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Article ; Online: Normothermic Regional Perfusion in Controlled Donation After Circulatory Determination of Death Simultaneous Pancreas - Kidney Transplantation.

Gómez-Dueñas, Gonzalo / Durán, Manuel / Calleja-Lozano, Rafael / Arjona-Sánchez, Álvaro / Sánchez-Hidalgo, Juan Manuel / Rodríguez-Ortiz, Lidia / Ayllón-Terán, Maria Dolores / Campos-Hernández, Juan Pablo / Rodríguez-Benot, Alberto / Briceño, Javier

Transplantation proceedings

2023 Volume 55, Issue 10, Page(s) 2259–2261

Abstract: Background: Simultaneous pancreas-kidney transplantation is the optimal treatment for patients with type 1 diabetes and renal failure. The use of pancreas grafts from donation after circulatory death (DCD), using normothermic regional perfusion (NRP), ... ...

Abstract	Background: Simultaneous pancreas-kidney transplantation is the optimal treatment for patients with type 1 diabetes and renal failure. The use of pancreas grafts from donation after circulatory death (DCD), using normothermic regional perfusion (NRP), is still marginal worldwide, mainly due to possible additional risks of graft dysfunction and complications compared with grafts from donors after brain death. Methods: Case series of patients who underwent simultaneous pancreas-kidney transplantation after DCD-NRP between January 2018 and September 2022. This study evaluated early postoperative grafts and survival outcomes. Results: Four patients were included. One patient lost the pancreatic graft due to arterial thrombosis requiring transplantectomy. Another patient required a laparotomy due to hemoperitoneum. Overall, 1-year pancreas and kidney graft survival was 75% and 100%, respectively. One patient developed a lymphoma during the follow-up. Conclusion: The use of pancreas grafts from DCD after NRP preservation is safe and feasible. Comparative studies with donors after brain death grafts and larger series are required to confirm the feasibility of DCD-NRP pancreas transplantation.
MeSH term(s)	Humans ; Brain Death ; Kidney Transplantation/adverse effects ; Organ Preservation/adverse effects ; Perfusion ; Tissue Donors ; Graft Survival ; Pancreas ; Death ; Tissue and Organ Procurement ; Retrospective Studies
Language	English
Publishing date	2023-11-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	82046-5
ISSN	1873-2623 ; 0041-1345
ISSN (online)	1873-2623
ISSN	0041-1345
DOI	10.1016/j.transproceed.2023.09.007
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Article ; Online: Short- and Long-Term Intestinal Complications After Combined Pancreas-Kidney Transplantation.

Durán Martínez, Manuel / Calleja Lozano, Rafael / Arjona-Sánchez, Álvaro / Sánchez-Hidalgo, Juan Manuel / Ayllón Terán, María Dolores / Rodríguez-Ortiz, Lidia / Campos Hernández, Pablo / Rodríguez-Benot, Alberto / Briceño Delgado, Javier

Transplantation proceedings

2022

Abstract: Background: Simultaneous pancreas-kidney (SPK) transplantation is the treatment of choice in patients with type 1 diabetes and end-stage renal disease, because it improves survival and quality of life. Currently, enteric exocrine drainage is the most ... ...

Abstract	Background: Simultaneous pancreas-kidney (SPK) transplantation is the treatment of choice in patients with type 1 diabetes and end-stage renal disease, because it improves survival and quality of life. Currently, enteric exocrine drainage is the most commonly used method. Intestinal complications continue to be a major cause of posttransplant morbidity despite improvements in surgical technique. This study analyzed early and late intestinal complications related to SPK transplantation. Materials and methods: We performed a retrospective analysis of 100 adult patients undergoing SPK transplantation between January 2009 and December 2019. We performed systemic venous drainage and exocrine enteric drainage with duodenojejunostomy. Statistical analysis was performed using SPSS v2. This study was performed in accordance with the Declaration of Istanbul and the 1964 Declaration of Helsinki. Informed consent was obtained from all participants involved in the study. Results: Ten patients had the following early intestinal complications (10%): ileus (n = 4), intestinal obstruction (n = 2), graft volvulus (n = 1), duodenal graft fistula (n = 1), and jejunal fistula after pancreas transplantation (n = 1). Two cases required relaparotomy: graft repositioning with Roux-en-Y conversion (n = 1) and Y-roux conversion (n = 1). Eight patients had repeated episodes of intestinal obstruction (8%), of whom 2 required surgery for resolution with 100% postoperative mortality. Conclusions: SPK transplantation with enteric drainage via duodenojejunostomy has a low rate of short- and long-term postoperative intestinal complications. Surgery in patients with recurrent intestinal obstruction has a high mortality risk and should be performed in reference transplant centers.
Language	English
Publishing date	2022-10-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	82046-5
ISSN	1873-2623 ; 0041-1345
ISSN (online)	1873-2623
ISSN	0041-1345
DOI	10.1016/j.transproceed.2022.09.014
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Article: The p53 Family Members p63 and p73 Roles in the Metastatic Dissemination: Interactions with microRNAs and TGFβ Pathway.

Rodriguez Calleja, Lidia / Lavaud, Melanie / Tesfaye, Robel / Brounais-Le-Royer, Bénédicte / Baud'huin, Marc / Georges, Steven / Lamoureux, François / Verrecchia, Franck / Ory, Benjamin

Cancers

2022 Volume 14, Issue 23

Abstract: TP53 (TP53), p73 (TP73), and p63 (TP63) are members of the p53 transcription factor family, which has many activities spanning from embryonic development through to tumor suppression. The utilization of two promoters and alternative mRNA splicing has ... ...

Abstract	TP53 (TP53), p73 (TP73), and p63 (TP63) are members of the p53 transcription factor family, which has many activities spanning from embryonic development through to tumor suppression. The utilization of two promoters and alternative mRNA splicing has been shown to yield numerous isoforms in p53, p63, and p73. TAp73 is thought to mediate apoptosis as a result of nuclear accumulation following chemotherapy-induced DNA damage, according to a number of studies. Overexpression of the nuclear ΔNp63 and ΔNp73 isoforms, on the other hand, suppresses TAp73's pro-apoptotic activity in human malignancies, potentially leading to metastatic spread or inhibition. Another well-known pathway that has been associated to metastatic spread is the TGF pathway. TGFs are a family of structurally related polypeptide growth factors that regulate a variety of cellular functions including cell proliferation, lineage determination, differentiation, motility, adhesion, and cell death, making them significant players in development, homeostasis, and wound repair. Various studies have already identified several interactions between the p53 protein family and the TGFb pathway in the context of tumor growth and metastatic spread, beginning to shed light on this enigmatic intricacy.
Language	English
Publishing date	2022-12-01
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14235948
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Article ; Online: Influence of Donor and Recipient Sex Matching in Simultaneous Pancreas-Kidney Transplantation Outcomes.

Sánchez Hidalgo, Juan Manuel / Durán Martínez, Manuel / Calleja Lozano, Rafael / Arjona Sánchez, Álvaro / Ayllón Terán, María Dolores / Rodríguez Ortiz, Lidia / Campos Hernández, Pablo / Rodríguez Benot, Alberto / Briceño Delgado, Francisco Javier

Transplantation proceedings

2021 Volume 53, Issue 9, Page(s) 2688–2691

Abstract: Background: Several studies in solid organ transplantation have shown a correlation between donor and recipient sex mismatch and risk of graft loss; however, it is possible influence is not well established. The aim of our study was to review the ... ...

Abstract	Background: Several studies in solid organ transplantation have shown a correlation between donor and recipient sex mismatch and risk of graft loss; however, it is possible influence is not well established. The aim of our study was to review the outcomes of pancreatic and kidney grafts in our series depending on sex matching. Methods: We retrospectively analyzed a cohort of 199 patients who underwent simultaneous pancreas-kidney transplantation from February 1989 to June 2019 at the Reina Sofia University Hospital. Results: Survival of patients in the series was 93.5% at 5 years, 84.3% at 10 years, and 71.5% at 15 years. In the sex-discordant group, survival of patients in the series at 5, 10, and 15 years was 94%, 82.3%, and 71.7% compared with 92.3%, 85.1%, and 72.2% in the concordant group, with no statistically significant differences (P = .86). Pancreatic graft survival censored for death at 5, 10, and 15 years was 79.5%, 60.8%, and 57.5% in the group with discordant sex vs 77.5%, 67.8%, and 65.5% in the concordant group, finding no statistically significant differences (P = .54). Kidney graft survival censored for death at 5, 10, and 15 years was 89.3%, 85%, and 78.1% in the sex-discordant group vs 87.3%, 83.5%. and 78.8% in the concordant group, with no differences (P = .69). No differences were observed between the 2 groups in the rate of serious postoperative complications or acute rejection. Conclusion: Our study shows that donor-recipient sex mismatch in simultaneous pancreas-kidney transplantation does not negatively influence perioperative outcomes and survival of the patient and both grafts.
MeSH term(s)	Female ; Graft Rejection ; Graft Survival ; Humans ; Kidney Transplantation/adverse effects ; Male ; Pancreas ; Pancreas Transplantation/adverse effects ; Retrospective Studies ; Tissue Donors
Language	English
Publishing date	2021-10-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	82046-5
ISSN	1873-2623 ; 0041-1345
ISSN (online)	1873-2623
ISSN	0041-1345
DOI	10.1016/j.transproceed.2021.09.004
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Article ; Online: Circulating Tumor Cells: A Review of Non-EpCAM-Based Approaches for Cell Enrichment and Isolation.

Gabriel, Marta Tellez / Calleja, Lidia Rodriguez / Chalopin, Antoine / Ory, Benjamin / Heymann, Dominique

Clinical chemistry

2016 Volume 62, Issue 4, Page(s) 571–581

Abstract: Background: Circulating tumor cells (CTCs) are biomarkers for noninvasively measuring the evolution of tumor genotypes during treatment and disease progression. Recent technical progress has made it possible to detect and characterize CTCs at the single- ...

Abstract	Background: Circulating tumor cells (CTCs) are biomarkers for noninvasively measuring the evolution of tumor genotypes during treatment and disease progression. Recent technical progress has made it possible to detect and characterize CTCs at the single-cell level in blood. Content: Most current methods are based on epithelial cell adhesion molecule (EpCAM) detection, but numerous studies have demonstrated that EpCAM is not a universal marker for CTC detection because it fails to detect both carcinoma cells that undergo epithelial-mesenchymal transition (EMT) and CTCs of mesenchymal origin. Moreover, EpCAM expression has been found in patients with benign diseases. A large proportion of the current studies and reviews about CTCs describe EpCAM-based methods, but there is evidence that not all tumor cells can be detected using this marker. Here we describe the most recent EpCAM-independent methods for enriching, isolating, and characterizing CTCs on the basis of physical and biological characteristics and point out the main advantages and disadvantages of these methods. Summary: CTCs offer an opportunity to obtain key biological information required for the development of personalized medicine. However, there is no universal marker of these cells. To strengthen the clinical utility of CTCs, it is important to improve existing technologies and develop new, non-EpCAM-based systems to enrich and isolate CTCs.
MeSH term(s)	Antigens, Neoplasm/blood ; Biomarkers, Tumor/blood ; Cell Adhesion Molecules/blood ; Cell Separation ; Epithelial Cell Adhesion Molecule ; Epithelial-Mesenchymal Transition ; Humans ; Neoplastic Cells, Circulating/chemistry ; Neoplastic Cells, Circulating/metabolism ; Single-Cell Analysis
Chemical Substances	Antigens, Neoplasm ; Biomarkers, Tumor ; Cell Adhesion Molecules ; EPCAM protein, human ; Epithelial Cell Adhesion Molecule
Language	English
Publishing date	2016-02-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80102-1
ISSN	1530-8561 ; 0009-9147
ISSN (online)	1530-8561
ISSN	0009-9147
DOI	10.1373/clinchem.2015.249706
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Article ; Online: Alternaria infectoria skin infection in a renal transplant recipient: an emerging phaeohyphomycosis of occidental countries?

Aragón-Miguel, Raquel / Calleja-Algarra, Alba / Morales-Raya, Carlos / López-Medrano, Francisco / Pérez-Ayala, Ana / Rodríguez-Peralto, Jose L / Ortiz-Romero, Pablo L / Maroñas-Jiménez, Lidia

International journal of dermatology

2017 Volume 56, Issue 7, Page(s) e153–e155

MeSH term(s)	Aged ; Alternariosis/immunology ; Alternariosis/pathology ; Alternariosis/therapy ; Antifungal Agents/therapeutic use ; Biopsy, Needle ; Combined Modality Therapy ; Communicable Diseases, Emerging/diagnosis ; Communicable Diseases, Emerging/epidemiology ; Communicable Diseases, Emerging/therapy ; Dermatologic Surgical Procedures/methods ; Europe ; Female ; Humans ; Immunocompromised Host/immunology ; Immunohistochemistry ; Kidney Transplantation/methods ; Lower Extremity ; Opportunistic Infections/diagnosis ; Opportunistic Infections/immunology ; Phaeohyphomycosis/pathology ; Phaeohyphomycosis/therapy ; Prognosis ; Treatment Outcome
Chemical Substances	Antifungal Agents
Language	English
Publishing date	2017-02-27
Publishing country	England
Document type	Case Reports ; Letter ; Review
ZDB-ID	412254-9
ISSN	1365-4632 ; 0011-9059 ; 1461-1244
ISSN (online)	1365-4632
ISSN	0011-9059 ; 1461-1244
DOI	10.1111/ijd.13563
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Article ; Online: miRNA-193a-5p repression of p73 controls Cisplatin chemoresistance in primary bone tumors.

Jacques, Camille / Calleja, Lidia Rodriguez / Baud'huin, Marc / Quillard, Thibaut / Heymann, Dominique / Lamoureux, François / Ory, Benjamin

Oncotarget

2016 Volume 7, Issue 34, Page(s) 54503–54514

Abstract: Osteosarcoma and Ewing Sarcoma are the two most common types of Bone Sarcomas, principally localized at the long bones of the extremities and mainly affecting adolescents and young adults. Cisplatin is one of the current options in the therapeutic ... ...

Abstract	Osteosarcoma and Ewing Sarcoma are the two most common types of Bone Sarcomas, principally localized at the long bones of the extremities and mainly affecting adolescents and young adults. Cisplatin is one of the current options in the therapeutic arsenal of drugs available to cure these aggressive cancers. Unfortunately, chemoresistance against this agent is still a major cause of patient relapse. Thus, a better understanding of the molecular pathways by which these drugs induce cancer cell death, together with a better delineation of the origins of chemoresistance are required to improve the success rate of current treatments. Furthermore, as p53 is frequently mutated in Bone Sarcomas, other pathways in these cancers must mediate drug-induced cell death. Here, we demonstrate for the first time that TAp73β, a p53-family protein, is implicated in Cisplatin-induced apoptosis of Bone Sarcomas'. Furthermore, while acquired resistance developed by cancer cells against such drugs can have multiple origins, it is now well accepted that epigenetic mechanisms involving microRNAs (miRNAs) are one of them. We show that miRNA-193a-5p modulates the viability, the clonogenic capacity and the Cisplatin-induced apoptosis of the Bone Sarcoma cells through inhibition of TAp73β. Collectively, these results shed light on the involvement of miR-193a-5p in Cisplatin chemoresistance of Bone Sarcomas', and they open the road to new therapeutic opportunities provided by targeting the miR-193a-5p/TAp73β axis in the context of these malignancies.
MeSH term(s)	Antineoplastic Agents/therapeutic use ; Bone Neoplasms/drug therapy ; Bone Neoplasms/pathology ; Cell Line, Tumor ; Cisplatin/pharmacology ; Cisplatin/therapeutic use ; Drug Resistance, Neoplasm ; Humans ; MicroRNAs/physiology ; Osteosarcoma/drug therapy ; Osteosarcoma/pathology ; Tumor Protein p73/physiology ; Tumor Suppressor Protein p53/physiology
Chemical Substances	Antineoplastic Agents ; MIRN193 microRNA, human ; MicroRNAs ; TP53 protein, human ; TP73 protein, human ; Tumor Protein p73 ; Tumor Suppressor Protein p53 ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2016-08-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.10950
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Article ; Online: Inhibition of BET proteins and epigenetic signaling as a potential treatment for osteoporosis.

Baud'huin, Marc / Lamoureux, François / Jacques, Camille / Rodriguez Calleja, Lidia / Quillard, Thibaut / Charrier, Céline / Amiaud, Jérome / Berreur, Martine / Brounais-LeRoyer, Bénédicte / Owen, Robert / Reilly, Gwendolen C / Bradner, James E / Heymann, Dominique / Ory, Benjamin

Bone

2017 Volume 94, Page(s) 10–21

Abstract: Histone modifications are important for maintaining the transcription program. BET proteins, an important class of "histone reading proteins", have recently been described as essential in bone biology. This study presents the therapeutic opportunity of ... ...

Abstract	Histone modifications are important for maintaining the transcription program. BET proteins, an important class of "histone reading proteins", have recently been described as essential in bone biology. This study presents the therapeutic opportunity of BET protein inhibition in osteoporosis. We find that the pharmacological BET protein inhibitor JQ1 rescues pathologic bone loss in a post-ovariectomy osteoporosis model by increasing the trabecular bone volume and restoring mechanical properties. The BET protein inhibition suppresses osteoclast differentiation and activity as well as the osteoblastogenesis in vitro. Moreover, we show that treated non-resorbing osteoclasts could still activate osteoblast differentiation. In addition, specific inhibition of BRD4 using RNA interference inhibits osteoclast differentiation but strongly activates osteoblast mineralization activity. Mechanistically, JQ1 inhibits expression of the master osteoclast transcription factor NFATc1 and the transcription factor of osteoblast Runx2. These findings strongly support that targeting epigenetic chromatin regulators such as BET proteins may offer a promising alternative for the treatment of bone-related disorders such as osteoporosis.
Language	English
Publishing date	2017-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	632515-4
ISSN	1873-2763 ; 8756-3282
ISSN (online)	1873-2763
ISSN	8756-3282
DOI	10.1016/j.bone.2016.09.020
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Zs.A 1571: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Targeting the epigenetic readers in Ewing sarcoma inhibits the oncogenic transcription factor EWS/Fli1.

Jacques, Camille / Lamoureux, François / Baud'huin, Marc / Rodriguez Calleja, Lidia / Quillard, Thibaut / Amiaud, Jérôme / Tirode, Franck / Rédini, Françoise / Bradner, James E / Heymann, Dominique / Ory, Benjamin

Oncotarget

2016 Volume 7, Issue 17, Page(s) 24125–24140

Abstract: Ewing Sarcoma is a rare bone and soft tissue malignancy affecting children and young adults. Chromosomal translocations in this cancer produce fusion oncogenes as characteristic molecular signatures of the disease. The most common case is the ... ...

Abstract	Ewing Sarcoma is a rare bone and soft tissue malignancy affecting children and young adults. Chromosomal translocations in this cancer produce fusion oncogenes as characteristic molecular signatures of the disease. The most common case is the translocation t (11; 22) (q24;q12) which yields the EWS-Fli1 chimeric transcription factor. Finding a way to directly target EWS-Fli1 remains a central therapeutic approach to eradicate this aggressive cancer. Here we demonstrate that treating Ewing Sarcoma cells with JQ1(+), a BET bromodomain inhibitor, represses directly EWS-Fli1 transcription as well as its transcriptional program. Moreover, the Chromatin Immuno Precipitation experiments demonstrate for the first time that these results are a consequence of the depletion of BRD4, one of the BET bromodomains protein from the EWS-Fli1 promoter. In vitro, JQ1(+) treatment reduces the cell viability, impairs the cell clonogenic and the migratory abilities, and induces a G1-phase blockage as well as a time- and a dose-dependent apoptosis. Furthermore, in our in vivo model, we observed a tumor burden delay, an inhibition of the global vascularization and an increase of the mice overall survival. Taken together, our data indicate that inhibiting the BET bromodomains interferes with EWS-FLi1 transcription and could be a promising strategy in the Ewing tumors context.
Language	English
Publishing date	2016-04-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.8214
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Article ; Online: Selective inhibition of BET bromodomain epigenetic signalling interferes with the bone-associated tumour vicious cycle.

Lamoureux, François / Baud'huin, Marc / Rodriguez Calleja, Lidia / Jacques, Camille / Berreur, Martine / Rédini, Françoise / Lecanda, Fernando / Bradner, James E / Heymann, Dominique / Ory, Benjamin

Nature communications

2014 Volume 5, Page(s) 3511

Abstract: The vicious cycle established between bone-associated tumours and bone resorption is the central problem with therapeutic strategies against primary bone tumours and bone metastasis. Here we report data to support inhibition of BET bromodomain proteins ... ...

Abstract	The vicious cycle established between bone-associated tumours and bone resorption is the central problem with therapeutic strategies against primary bone tumours and bone metastasis. Here we report data to support inhibition of BET bromodomain proteins as a promising therapeutic strategy that target simultaneously the three partners of the vicious cycle. Treatment with JQ1, a BET bromodomain inhibitor, reduces cell viability of osteosarcoma cells and inhibits osteoblastic differentiation both in vitro and in vivo. These effects are associated with transcriptional silencing of MYC and RUNX2, resulting from the depletion of BRD4 from their respective loci. Moreover, JQ1 also inhibits osteoclast differentiation by interfering with BRD4-dependent RANKL activation of NFATC1 transcription. Collectively, our data indicate that JQ1 is a potent inhibitor of osteoblast and osteoclast differentiation as well as bone tumour development.
MeSH term(s)	Adolescent ; Adult ; Aged ; Aged, 80 and over ; Animals ; Azepines/pharmacology ; Blotting, Western ; Bone Neoplasms/genetics ; Bone Neoplasms/pathology ; Bone Neoplasms/prevention & control ; Cell Line, Tumor ; Epigenesis, Genetic ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Male ; Mice ; Mice, Inbred C3H ; Mice, Nude ; Middle Aged ; Nuclear Proteins/genetics ; Osteosarcoma/genetics ; Osteosarcoma/pathology ; Osteosarcoma/prevention & control ; Proto-Oncogene Proteins c-myc/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Transcription Factors/genetics ; Triazoles/pharmacology ; Xenograft Model Antitumor Assays ; Young Adult
Chemical Substances	(+)-JQ1 compound ; Azepines ; BRD4 protein, human ; Nuclear Proteins ; Proto-Oncogene Proteins c-myc ; Transcription Factors ; Triazoles
Language	English
Publishing date	2014-03-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2041-1723
ISSN (online)	2041-1723
DOI	10.1038/ncomms4511
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