{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,7]],"date-time":"2026-11-07T04:05:45Z","timestamp":1794024345564,"version":"4.8.0"},"reference-count":82,"publisher":"American Society of Hematology","issue":"25","license":[{"start":{"date-parts":[[2024,3,29]],"date-time":"2024-03-29T00:00:00Z","timestamp":1711670400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2024,6,20]]},"abstract":"<jats:sec>\n                  <jats:title>Abstract<\/jats:title>\n                  <jats:p>Immunogenic cell death (ICD) is a form of cell death by which cancer treatments can induce a clinically relevant antitumor immune response in a broad range of cancers. In multiple myeloma (MM), the proteasome inhibitor bortezomib is an ICD inducer and creates durable therapeutic responses in patients. However, eventual relapse and resistance to bortezomib appear inevitable. Here, by integrating patient transcriptomic data with an analysis of calreticulin (CRT) protein interactors, we found that GABA type A receptor\u2013associated protein (GABARAP) is a key player whose loss prevented tumor cell death from being perceived as immunogenic after bortezomib treatment. GABARAP is located on chromosome 17p, which is commonly deleted in patients with high risk MM. GABARAP deletion impaired the exposure of the eat-me signal CRT on the surface of dying MM cells in\u00a0vitro and in\u00a0vivo, thus reducing tumor cell phagocytosis by dendritic cells and the subsequent antitumor T-cell response. Low GABARAP was independently associated with shorter survival in patients with MM and reduced tumor immune infiltration. Mechanistically, we found that GABARAP deletion blocked ICD signaling by decreasing autophagy and altering Golgi apparatus morphology, with consequent defects in the downstream vesicular transport of CRT. Conversely, upregulating autophagy using rapamycin restored Golgi morphology, CRT exposure, and ICD signaling in GABARAPKO cells undergoing bortezomib treatment. Therefore, coupling an ICD inducer, such as bortezomib, with an autophagy inducer, such as rapamycin, may improve patient outcomes in MM, in which low GABARAP in the form of del(17p) is common and leads to worse outcomes.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1182\/blood.2023022777","type":"journal-article","created":{"date-parts":[[2024,3,29]],"date-time":"2024-03-29T16:12:29Z","timestamp":1711728749000},"page":"2612-2626","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":25,"title":["Loss of GABARAP mediates resistance to immunogenic chemotherapy in multiple myeloma"],"prefix":"10.1182","volume":"143","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4569-0095","authenticated-orcid":false,"given":"Annamaria","family":"Gulla","sequence":"first","affiliation":[{"name":"1Department of Medical Oncology, Candiolo Cancer Institute, Fondazione del Piemonte per l'Oncologia-IRCCS, Candiolo, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8850-0442","authenticated-orcid":false,"given":"Eugenio","family":"Morelli","sequence":"additional","affiliation":[{"name":"1Department of Medical Oncology, Candiolo Cancer Institute, Fondazione del Piemonte per l'Oncologia-IRCCS, Candiolo, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Megan","family":"Johnstone","sequence":"additional","affiliation":[{"name":"2Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8760-1794","authenticated-orcid":false,"given":"Marcello","family":"Turi","sequence":"additional","affiliation":[{"name":"1Department of Medical Oncology, Candiolo Cancer Institute, Fondazione del Piemonte per l'Oncologia-IRCCS, Candiolo, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9978-5682","authenticated-orcid":false,"given":"Mehmet K.","family":"Samur","sequence":"additional","affiliation":[{"name":"2Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA"},{"name":"3Department of Data Sciences, Dana-Farber Cancer Institute, Boston, MA"},{"name":"4Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1522-4504","authenticated-orcid":false,"given":"Cirino","family":"Botta","sequence":"additional","affiliation":[{"name":"5Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties, University of Palermo, Palermo, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-7993-8639","authenticated-orcid":false,"given":"Selma","family":"Cifric","sequence":"additional","affiliation":[{"name":"2Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pietro","family":"Folino","sequence":"additional","affiliation":[{"name":"2Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, 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