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Melanoma:Molecular genetics,metastasis,targeted therapies,immunotherapies,and therapeutic resistance 被引量:3
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作者 William Wagstaff Rimel N.Mwamba +12 位作者 Karina Grullon Mikhayla Armstrong Piao Zhao Bryce Hendren-Santiago Kevin H.Qin Alexander J.Li daniel a.hu Andrew Youssef Russell R.Reid Hue H.Luu Le Shen Tong-Chuan He Rex C.Haydon 《Genes & Diseases》 SCIE 2022年第6期1608-1623,共16页
Cutaneous melanoma is a common cancer and cases have steadily increased since the mid 70s.For some patients,early diagnosis and surgical removal of melanomas is lifesaving,while other patients typically turn to molecu... Cutaneous melanoma is a common cancer and cases have steadily increased since the mid 70s.For some patients,early diagnosis and surgical removal of melanomas is lifesaving,while other patients typically turn to molecular targeted therapies and immunotherapies as treatment options.Easy sampling of melanomas allows the scientific community to identify the most prevalent mutations that initiate melanoma such as the BRAF,NRAS,and TERT genes,some of which can be therapeutically targeted.Though initially effective,many tumors acquire resistance to the targeted therapies demonstrating the need to investigate compensatory pathways.Immunotherapies represent an alternative to molecular targeted therapies.However,inter-tumoral immune cell populations dictate initial therapeutic response and even tumors that responded to treatment develop resistance in the long term.As the protocol for combination therapies develop,so will our scientific understanding of the many pathways at play in the progression of melanoma.The future direction of the field may be to find a molecule that connects all of the pathways.Meanwhile,noncoding RNAs have been shown to play important roles in melanoma development and progression.Studying noncoding RNAs may help us to understand how resistance e both primary and acquired e develops;ultimately allow us to harness the true potential of current therapies.This review will cover the basic structure of the skin,the mutations and pathways responsible for transforming melanocytes into melanomas,the process by which melanomas metastasize,targeted therapeutics,and the potential that noncoding RNAs have as a prognostic and treatment tool. 展开更多
关键词 BRAF inhibitors Checkpoint inhibitors Drug resistance IMMUNOTHERAPY MELANOMA Melanoma metastasis Skin cancer Targeted therapy Therapeutic resistance
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SATB2:A versatile transcriptional regulator of craniofacial and skeleton development,neurogenesis and tumorigenesis,and its applications in regenerative medicine 被引量:2
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作者 Xia Huang Qiuman Chen +17 位作者 Wenping Luo Mikhail Pakvasa Yuxin Zhang Liwen Zheng Shuang Li Zhuohui Yang Huan Zeng Fang Liang Fugui Zhang daniel a.hu Kevin H.Qin Eric J.Wang David S.Qin Russell R.Reid Tong-Chuan He Aravind Athiviraham Mostafa El Dafrawy Hongmei Zhang 《Genes & Diseases》 SCIE 2022年第1期95-107,I0005,共14页
SATB2(special AT-rich sequence-binding protein 2)is a member of the special AT-rich binding protein family.As a transcription regulator,SATB2 mainly integrates higher-order chromatin organization.SATB2 expression appe... SATB2(special AT-rich sequence-binding protein 2)is a member of the special AT-rich binding protein family.As a transcription regulator,SATB2 mainly integrates higher-order chromatin organization.SATB2 expression appears to be tissue-and stage-specific,and is governed by several cellular signaling molecules and mediators.Expressed in branchial arches and osteoblast-lineage cells,SATB2 plays a significant role in craniofacial pattern and skeleton development.In addition to regulating osteogenic differentiation,SATB2 also displays versatile functions in neural development and cancer progression.As an osteoinductive factor,SATB2 holds great promise in improving bone regeneration toward bone defect repair.In this review,we have summarized our current understanding of the physiological and pathological functions of SATB2 in craniofacial and skeleton development,neurogenesis,tumorigenesis and regenerative medicine. 展开更多
关键词 Bone regeneration DEVELOPMENT NEUROGENESIS SATB2 TUMORIGENESIS
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