LIVIVO - Search results -

Search results

Result 1 - 10 of total 40

Search options

Article ; Online: Promises and Challenges of Immunogenic Chemotherapy in Multiple Myeloma.

Johnstone, Megan / Vinaixa, Delaney / Turi, Marcello / Morelli, Eugenio / Anderson, Kenneth Carl / Gulla, Annamaria

2022 Volume 11, Issue 16

Abstract: Immunological tolerance of myeloma cells represents a critical obstacle in achieving long-term disease-free survival for multiple myeloma (MM) patients. Over the past two decades, remarkable preclinical efforts to understand MM biology have led to the ... ...

Abstract	Immunological tolerance of myeloma cells represents a critical obstacle in achieving long-term disease-free survival for multiple myeloma (MM) patients. Over the past two decades, remarkable preclinical efforts to understand MM biology have led to the clinical approval of several targeted and immunotherapeutic agents. Among them, it is now clear that chemotherapy can also make cancer cells "visible" to the immune system and thus reactivate anti-tumor immunity. This knowledge represents an important resource in the treatment paradigm of MM, whereas immune dysfunction constitutes a clear obstacle to the cure of the disease. In this review, we highlight the importance of defining the immunological effects of chemotherapy in MM with the goal of enhancing the clinical management of patients. This area of investigation will open new avenues of research to identify novel immunogenic anti-MM agents and inform the optimal integration of chemotherapy with immunotherapy.
MeSH term(s)	Humans ; Immunotherapy ; Multiple Myeloma
Language	English
Publishing date	2022-08-14
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11162519
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Article ; Online: DIS3

Haematologica

2024 Volume 109, Issue 1, Page(s) 231–244

Abstract: DIS3 gene mutations occur in approximately 10% of patients with multiple myeloma (MM); furthermore, DIS3 expression can be affected by monosomy 13 and del(13q), found in roughly 40% of MM cases. Despite the high incidence of DIS3 mutations and deletions, ...

Abstract	DIS3 gene mutations occur in approximately 10% of patients with multiple myeloma (MM); furthermore, DIS3 expression can be affected by monosomy 13 and del(13q), found in roughly 40% of MM cases. Despite the high incidence of DIS3 mutations and deletions, the biological significance of DIS3 and its contribution to MM pathogenesis remain poorly understood. In this study we investigated the functional role of DIS3 in MM, by exploiting a loss-of-function approach in human MM cell lines. We found that DIS3 knockdown inhibits proliferation in MM cell lines and largely affects cell cycle progression of MM plasma cells, ultimately inducing a significant increase in the percentage of cells in the G0/G1 phase and a decrease in the S and G2/M phases. DIS3 plays an important role not only in the control of the MM plasma cell cycle, but also in the centrosome duplication cycle, which are strictly co-regulated in physiological conditions in the G1 phase. Indeed, DIS3 silencing leads to the formation of supernumerary centrosomes accompanied by the assembly of multipolar spindles during mitosis. In MM, centrosome amplification is present in about a third of patients and may represent a mechanism leading to genomic instability. These findings strongly prompt further studies investigating the relevance of DIS3 in the centrosome duplication process. Indeed, a combination of DIS3 defects and deficient spindle-assembly checkpoint can allow cells to progress through the cell cycle without proper chromosome segregation, generating aneuploid cells which ultimately lead to the development of MM.
MeSH term(s)	Humans ; Multiple Myeloma/pathology ; Centrosome/metabolism ; Centrosome/pathology ; Mitosis ; Cell Cycle/genetics ; Genomic Instability ; Exosome Multienzyme Ribonuclease Complex/metabolism
Chemical Substances	DIS3 protein, human (EC 3.1.13.-) ; Exosome Multienzyme Ribonuclease Complex (EC 3.1.-)
Language	English
Publishing date	2024-01-01
Publishing country	Italy
Document type	Journal Article
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2023.283274
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uh III Zs.76: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: GPER1 Activation Exerts Anti-Tumor Activity in Multiple Myeloma.

Gallo Cantafio, Maria Eugenia / Torcasio, Roberta / Scionti, Francesca / Mesuraca, Maria / Ronchetti, Domenica / Pistoni, Mariaelena / Bellizzi, Dina / Passarino, Giuseppe / Morelli, Eugenio / Neri, Antonino / Viglietto, Giuseppe / Amodio, Nicola

Cells

2023 Volume 12, Issue 18

Abstract: G protein-coupled estrogen receptor 1 (GPER1) activation is emerging as a promising therapeutic strategy against several cancer types. While GPER targeting has been widely studied in the context of solid tumors, its effect on hematological malignancies ... ...

Abstract	G protein-coupled estrogen receptor 1 (GPER1) activation is emerging as a promising therapeutic strategy against several cancer types. While GPER targeting has been widely studied in the context of solid tumors, its effect on hematological malignancies remains to be fully understood. Here, we show that GPER1 mRNA is down-regulated in plasma cells from overt multiple myeloma (MM) and plasma cell leukemia patients as compared to normal donors or pre-malignant conditions (monoclonal gammopathy of undetermined significance and smoldering MM); moreover, lower GPER1 expression associates with worse overall survival of MM patients. Using the clinically applicable GPER1-selective agonist G-1, we demonstrate that the pharmacological activation of GPER1 triggered in vitro anti-MM activity through apoptosis induction, also overcoming the protective effects exerted by bone marrow stromal cells. Noteworthy, G-1 treatment reduced in vivo MM growth in two distinct xenograft models, even bearing bortezomib-resistant MM cells. Mechanistically, G-1 upregulated the miR-29b oncosuppressive network, blunting an established miR-29b-Sp1 feedback loop operative in MM cells. Overall, this study highlights the druggability of GPER1 in MM, providing the first preclinical framework for further development of GPER1 agonists to treat this malignancy.
MeSH term(s)	Humans ; Multiple Myeloma/drug therapy ; Multiple Myeloma/genetics ; Hematologic Neoplasms ; Smoldering Multiple Myeloma ; Plasma Cells ; MicroRNAs
Chemical Substances	MicroRNAs
Language	English
Publishing date	2023-09-07
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12182226
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: BRD9 Degradation Disrupts Ribosome Biogenesis in Multiple Myeloma.

Kurata, Keiji / Samur, Mehmet K / Liow, Priscilla / Wen, Kenneth / Yamamoto, Leona / Liu, Jiye / Morelli, Eugenio / Gulla, Annamaria / Tai, Yu-Tzu / Qi, Jun / Hideshima, Teru / Anderson, Kenneth C

Clinical cancer research : an official journal of the American Association for Cancer Research

2023 Volume 29, Issue 9, Page(s) 1807–1821

Abstract: Purpose: BRD9 is a defining component of the noncanonical SWI/SNF complex, which regulates gene expression by controlling chromatin dynamics. Although recent studies have found an oncogenic role for BRD9 in multiple cancer types including multiple ... ...

Abstract	Purpose: BRD9 is a defining component of the noncanonical SWI/SNF complex, which regulates gene expression by controlling chromatin dynamics. Although recent studies have found an oncogenic role for BRD9 in multiple cancer types including multiple myeloma, its clinical significance and oncogenic mechanism have not yet been elucidated. Here, we sought to identify the clinical and biological impact of BRD9 in multiple myeloma, which may contribute to the development of novel therapeutic strategies. Experimental design: We performed integrated analyses of BRD9 in vitro and in vivo using multiple myeloma cell lines and primary multiple myeloma cells in established preclinical models, which identified the molecular functions of BRD9 contributing to multiple myeloma cell survival. Results: We found that high BRD9 expression was a poor prognostic factor in multiple myeloma. Depleting BRD9 by genetic (shRNA) and pharmacologic (dBRD9-A; proteolysis-targeting chimera; BRD9 degrader) approaches downregulated ribosome biogenesis genes, decreased the expression of the master regulator MYC, and disrupted the protein-synthesis maintenance machinery, thereby inhibiting multiple myeloma cell growth in vitro and in vivo in preclinical models. Importantly, we identified that the expression of ribosome biogenesis genes was associated with the disease progression and prognosis of patients with multiple myeloma. Our results suggest that BRD9 promotes gene expression by predominantly occupying the promoter regions of ribosome biogenesis genes and cooperating with BRD4 to enhance the transcriptional function of MYC. Conclusions: Our study identifies and validates BRD9 as a novel therapeutic target in preclinical models of multiple myeloma, which provides the framework for the clinical evaluation of BRD9 degraders to improve patient outcome.
MeSH term(s)	Humans ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Multiple Myeloma/genetics ; Nuclear Proteins/genetics ; Ribosomes/genetics ; Ribosomes/metabolism ; Cell Cycle Proteins
Chemical Substances	Transcription Factors ; Nuclear Proteins ; BRD4 protein, human ; Cell Cycle Proteins ; BRD9 protein, human
Language	English
Publishing date	2023-02-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-22-3668
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4223: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: CRISPR Interference (CRISPRi) and CRISPR Activation (CRISPRa) to Explore the Oncogenic lncRNA Network.

Morelli, Eugenio / Gulla', Annamaria / Amodio, Nicola / Taiana, Elisa / Neri, Antonino / Fulciniti, Mariateresa / Munshi, Nikhil C

Methods in molecular biology (Clifton, N.J.)

2021 Volume 2348, Page(s) 189–204

Abstract: The human genome contains thousands of long noncoding RNAs (lncRNAs), even outnumbering protein-coding genes. These molecules can play a pivotal role in the development and progression of human disease, including cancer, and are susceptible to ... ...

Abstract	The human genome contains thousands of long noncoding RNAs (lncRNAs), even outnumbering protein-coding genes. These molecules can play a pivotal role in the development and progression of human disease, including cancer, and are susceptible to therapeutic intervention. Evidence of biologic function, however, is still missing for the vast majority of them. Both loss-of-function (LOF) and gain-of-function (GOF) studies are therefore necessary to advance our understanding of lncRNA networks and programs driving tumorigenesis. Here, we describe a protocol to perform lncRNA's LOF or GOF studies in multiple myeloma (MM) cells, using CRISPR interference (CRISPRi) or CRISPR activation (CRISPRa) technologies, respectively. These approaches have many advantages, including applicability to large-scale genetic screens in mammalian cells and possible reversibility of modulating effects; moreover, CRISPRa offers the unique opportunity to enhance lncRNA expression at the site of transcription, with relevant biologic implications.
MeSH term(s)	CRISPR-Cas Systems ; Cell Line, Tumor ; Clustered Regularly Interspaced Short Palindromic Repeats ; Gene Editing ; Gene Expression Regulation, Neoplastic ; Gene Regulatory Networks ; Genetic Vectors/genetics ; Humans ; Multiple Myeloma/genetics ; Mutation ; Oncogenes/genetics ; RNA, Guide, CRISPR-Cas Systems ; RNA, Long Noncoding/genetics ; Transduction, Genetic
Chemical Substances	RNA, Guide, CRISPR-Cas Systems ; RNA, Long Noncoding
Language	English
Publishing date	2021-06-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1581-2_13
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾
- Full text online
- Order with fees

Article ; Online: In Vitro Silencing of lncRNAs Using LNA GapmeRs.

Taiana, Elisa / Favasuli, Vanessa / Ronchetti, Domenica / Morelli, Eugenio / Tassone, Pierfrancesco / Viglietto, Giuseppe / Munshi, Nikhil C / Neri, Antonino / Amodio, Nicola

Methods in molecular biology (Clifton, N.J.)

2021 Volume 2348, Page(s) 157–166

Abstract: Despite substantial advancements have been achieved in the identification of long noncoding RNA (lncRNA) molecules, many challenges still remain into their functional characterization. Loss-of-function approaches are needed to study oncogenic lncRNAs, ... ...

Abstract	Despite substantial advancements have been achieved in the identification of long noncoding RNA (lncRNA) molecules, many challenges still remain into their functional characterization. Loss-of-function approaches are needed to study oncogenic lncRNAs, which appear more difficult to knock down by RNA interference as compared to mRNAs. In this chapter, we present a protocol based on the use of a novel class of antisense oligonucleotides, named locked nucleic acid (LNA) GapmeRs, to inhibit the oncogenic lncRNA NEAT1 in multiple myeloma cells. Overall, this approach holds many advantages, including its possible independence from delivery reagents as well as the capability to knock down lncRNAs even in hard-to-transfect suspension cells, like hematopoietic cells.
MeSH term(s)	Biomarkers, Tumor ; Cell Line, Tumor ; Electroporation ; Gene Knockdown Techniques ; Gene Silencing ; Humans ; Oligonucleotides ; RNA Interference ; RNA, Long Noncoding/genetics ; RNA, Messenger ; Transfection
Chemical Substances	Biomarkers, Tumor ; NEAT1 long non-coding RNA, human ; Oligonucleotides ; RNA, Long Noncoding ; RNA, Messenger ; locked nucleic acid
Language	English
Publishing date	2021-06-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1581-2_10
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾
- Full text online
- Order with fees

Article ; Online: Epigenetic regulation of CD38/CD48 by KDM6A mediates NK cell response in multiple myeloma.

Nature communications

2024 Volume 15, Issue 1, Page(s) 1367

Abstract: Anti-CD38 monoclonal antibodies like Daratumumab (Dara) are effective in multiple myeloma (MM); however, drug resistance ultimately occurs and the mechanisms behind this are poorly understood. Here, we identify, via two in vitro genome-wide CRISPR ... ...

Abstract	Anti-CD38 monoclonal antibodies like Daratumumab (Dara) are effective in multiple myeloma (MM); however, drug resistance ultimately occurs and the mechanisms behind this are poorly understood. Here, we identify, via two in vitro genome-wide CRISPR screens probing Daratumumab resistance, KDM6A as an important regulator of sensitivity to Daratumumab-mediated antibody-dependent cellular cytotoxicity (ADCC). Loss of KDM6A leads to increased levels of H3K27me3 on the promoter of CD38, resulting in a marked downregulation in CD38 expression, which may cause resistance to Daratumumab-mediated ADCC. Re-introducing CD38 does not reverse Daratumumab-mediated ADCC fully, which suggests that additional KDM6A targets, including CD48 which is also downregulated upon KDM6A loss, contribute to Daratumumab-mediated ADCC. Inhibition of H3K27me3 with an EZH2 inhibitor resulted in CD38 and CD48 upregulation and restored sensitivity to Daratumumab. These findings suggest KDM6A loss as a mechanism of Daratumumab resistance and lay down the proof of principle for the therapeutic application of EZH2 inhibitors, one of which is already FDA-approved, in improving MM responsiveness to Daratumumab.
MeSH term(s)	Humans ; Multiple Myeloma/drug therapy ; Multiple Myeloma/genetics ; Epigenesis, Genetic ; Histones/metabolism ; ADP-ribosyl Cyclase 1 ; Killer Cells, Natural
Chemical Substances	Histones ; ADP-ribosyl Cyclase 1 (EC 3.2.2.6)
Language	English
Publishing date	2024-02-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-45561-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Book: Scritti di Eugenio Morelli

Morelli, Eugenio

1964

Author's details	Eugenio Morelli
Language	Italian
Size	XVIII, 1034 S.
Publisher	Capelli
Publishing place	s.l.
Publishing country	Italy
Document type	Book
Remark	Bibliothek H. W. Knipping: 1990 A 245
HBZ-ID	HT011239257
Database	Catalogue ZB MED Medicine, Health

In stock of ZB MED Cologne/Königswinter

Shelf mark	Loan status	Location
1990 A 245	order for loan	Magazin

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Loss of GABARAP mediates resistance to immunogenic chemotherapy in multiple myeloma.

Gulla, Annamaria / Morelli, Eugenio / Johnstone, Megan / Turi, Marcello / Samur, Mehmet K / Botta, Cirino / Cifric, Selma / Folino, Pietro / Vinaixa, Delaney / Barello, Francesca / Clericuzio, Cole / Favasuli, Vanessa Katia / Maisano, Domenico / Talluri, Srikanth / Prabhala, Rao H / Bianchi, Giada / Fulciniti, Mariateresa / Wen, Kenneth / Kurata, Keiji /

Liu, Jiye / Penailillo, Johany / Bragoni, Alberto / Sapino, Anna / Richardson, Paul G / Chauhan, Dharminder / Carrasco, Ruben D / Hideshima, Teru / Munshi, Nikhil C / Anderson, Kenneth C

Blood

2024

Abstract: Immunogenic cell death (ICD) is a form of cell death by which cancer treatments can induce a clinically relevant anti-tumor immune response in a broad range of cancers. In multiple myeloma (MM), the proteasome inhibitor bortezomib is an ICD inducer and ... ...

Abstract	Immunogenic cell death (ICD) is a form of cell death by which cancer treatments can induce a clinically relevant anti-tumor 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 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 high-risk MM patients. GABARAP deletion impaired the exposure of the eat-me signal CRT on the surface of dying MM cells in vitro and in vivo, thus reducing tumor cell phagocytosis by dendritic cells and the subsequent anti-tumor T cell response. Low GABARAP was independently associated with shorter MM patient survival 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, like bortezomib, with an autophagy inducer, like rapamycin, may improve patient outcomes in MM, where low GABARAP in the form of del(17p) is common and leads to worse outcomes.
Language	English
Publishing date	2024-03-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2023022777
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uh III Zs.140: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 364: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: CDK7 controls E2F- and MYC-driven proliferative and metabolic vulnerabilities in multiple myeloma.

Blood

2023 Volume 141, Issue 23, Page(s) 2841–2852

Abstract: Therapeutic targeting of CDK7 has proven beneficial in preclinical studies, yet the off-target effects of currently available CDK7 inhibitors make it difficult to pinpoint the exact mechanisms behind MM cell death mediated by CDK7 inhibition. Here, we ... ...

Abstract	Therapeutic targeting of CDK7 has proven beneficial in preclinical studies, yet the off-target effects of currently available CDK7 inhibitors make it difficult to pinpoint the exact mechanisms behind MM cell death mediated by CDK7 inhibition. Here, we show that CDK7 expression positively correlates with E2F and MYC transcriptional programs in cells from patients with multiple myeloma (MM); its selective targeting counteracts E2F activity via perturbation of the cyclin-dependent kinases/Rb axis and impairs MYC-regulated metabolic gene signatures translating into defects in glycolysis and reduced levels of lactate production in MM cells. CDK7 inhibition using the covalent small-molecule inhibitor YKL-5-124 elicits a strong therapeutic response with minimal effects on normal cells, and causes in vivo tumor regression, increasing survival in several mouse models of MM including a genetically engineered mouse model of MYC-dependent MM. Through its role as a critical cofactor and regulator of MYC and E2F activity, CDK7 is therefore a master regulator of oncogenic cellular programs supporting MM growth and survival, and a valuable therapeutic target providing rationale for development of YKL-5-124 for clinical use.
MeSH term(s)	Animals ; Mice ; Cyclin-Dependent Kinase-Activating Kinase ; Cyclin-Dependent Kinases/genetics ; Cyclin-Dependent Kinases/metabolism ; Multiple Myeloma/genetics
Chemical Substances	Cyclin-Dependent Kinase-Activating Kinase (EC 2.7.11.22) ; Cyclin-Dependent Kinases (EC 2.7.11.22) ; Cdk7 protein, mouse
Language	English
Publishing date	2023-03-04
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2022018885
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uh III Zs.140: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 364: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito