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| 1 | Tom20 senses iron-activated ROS signaling to promote melanoma cell pyroptosis显示文摘Iron has been shown to trigger oxidative stress by elevating reactive oxygen species (ROS) and to participate in different modes of cell death,such as ferroptosis,apoptosis and necroptosis. However,whether iron-elevated ROS is also linked to pyroptosis has not been reported. Here,we demonstrate that iron-activated ROS can induce pyroptosis via a Tom20-Bax-caspase-GSDME pathway. In melanoma cells,iron enhanced ROS signaling initiated by CCCP,causing the oxidation and oligomerization of the mitochondrial outer membrane protein Tom20. Bax is recruited to mitochondria by oxidized Tom20,which facilitates cytochrome c release to cytosol to activate caspase-3;eventually triggering pyroptotic death by inducing GSDME cleavage. Therefore,ROS acts as a causative factor and Tom20 senses ROS signaling for iron-driven pyroptotic death of melanoma cells. Since iron activates ROS for GSDME-dependent pyroptosis induction and melanoma cells specifically express a high level of GSDME,iron may be a potential candidate for melanoma therapy. Based on the functional mechanism of iron shown above,we further demonstrate that iron supplementation at a dosage used in iron-deficient patients is sufficient to maximize the anti-tumor effect of clinical ROS-inducing drugs to inhibit xenograft tumor growth and metastasis of melanoma cells through GSDME-dependent pyroptosis. Moreover,no obvious side effects are observed in the normal tissues and organs of mice during the combined treatment of clinical drugs and iron. This study not only identifies iron as a sensitizer amplifying ROS signaling to drive pyroptosis,but also implicates a novel iron-based intervention strategy for melanoma therapy. | Bo Zhou Jia-yuan Zhang Xian-shuo Liu Hang-zi Chen Yuan-li Ai Kang Cheng Ru-yue Sun Dawang Zhou Jiahuai Han Qiao Wu | 2018 | Cell Research2018，28，12： | 52 |
| 2 | 免疫检查点抑制剂治疗中免疫相关不良反应的临床表现及处理显示文摘免疫检查点阻断治疗是当今备受瞩目的新兴肿瘤治疗方式。不同于以往其他治疗方式,免疫检查点抑制剂靶向机体免疫系统而非肿瘤细胞,旨在恢复并促进效应T细胞特异性识别和杀伤肿瘤细胞的功能,系统性增强全身的抗肿瘤免疫反应,因而代表了当前肿瘤治疗模式的转变。迄今多个临床试验已证实免疫检查点抑制剂在晚期黑色素瘤、 | 王巧红 吴霞(指导) | 2017 | 中国免疫学杂志2017，33，4： | 19 |
| 3 | Eukaryotic elongation factor-2 kinase regulates the cross-talk between autophagy and pyroptosis in doxorubicin-treated human melanoma cells in vitro显示文摘Eukaryotic elongation factor-2 kinase (eEF-2K), a negative regulator of protein synthesis, has been shown to play an important role in modulating autophagy and apoptosis in tumor cells under various stresses. In this study, we investigated the regulatory role of eEF-2K in pyroptosis (a new form of programmed necrosis) in doxorubicin-treated human melanoma cells. We found that doxorubicin (0.5-5 μmol/L) induced pyroptosis in melanoma cell lines SK-MEL-5, SK-MEL-28, and A-375 with high expression of DFNA5, but not in human breast cancer cell line MCF-7 with little expression of DFNA5. On the other hand, doxorubicin treatment activated autophagy in the melanoma cells;inhibition of autophagy by transfecting the cells with siRNA targeting Beclin1 or by pretreatment with chloroquine (20 μmol/L) significantly augmented pyroptosis, thus sensitizing the melanoma cells to doxorubicin. We further demonstrated that doxorubicin treatment activated eEF-2K in the melanoma cells, and silencing of eEF-2K blunted autophagic responses, but promoted doxorubicin-induced pyroptotic cell death. Taken together, the above results demonstrate that eEF-2K dictates the cross-talk between pyroptosis and autophagy in doxorubicin-treated human melanoma cells;suppression of eEF-2K results in inhibiting autophagy and augmenting pyroptosis, thus modulating the sensitivity of melanoma cells to doxorubicin, suggesting that targeting eEF-2K may reinforce the antitumor ef?cacy of doxorubicin, offering a new insight into tumor chemotherapy. | Pian Yu Hai-yan Wang Min Tian Ao-xue Li Xi-sha Chen Xin-luan Wang Yi Zhang Yan Cheng | 2019 | Acta Pharmacologica Sinica2019，40，9： | 19 |
| 4 | Primary hepatic epithelioid angiomyolipoma: A malignant potential tumor which should be recognized显示文摘AIM: To improve the clinical diagnosis and recognition of hepatic epithelioid angiomyolipoma(HEAML).METHODS: Four cases of primary HEAML were confirmed based on the pathology archive system in our hospital from January 2009 to November 2015. The general state, clinical symptoms, imaging manifestations, histological results and immunohistochemistry of these patients were retrospectively reviewed and analyzed. Studies of HEAML published in the last 15 years were collected from Pub Med and MEDLINE to summarize the clinical symptoms, imaging characteristics, pathological features and management of HEAML.RESULTS: Four cases of primary HEAML were retrieved from our archives. These included three female patients and one male patient, with a mean age of 41.8 ± 11.5 years(ranging from 31 to 56 years). The meantumor size was 7.3 ± 5.5 cm(ranging from 3.0 to 15 cm). In the contrast-enhanced imaging, the tumor was obviously enhanced in the arterial phase, but enhanced continuously or exhibited a slow-density masse during the venous and delayed phases. Histologically, the tumors mainly consisted of epithelioid cells that comprised approximately 95% of the total neoplastic mass. Although no metastases occurred in our patients, pathological studies revealed necrosis, mitotic figures and liver invasion in two patients, which indicates aggressive behavior. Immunohistochemical staining revealed that human melanoma black 45(HMB-45) and Melan-A were positive in 4 cases. We only identified 81 cases with primary HEAML, including our present patients, from 26 articles available from Pub Med and MEDLINE. The majority of the papers were published as case reports. Only 5(5/75, 6%) cases were associated with tuberous sclerosis complex(TSC). More than half(35/66) were discovered incidentally upon physical examination. Approximately 65%(22/34) of the patients were misdiagnosed with HCC or other tumors before surgery. Approximately 10%(8/81) of the patients with HEAML had recurrence or metastasis after surgery, which was a very high and alarming rate.CONCLUSION: HEAML is a very rare primary hepatic tumor that is often misdiagnosed before surgery. Patients should be followed closely after surgery because of its malignant potential. | Jie Liu Cheng-Wu Zhang De-Fei Hong Ran Tao Yuan Chen Min-Jie Shang Yu-Hua Zhang | 2016 | World Journal of Gastroenterology2016，22，20： | 18 |
| 5 | IDO1 in cancer: a Gemini of immune checkpoints显示文摘Indoleamine 2,3-dioxygenase 1(IDO1)is a rate-limiting metabolic enzyme that converts the essential amino acid tryptophan(Trp)into downstream catabolites known as kynurenines.Coincidently,numerous studies have demonstrated that IDO1 is highly expressed in multiple types of human cancer.Preclinical studies have further introduced an interesting paradox:while single-agent treatment with IDO1 enzyme inhibitor has a negligible effect on decreasing the established cancer burden,approaches combining select therapies with IDO1 blockade tend to yield a synergistic benefit against tumor growth and/or animal subject survival.Given the high expression of IDO1 among multiple cancer types along with the lack of monotherapeutic efficacy,these data suggest that there is a more complex mechanism of action than previously appreciated.Similar to the dual faces of the astrological Gemini,we highlight the multiple roles of IDO1 and review its canonical association with IDO1-dependent tryptophan metabolism,as well as documented evidence confirming the dispensability of enzyme activity for its immunosuppressive effects.The gene transcript levels for IDO1 highlight its strong association with T-cell infiltration,but the lack of a universal prognostic significance among all cancer subtypes.Finally,ongoing clinical trials are discussed with consideration of IDO1-targeting strategies that enhance the efficacy of immunotherapy for cancer patients。 | Lijie Zhai Erik Ladomersky Alicia Lenzen Brenda Nguyen Ricky Patel Kristen L Lauing Meijing Wu Derek A Wainwright | 2018 | Cellular & Molecular Immunology2018，15，5： | 17 |
| 6 | Endoplasmic reticulum stress-mediated pathways to both apoptosis and autophagy: Significance for melanoma treatment显示文摘Melanoma is the most aggressive form of skin cancer.Disrupted intracellular signaling pathways are responsible for melanoma's extraordinary resistance to current chemotherapeutic modalities. The pathophysiologic basis for resistance to both chemo- and radiation therapy is rooted in altered genetic and epigenetic mechanisms that, in turn, result in the impairing of cell death machinery and/or excessive activation of cell growth and survival-dependent pathways. Although most current melanoma therapies target mitochondrial dysregulation,there is increasing evidence that endoplasmic reticulum(ER) stress-associated pathways play a role in the potentiation,initiation and maintenance of cell death machinery and autophagy. This review focuses on the reliability of ER-associated pathways as therapeutic targets for melanoma treatment. | Mohamed Hassan Denis Selimovic Matthias Hannig Youssef Haikel Robert T Brodell Mossaad Megahed | 2015 | World Journal of Experimental Medicine2015，5，4： | 15 |
| 7 | The TLR7 agonists imiquimod and gardiquimod improve DC-based immunotherapy for melanoma in mice显示文摘Toll-like receptors(TLRs)are a family of highly conserved germline-encoded pattern-recognition receptors that are essential for host immune responses.TLR ligands represent a promising class of immunotherapeutics or vaccine adjuvants with the potential to generate an effective antitumor immune response.The TLR7/8 agonists have aroused interest because they not only activate antigen-presenting cells but also promote activation of T and natural killer(NK)cells.However,the exact mechanism by which stimulation of these TLRs promotes immune responses remains unclear,and different TLR7/8 agonists have been found to induce different responses.In this study,we demonstrate that both gardiquimod and imiquimod promote the proliferation of murine splenocytes,stimulate the activation of splenic T,NK and natural killer T(NKT)cells,increase the cytolytic activity of splenocytes against B16 and MCA-38 tumor cell lines,and enhance the expression of costimulatory molecules and IL-12 by macrophages and bone marrow-derived dendritic cells(DCs).In a murine model,both agonists improved the antitumor effects of tumor lysate-loaded DCs,resulting in delayed growth of subcutaneous B16 melanoma tumors and suppression of pulmonary metastasis.Further,we found that gardiquimod demonstrated more potent antitumor activity than imiquimod.These results suggest that TLR7/8 agonists may serve as potent innate and adaptive immune response modifiers in tumor therapy.More importantly,they can be used as vaccine adjuvants to potentiate the efficiency of DC-based tumor immunotherapy. | Fang Ma Jianhua Zhang Jian Zhang Cai Zhang | 2010 | Cellular & Molecular Immunology2010，7，5： | 13 |
| 8 | Boron delivery agents for neutron capture therapy of cancer显示文摘Boron neutron capture therapy(BNCT)is a binary radiotherapeutic modality based on the nuclear capture and fission reactions that occur when the stable isotope,boron-10,is irradiated with neutrons to produce high energy alpha particles.This review will focus on tumor-targeting boron delivery agents that are an essential component of this binary system.Two low molecular weight boron-containing drugs currently are being used clinically,boronopheny-lalanine(BPA)and sodium borocaptate(BSH).Although they are far from being ideal,their therapeutic efficacy has been demonstrated in patients with high grade gliomas,recurrent tumors of the head and neck region,and a much smaller number with cutaneous and extra-cutaneous melanomas.Because of their limitations,great effort has been expended over the past 40 years to develop new boron delivery agents that have more favorable biodistribution and uptake for clinical use.These include boron-containing porphyrins,amino acids,polyamines,nucleosides,peptides,monoclonal antibodies,liposomes,nanoparticles of various types,boron cluster compounds and co-polymers.Cur-rently,however,none of these have reached the stage where there is enough convincing data to warrant clinical biodistribution studies.Therefore,at present the best way to further improve the clinical efficacy of BNCT would be to optimize the dosing paradigms and delivery of BPA and BSH,either alone or in combination,with the hope that future research will identify new and better boron delivery agents for clinical use. | Rolf F.Barth Peng Mi Weilian Yang | 2018 | Cancer Communications2018，38，1： | 13 |
| 9 | Chinese guidelines for diagnosis and treatment of melanoma 2018(English version)显示文摘1. Overview2. Screening and diagnosis2.1 Surveillance and screening of high-risk population2.2 Diagnosis of melanoma2.2.1 Clinical symptoms2.2.2 Imaging diagnosis2.2.3 Laboratory tests2.2.4 Focus biopsy2.3 Pathological diagnosis of melanoma2.3.1 Criteria for pathological diagnosis2.3.2 Standard pathological diagnosis of melanoma2.3.3 Pathological report of melanoma2.4 Clinical diagnostic criteria and route map of melanoma3. Staging4. Treatment4.1 Surgical treatment4.1.1 Wide excision4.1.2 Sentinel lymph node biopsy (SLNB). | 无 | 2019 | Chinese Journal of Cancer Research2019，31，4： | 9 |
| 10 | Colonic ulcerations may predict steroid-refractory course in patients with ipilimumab-mediated enterocolitis显示文摘AIM To investigate management of patients who develop ipilimumab-mediated enterocolitis, including association of endoscopic findings with steroid-refractory symptoms and utility of infliximab as second-line therapy.METHODS We retrospectively reviewed all patients at our centerwith metastatic melanoma who were treated with ipilimumab between March 2011 and May 2014. All patients received a standard regimen of intravenous ipilimumab 3 mg/kg every 3 wk for four doses or until therapy was stopped due to toxicity or disease progression. Basic demographic and clinical data were collected on all patients. For patients who developed grade 2 or worse diarrhea(increase of 4 bowel movements per day), additional data were collected regarding details of gastrointestinal symptoms, endoscopic findings and treatment course. Descriptive statistics were used.RESULTS A total of 114 patients were treated with ipilimumab during the study period and all were included. Sixteen patients(14%) developed ≥ grade 2 diarrhea. All patients were treated with high-dose corticosteroids(1-2 mg/kg prednisone daily or equivalent). Nine of 16 patients(56%) had ongoing diarrhea despite highdose steroids. Steroid-refractory patients received one dose of intravenous infliximab at 5 mg/kg, and all but one had brisk resolution of diarrhea. Fourteen of the patients underwent either colonoscopy or sigmoidoscopy with variable endoscopic findings, ranging from mild erythema to colonic ulcers. Among 8 patients with ulcers demonstrated by sigmoidoscopy or colonoscopy, 7 patients(88%) developed steroidrefractory symptoms requiring infliximab. With a median follow-up of 264 d, no major adverse events associated with prednisone or infliximab were reported.CONCLUSION In patients with ipilimumab-mediated enterocolitis, the presence of colonic ulcers on endoscopy was associated with a steroid-refractory course. | Animesh Jain Evan J Lipson William H Sharfman Steven R Brant Mark G Lazarev | 2017 | World Journal of Gastroenterology2017，23，11： | 8 |
| 11 | Metastatic tumors to the pancreas: The role of surgery显示文摘Pancreatic metastases from other primary malignancies are a rare entity. By far, the most common primary cancer site resulting in an isolated pancreatic metastasis is the kidney, followed by colorectal cancer, melanoma, breast cancer, lung carcinoma and sarcoma. Only few data on the surgical outcome of pancreatic resections performed for metastases from other primary tumor have been published, and there are no guidelines to address the surgical treatment for these patients. In this study, we performed a review of the published literature, focusing on the early and long-term results of surgery for the most frequent primary tumors metastasizing to the pancreas. Results for the Literature's analysis show that in last years an increasing number of surgical resections have been performed in selected patients with limited pancreatic disease. Pancreatic resection for metastatic disease can be performed with acceptable mortality and morbidity rates. The usefulness of pancreatic resection is mainly linked to the biology of the primary tumor metastasizing to the pancreas. The benefit of metastasectomy in terms of patient survival has been observed for metastases from renal cell cancer, while for other primary tumors, such as lung and breast cancers, the role of surgery is mainly palliative. | Cosimo Sperti Lucia Moletta Giuseppe Patanè | 2014 | World Journal of Gastrointestinal Oncology2014，6，10： | 8 |
| 12 | Oncolytic adenovirus-mediated MDA-7/IL-24 overexpression enhances antitumor activity in hepatocellular carcinoma cell lines显示文摘BACKGROUND:Melanoma differentiation-associated gene-7 (MDA-7)/interleukin-24(IL-24)is a novel tumor suppressor gene,which has suppressor activity in a broad spectrum of human cancer cells.We investigated the effect of the replication-competent oncolytic adenovirus SG600-IL24 and replication-incompetent adenovirus Ad.IL-24,both expressing human MDA-7/IL-24 on the hepatocellular carcinoma cell lines HepG2,Hep3B,SMMC-7721,HCCLM3,and the normal liver cell line L02. METHODS:Hepatocellular carcinoma cell lines and the normal liver cell line were infected with SG600-IL24 and Ad.IL-24.The mRNA and protein expression of MDA-7/IL-24 in infected cells was confirmed by RT-PCR,ELISA,and Western blotting.MTT assay was used to investigate the proliferation effect.Hoechst staining and Annexin-V and PI staining were performed to study the MDA-7/IL-24 gene expressed in HCC cell lines and the normal liver cell line.Flow cytometry was used to analyse the cell cycle. RESULTS:RT-PCR,ELISA and Western blotting confirmed that the exogenous MDA-7/IL-24 gene was highly expressed in cells infected with SG600-IL24.MTT and apoptosis detection indicated that SG600-IL24 induced growth suppression promoted apoptosis,and blocked cancer cell lines in the G2/M phase in hepatocellular carcinoma cell lines but not in the normal liver cell line. CONCLUSIONS:SG600-IL24 selectively induces growth suppression and apoptosis in hepatocellular carcinoma cell lines in vitro but not in the normal liver cell line L02. Compared with Ad.IL-24,SG600-IL24 dramatically enhances antitumor activity in hepatocellular carcinoma cell lines. | Xiao, Chao-Wen Xue, Xin-Bo Zhang, Hui Gao, Wei Yu, Yuan Chen, Kun Zheng, Jian-Wei Wang, Cong-Jun | 2010 | Hepatobiliary & Pancreatic Diseases International2010，9，6： | 8 |
| 13 | Novel circular RNA expression profile of uveal melanoma revealed by microarray显示文摘Objective: The present study aimed to investigate circular RNA(circRNA) expression in uveal melanoma(UM).Methods: First,we used microarray to compare the expression profiles of circRNA in five UM samples and five normal uvea tissues.Next,bioinformatics analyses,including gene ontology(GO) analysis and pathway analysis,were applied to study these differentially expressed circRNAs to predict pathogenic pathways that may be involved.Quantitative real-time polymerase chain reaction(qRT-PCR) in 20 UM samples and 20 normal uvea samples was used to confirm the circRNA expression profiles obtained from the microarray data.Finally,we analyzed the interaction between validated circRNAs and their potential cancer-associated miRNA targets.Results: In total,50,579 circRNAs [fold change(FC) ≥2.0; P<0.05],including 20,654 up-regulated and 29,925 down-regulated circRNAs,were identified as differentially expressed between UM tissues and normal uvea tissues.We used qRT-PCR to verify seven dysregulated circRNAs indicated by the microarray data,including hsa_circ_0119873,hsa_circ_0128533,hsa_circ_0047924,hsa_circ_0103232,hsa-circRNA10628-6,hsa_circ_0032148 and hsa_circ_0133460,which may be promising candidates to study future molecular mechanisms.Conclusions: This study explored,for the first time,the abnormal expression of circRNAs in UM and described the expression profile of circRNAs,providing a new potential target for the mechanism of UM and future treatment of UM. | Xuan Yang Yang Li Yueming Liu Xiaolin Xu Yingzhi Wang Yanni Yan Wenjia Zhou Jingyan Yang Wenbin Wei | 2018 | Chinese Journal of Cancer Research2018，30，6： | 6 |
| 14 | Adenovirus vector expressing mda-7 selectively kills hepatocellular carcinoma cell line Hep3B显示文摘BACKGROUND:Melanoma differentiation associated gene-7(mda-7)is a novel tumor suppressor gene,which has suppressor activity in a broad spectrum of human cancer cells both in vitro and in vivo through activation of various intracellular signaling pathways.In this study, we investigated the potential effect of mda-7 on human hepatocellular carcinoma(HCC)in vitro. METHODS:Cells from the human HCC cell line Hep3B and the human liver cell line L-02 were assigned to three groups. One was cultured in Dulbecco's modified Eagle's medium without serum(control).The others were transfected with adenovirus expressing the mda-7 gene(Ad.mda-7)or adenovirus vector serving as negative control(Ad.vec).The expression of MDA-7 and Bcl-2 proteins in Hep3B and L-02 cells was confirmed by the reverse transcriptase-polymerase chain reaction and enzyme-linked immunosorbent assay. The methyl thiazolyl tetrazolium colorimetric assay and flow cytometry were used to assess tumor cell proliferation and the cell cycle.Hoechst and Annexin-V/propidium iodide staining were used to study mda-7 gene expression in Hep3B and L-02 cells.The expression of MDA-7,Bcl-2 and Bax proteins were detected by Western blotting.RESULTS:The mda-7 gene was expressed in Hep3B and L-02 cells.The protein concentrations of MDA-7 in supernatants were 790 and 810 pg/ml,respectively.mda-7 induced Hep3B growth suppression and apoptosis,compared with Ad.mda-7 and control(P<0.01).In addition,cell block in G2/M was identified by exposure of HCC cells to secreted MDA-7 protein,but this was not found in L-02.The gene expression of Bcl-2 was markedly decreased in Hep3B but not in L-02. CONCLUSIONS:mda-7 selectively induces growth inhibi- tion and apoptosis in the HCC cell line Hep3B but not in the normal liver cell line L-02 via downregulating the anti- apoptosis protein Bcl-2.It could be an ideal gene for gene therapy in HCC. | Xue, Xin-Bo Chen, Kun Wang, Cong-Jun Zheng, Jian-Wei Yu, Yuan Peng, Zhi-Hai Wu, Zai-De | 2008 | Hepatobiliary & Pancreatic Diseases International2008，7，5： | 6 |
| 15 | Galectin-1-mediated biochemical controls of melanoma and glioma aggressive behavior显示文摘Gliomas and melanomas are associated with dismal prognosis because of their marked intrinsic resistance to proapoptotic stimuli,such as conventional chemotherapy and radiotherapy,as well as their ability to escape immune cell attacks.In addition,gliomas and melanomas display pronounced neoangiogenesis.Galectin-1 is a hypoxia-sensitive protein,which is abundantly secreted by glioma and melanoma cells,which displays marked proangiogenic effects.It also provides immune tolerogenic environments to melanoma and glioma cells through the killing of activated T cells that attack these tumor cells.Galectin-1 protects glioma and melanoma cells against cytotoxic insults(including chemotherapy and radiotherapy) through a direct role in the unfolded protein response.Altogether,these facts clearly point to galectin-1 as an important target to be combated in gliomas and melanomas in order to:(1) weaken the defenses of these two types of cancers against radiotherapy,chemotherapy and immunotherapy/vaccine therapy;and(2) reinforce antiangiogenic therapies.In the present article,we review the biochemical and molecular biology-related pathways controlled by galectin-1,which are actually beneficial for melanoma and glioma cells,and therefore detrimental for melanoma and glioma patients. | Florence Lefranc Véronique Mathieu Robert Kiss | 2011 | World Journal of Biological Chemistry2011，2，9： | 6 |
| 16 | COX-2 as a potential biomarker and therapeutic target in melanoma显示文摘With a constantly increasing incidence,cutaneous melanoma has raised the need for a better understanding of its complex microenvironment that may further guide therapeutic options.Melanoma is a model tumor in immuno-oncology.Inflammation represents an important hallmark of cancer capable of inducing and sustaining tumor development.The inflammatory process also orchestrates the adaptative immunosuppression of tumor cells that helps them to evade immune destruction.Besides its role in proliferation,angiogenesis,and apoptosis,cyclooxygenase-2(COX-2)is a well-known promoter of immune suppression in melanoma.COX-2 inhibitors are closely involved in this condition.This review attempts to answer two controversial questions:is COX-2 a valuable prognostic factor?Among all COX-2 inhibitors,is celecoxib a suitable adjuvant in melanoma therapy? | Diana Valentina Tudor Ioana Baldea Mihai Lupu Teodor Kacso Eniko Kutasi Andreea Hopartean Roland Stretea Adriana Gabriela Filip | 2020 | Cancer Biology & Medicine2020，17，1： | 6 |
| 17 | Endoscopic submucosal dissection as excisional biopsy for anorectal malignant melanoma:A case report显示文摘BACKGROUND Anorectal malignant melanoma (AMM) is a rare disorder with an extremely poor prognosis. Although there is currently no consensus on the treatment methods for AMM, surgical procedures have been the most common treatment methods used until now. We recently encountered a case of AMM that we diagnosed using endoscopic submucosal dissection (ESD). To our knowledge, this is the first case of ESD for AMM, suggesting that ESD can potentially be a diagnostic and treatment method for AMM. CASE SUMMARY A 77-year-old woman visited our hospital with a chief complaint of anal bleeding and a palpable rectal mass. Colonoscopy revealed a 20-mm protruded lesion in the lower rectum. After obtaining biopsy specimens from the lesion, although a malignant rectal tumor was suspected, a definitive diagnosis was not made. Endoscopic ultrasonography revealed tumor invasion into the submucosal layer but not the muscular layer. Therefore, we performed an excisional biopsy using ESD. Immunohistochemical examination of the ESD-resected specimen revealed tumor cells positive for Human Melanin Black-45, Melan-A, and S-100. Moreover, the tumor cells lacked melanin pigment;thus, a diagnosis of amelanotic AMM was made. Although the AMM had massively invaded the submucosal layer and both lymphatic and venous invasion were present, we closely monitored the patient without any additional therapy on the basis of her request. Six months after ESD, local recurrence was detected, and the patient consented to wide local excision. CONCLUSION It is suggested that ESD is a potential diagnostic and treatment method for AMM. | Shigeo Manabe Yoshio Boku Michiyo Takeda Fumitaka Usui Ikuhiro Hirata Shuji Takahashi | 2019 | World Journal of Clinical Cases2019，7，13： | 6 |
| 18 | Novel biomarkers and therapeutic targets for optimizing the therapeutic management of melanomas显示文摘Cutaneous malignant melanoma is the most aggressive form of skin cancer with an extremely poor survival rate for the patients diagnosed with locally invasive and metastatic disease states. Intensive research has led in last few years to an improvement of the early detection and curative treatment of primary cutaneous melanomas that are confined to the skin by tumor surgical resection. However, locally advanced and disseminated melanomas are generally resistant to conventional treatments, including ionizing radiation, systemic chemotherapy, immunotherapy and/or adjuvant stem cellbased therapies, and result in the death of patients. The rapid progression of primary melanomas to locally invasive and/or metastatic disease states remains a major obstacle for an early effective diagnosis and a curative therapeutic intervention for melanoma patients. Importantly, recent advances in the melanoma research have led to the identification of different gene products that are often implicated in the malignant transforma-tion of melanocytic cells into melanoma cells, including melanoma stem/progenitor cells, during melanoma initiation and progression to locally advanced and metastatic disease states. The frequent deregulated genes products encompass the oncogenic B-Raf V600 E and N-RasQ 61 R mutants, different receptor tyrosine kinases and developmental pathways such as epidermal growth factor receptor(EGFR), stem cell-like factor(SCF) receptor KIT, hedgehog, Wnt/β-catenin, Notch, stromal cell-derived factor-1(SDF-1)/CXC chemokine receptor-4(CXCR4) and vascular endothelial growth factor(VEGF)/VEGFR receptor. These growth factors can cooperate to activate distinct tumorigenic downstream signaling elements and epithelial-mesenchymal transition(EMT)-associated molecules, including phosphatidylinositol 3'-kinase(PI3K)/Akt/ molecular target of rapamycin(mT OR), nuclear factor-kappaB(NF-κB), macrophage inhibitory cytokine-1(MIC-1), vimentin, snail and twist. Of therapeutic relevance, these deregulated signal transduction components constitute new potential biomarkers and therapeutic targets of great clinical interest for improving the efficacy of current diagnostic and prognostic methods and management of patients diagnosed with locally advanced, metastatic and/or relapsed melanomas. | Murielle Mimeault Surinder K Batra | 2012 | World Journal of Clinical Oncology2012，3，3： | 5 |
| 19 | Surgery for gastrointestinal malignant melanoma:Experience from surgical training center显示文摘AIM:To characterize clinical features,surgery,outcome,and survival of malignant melanoma(MM) of the gastrointestinal(GI) tract in a surgical training center in Bangkok,Thailand. METHODS:A retrospective review was performed for all patients with MM of the GI tract treated at our institution between 1997 and 2007. RESULTS:Fourteen patients had GI involvement either in a metastatic form or as a primary melanoma. Thirteen patients with sufficient data were reviewed. The median age of the patients was 66 years(range:32-87 years) .Ten patients were female and three were male.Seven patients had primary melanomas of the anal canal,stomach and the sigmoid colon(5,1 and 1 cases,respectively) .Seven patients underwent curative resections:three abdominoperineal resections,two wide local excisions,one total gastrectomy andone sigmoidectomy.Six patients had distant metastatic lesions at the time of diagnosis,which made curative resection an inappropriate choice.Patients who underwent curative resection exhibited a longer mean survival time(29.7 mo,range:10-96 mo) than did patients in the palliative group(4.8 mo,P=0.0006) . CONCLUSION:GI MM had an unfavorable prognosis,except in patients who underwent curative resection(53.8%of cases) ,who had a mean survival of 29.7 mo. | Thawatchai Akaraviputh Satida Arunakul Varut Lohsiriwat Cherdsak Iramaneerat Atthaphorn Trakarnsanga | 2010 | World Journal of Gastroenterology2010，16，6： | 5 |
| 20 | Detection of AFPmRNA and melanoma anti-gen gene-1mRNA as markers of disseminated hepatocellular carcinoma cells in blood显示文摘 | | 2005 | Hepatobiliary & Pancreatic Diseases International2005，4，2： | 5 |
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