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A single-cell atlas characterizes dysregulation of the bone marrow immune microenvironment associated with outcomes in multiple myeloma.

William C PilcherLijun YaoEdgar Gonzalez-KozlovaYered Pita-JuarezDimitra KaragkouniChaitanya R AcharyaMarina E MichaudMark HamiltonShivani NandaYizhe SongKazuhito SatoJulia T WangSarthak SatpathyYuling MaJessica SchulmanDarwin D'SouzaReyka G JayasingheGiulia CheloniMojtaba BakhtiariNick PabustanKai NieJennifer A FoltzIsabella SaldarriagaRania AlaaeldinEva LepistoRachel ChenMark A FialaBeena E ThomasApril CookJunia Vieira Dos SantosI-Ling ChiangIgor FigueiredoJulie FortierMichael SladeStephen T OhMichael P RettigEmilie AndersonYing LiSurendra DasariMichael A StrausbauchVernadette A Simonnull nullAdeeb H RahmanZhihong ChenAlessandro LaganaJohn F DiPersioJacalyn RosenblattSeunghee Kim-SchulzeMadhav V DhodapkarSagar LonialShaji KumarManoj K BhasinTaxiarchis KourelisRavi VijDavid AviganHearn J ChoGeorge MulliganLi DingSacha GnjaticIoannis S VlachosManoj Bhasin
Published in: bioRxiv : the preprint server for biology (2024)
Multiple Myeloma (MM) remains incurable despite advances in treatment options. Although tumor subtypes and specific DNA abnormalities are linked to worse prognosis, the impact of immune dysfunction on disease emergence and/or treatment sensitivity remains unclear. We established a harmonized consortium to generate an Immune Atlas of MM aimed at informing disease etiology, risk stratification, and potential therapeutic strategies. We generated a transcriptome profile of 1,149,344 single cells from the bone marrow of 263 newly diagnosed patients enrolled in the CoMMpass study and characterized immune and hematopoietic cell populations. Associating cell abundances and gene expression with disease progression revealed the presence of a proinflammatory immune senescence-associated secretory phenotype in rapidly progressing patients. Furthermore, signaling analyses suggested active intercellular communication involving APRIL-BCMA, potentially promoting tumor growth and survival. Finally, we demonstrate that integrating immune cell levels with genetic information can significantly improve patient stratification.
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