Evidence map›Paper›PMID 39039072›Full record

ArticleCell discovery2024

Proteogenomic insights into the biology and treatment of pan-melanoma.

Hang Xiang, Rongkui Luo, Yunzhi Wang, Bing Yang, Sha Xu, Wen Huang, Shaoshuai Tang, Rundong Fang, Lingli Chen, Na Zhu and 9 more

Erratum issuedAbstract read
In one paragraph

Article in Cell discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors.

Hang Xiang *State Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Department of Plastic and Reconstructive Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Rongkui Luo *Department of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China.
Yunzhi Wang *State Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Department of Plastic and Reconstructive Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Bing Yang *State Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Department of Plastic and Reconstructive Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Sha Xu *State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.
Wen HuangDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China.
Shaoshuai TangState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Department of Plastic and Reconstructive Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Rundong FangState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Department of Plastic and Reconstructive Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Lingli ChenDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China.
Na ZhuDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China.
Zixiang YuDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China.
Sujie AkesuDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China.
Chuanyuan WeiDepartment of Plastic and Reconstructive Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0001-5580-6499
Chen XuDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China. xu.chen@zs-hospital.sh.cn.
Yuhong ZhouDepartment of Medical Oncology, Zhongshan Hospital, Fudan University, Shanghai, China. zhou.yuhong@zs-hospital.sh.cn.
Jianying GuDepartment of Plastic and Reconstructive Surgery, Zhongshan Hospital, Fudan University, Shanghai, China. gu.jianying@zs-hospital.sh.cn.
Jianyuan ZhaoInstitute for Developmental and Regenerative Cardiovascular Medicine, MOE-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. zhaojy@vip.163.com.
Yingyong HouDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China. hou.yingyong@zs-hospital.sh.cn.
Chen DingState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Department of Plastic and Reconstructive Surgery, Zhongshan Hospital, Fudan University, Shanghai, China. chend@fudan.edu.cn.ORCID http://orcid.org/0000-0001-8673-3464

Funding

China Postdoctoral Science Foundation 2023TQ0063; GZC20230524National Natural Science Foundation of China (National Science Foundation of China) 32201212National Natural Science Foundation of China (National Science Foundation of China) 32330062; 31972933National Natural Science Foundation of China (National Science Foundation of China) 82101750
6 · The paper itself

Abstract

Melanoma is one of the most prevalent skin cancers, with high metastatic rates and poor prognosis. Understanding its molecular pathogenesis is crucial for improving its diagnosis and treatment. Integrated analysis of multi-omics data from 207 treatment-naïve melanomas (primary-cutaneous-melanomas (CM, n = 28), primary-acral-melanomas (AM, n = 81), primary-mucosal-melanomas (MM, n = 28), metastatic-melanomas (n = 27), and nevi (n = 43)) provides insights into melanoma biology. Multivariate analysis reveals that PRKDC amplification is a prognostic molecule for melanomas. Further proteogenomic analysis combined with functional experiments reveals that the cis-effect of PRKDC amplification may lead to tumor proliferation through the activation of DNA repair and folate metabolism pathways. Proteome-based stratification of primary melanomas defines three prognosis-related subtypes, namely, the ECM subtype, angiogenesis subtype (with a high metastasis rate), and cell proliferation subtype, which provides an essential framework for the utilization of specific targeted therapies for particular melanoma subtypes. The immune classification identifies three immune subtypes. Further analysis combined with an independent anti-PD-1 treatment cohort reveals that upregulation of the MAPK7-NFKB signaling pathway may facilitate T-cell recruitment and increase the sensitivity of patients to immunotherapy. In contrast, PRKDC may reduce the sensitivity of melanoma patients to immunotherapy by promoting DNA repair in melanoma cells. These results emphasize the clinical value of multi-omics data and have the potential to improve the understanding of melanoma treatment.

Identifiers

PMID39039072
PMCPMC11263678

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.