Circulating tumor cells in myeloma are a compound biomarker for bone marrow high-risk genomic alterations and tumor load

作者
Cathelijne Fokkema,Luca Bertamini,Madelon M.E. de Jong,Sabrin Tahri,Davine Hofste op Bruinink,Zoltán Kellermayer,Natalie Papazian,Chelsea den Hollander,Michael Vermeulen,Elodie C.G. Stoetman,Gregory van Beek,Remco Hoogenboezem,Vincent H. J. van der Velden,Cyrille Hulin,Aurore Perrot,Philippe Moreau,Melissa Rowe,Diego Vieyra,Robin Carson,Mark van Duin
出处
期刊:Blood [Elsevier BV]
标识
DOI:10.1182/blood.2025030083
摘要

High levels of circulating tumor cells (CTC) are a powerful predictor of poor outcomes in newly diagnosed multiple myeloma, yet the mechanistic underpinnings of this correlation remain unknown. To investigate whether CTC-related pathobiology is driven by a specific circulating tumor cell subset, paired bone marrow and blood samples from newly-diagnosed multiple myeloma patients were analyzed by single-cell transcriptomics and whole-genome sequencing. This revealed that down to the individual clone level, CTCs and paired bone marrow cells are transcriptionally similar, without evidence for a distinct circulating population. In contrast, bone marrow myeloma cells from patients with high CTC levels showed increased proliferation and unbalanced primary genetic events, including enrichment for MAF and CCND translocations. To investigate impact of heterogenic genomic events on CTC levels, whole-exome and bulk-RNA sequencing from the MMRF CoMMpass dataset were analyzed and validated in our in-house datasets. Bone marrow tumor cells from patients with high CTC levels were uniformly characterized by transcriptomic signatures of proliferation. Additionally, CTC levels were uniquely dependent on primary genomic events, as well as high-risk secondary genomic events, including amplification1q, deletion1p, deletion13q, biallelic TP53 mutations, and increased APOBEC-induced mutations even in patients without MAF translocations. Finally, we developed a model that predicts the impact of genetic alterations and tumor burden on CTC levels. In sum, we show that CTC are the net result of tumor burden, primary translocations, and secondary genomic events, making CTC a powerful biomarker for genomics-driven high-risk disease in newly diagnosed myeloma patients.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
子不语完成签到,获得积分10
刚刚
吴梦丽完成签到,获得积分10
1秒前
雪梨完成签到,获得积分10
1秒前
keke完成签到 ,获得积分10
1秒前
Beton_X完成签到,获得积分10
1秒前
2秒前
KIVA完成签到,获得积分10
2秒前
3秒前
urologywang完成签到 ,获得积分10
3秒前
wang完成签到 ,获得积分10
3秒前
珍珠奶茶加芋圆完成签到,获得积分10
3秒前
wys完成签到,获得积分20
3秒前
YYY完成签到 ,获得积分10
3秒前
蓝天发布了新的文献求助30
3秒前
年糕完成签到,获得积分10
4秒前
ERIC完成签到,获得积分10
4秒前
4秒前
treasure完成签到,获得积分10
4秒前
认真幼萱应助PDD1235采纳,获得10
4秒前
小叶子完成签到,获得积分10
4秒前
火星上如松完成签到 ,获得积分10
5秒前
彦卿发布了新的文献求助10
5秒前
Starry完成签到,获得积分10
5秒前
Akim应助jkhjkhj采纳,获得10
5秒前
Minton完成签到,获得积分10
6秒前
Su完成签到,获得积分20
6秒前
Crazy完成签到 ,获得积分10
7秒前
东岭黄沙完成签到 ,获得积分10
7秒前
7秒前
7秒前
深情隶完成签到,获得积分10
7秒前
研友_8oYg4n发布了新的文献求助10
8秒前
东山完成签到,获得积分10
8秒前
saberLee完成签到,获得积分10
8秒前
一蓑烟雨完成签到,获得积分10
8秒前
4399完成签到,获得积分10
9秒前
czzlancer完成签到,获得积分0
9秒前
77发布了新的文献求助10
9秒前
9秒前
拼搏的黑夜完成签到,获得积分10
9秒前
高分求助中
Principles of Economics, 11th Edition 10000
University Physics with Modern Physics, 16th edition 10000
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Molecular Mechanisms of Photosynthesis, 4th Edition 1000
Organic Reactions, Volume 116 1000
Matrix Methods in Data Mining and Pattern Recognition 510
Social Skills Improvement System-Rating Scales--Chinese Version 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7253146
求助须知:如何正确求助?哪些是违规求助? 8875268
关于积分的说明 18735959
捐赠科研通 6933704
什么是DOI,文献DOI怎么找? 3199860
关于科研通互助平台的介绍 2374614
邀请新用户注册赠送积分活动 2174531