. We found that BANCR was abnormally overexpressed in human malignant melanoma cell lines and tissues, and increased with tumor stages by quantitative PCR. BANCR knockdown induced by shRNA transfection significantly inhibited proliferation of tumor cells and inactivated MAPK pathway, especially by silencing the ERK1/2 and JNK component. Moreover, combination treatment of BANCR knockdown and suppression ERK1/2 or JNK (induced by specific inhibitors U0126 or SP600125 respectively) produced synergistic inhibitory effects in vitro. And the inhibitory effects induced by ERK1/2 or JNK could be rescued by BANCR overexpression. By tumorigenicity assay in BALB/c nude mice, we further found that BANCR knockdown inhibited tumor growth in vivo. In addition, patients with high expression of BANCR had a lower survival rate. Taken together, we confirmed the abnormal upregulation of a novel lncRNA, BANCR, in human malignant melanoma. BANCR was involved in melanoma cell proliferation both in vitro and in vivo. The linkage between BANCR and MAPK pathway may provide a novel interpretation for the mechanism of proliferation regulation in malignant melanoma.
    Full-text · Article · Jun 2014
    • "It causes high mortality rate [18]. Gold standard of primary melanoma is surgery; but combined therapy, such as chemotherapy, immunotherapy, or radiotherapy, is necessary to advanced or metastatic melanoma [19, 20]. The Raf protein/mitogen-activated protein kinase/extracellular-signal-regulated kinase (RAF/MAPK/ERK) signal pathway has thus become a molecular target for therapeutic design of advanced melanoma harboring the B-RAF gene mutation [21, 22]. "
    [Show abstract] [Hide abstract] ABSTRACT: One has found an important cell cycle controller. This guard can decide the cell cycle toward proliferation or quiescence. Cyclin-dependent kinase 2 (CDK2) is a unique target among the CDK family in melanoma therapy. We attempted to find out TCM compounds from TCM Database@Taiwan that have the ability to inhibit the activity of CDK2 by systems biology. We selected Tetrahydropalmatine, Reserpiline, and (+)-Corydaline as the candidates by docking and screening results for further survey. We utilized support vector machine (SVM), multiple linear regression (MLR) models and Bayesian network for validation of predicted activity. By overall analysis of docking results, predicted activity, and molecular dynamics (MD) simulation, we could conclude that Tetrahydropalmatine, Reserpiline, and (+)-Corydaline had better binding affinity than the control. All of them had the ability to inhibit the activity of CDK2 and might have the opportunity to be applied in melanoma therapy.
    Full-text · Article · Jun 2014
Show more