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52. Contributors

Author

Akanksha, Samuel, primary, Allione, Alessandra, additional, Álvarez-Perez, Juan Carlos, additional, Andrades, Alvaro, additional, Arenas, Alberto M., additional, Baliñas-Gavira, Carlos, additional, Barth, Dominik A., additional, Bielowski, Anna, additional, Biswas, Roopa, additional, Boeri, Mattia, additional, Broseghini, Elisabetta, additional, Calin, George A., additional, Calura, Enrica, additional, Casalone, Elisabetta, additional, Constâncio, Vera, additional, Cosentino, Giulia, additional, Costa, Marina C., additional, Croce, Carlo M., additional, Cuadros, Marta, additional, Cutucache, Christine E., additional, Davidson, Ben, additional, Dika, Emi, additional, Dilmac, Sayra, additional, Dragomir, Mihnea P., additional, Drula, Rares, additional, Enguita, Francisco J., additional, Feng, Zhaohui, additional, Ferracin, Manuela, additional, Fornari, Francesca, additional, Fortunato, Orazio, additional, Gabriel, André F., additional, García, Daniel J., additional, Gramantieri, Laura, additional, Henrique, Rui, additional, Hu, Wenwei, additional, Iorio, Marilena V., additional, Jerónimo, Carmen, additional, Kamboj, Sakshi, additional, Kumar, Manoj, additional, Lawrie, Charles Henderson, additional, Leitão, Ana Lúcia, additional, Liu, Juan, additional, Lovat, Francesca, additional, Masatti, Laura, additional, Matullo, Giuseppe, additional, Medina, Pedro P., additional, Mohapatra, Swati, additional, Moisoiu, Vlad, additional, Negrini, Massimo, additional, Nguyen, Vu Hong Loan, additional, Anderson O’Brien, Jacob, additional, Ozpolat, Bulent, additional, Pardini, Barbara, additional, Patiño-Mercau, Juan Rodrigo, additional, Pazzaglia, Laura, additional, Peinado, Paola, additional, Pekarsky, Yuri, additional, Peng, Chun, additional, Petrescu, George E.D., additional, Pichler, Martin, additional, Plantamura, Ilaria, additional, Reich, Reuven, additional, Rodriguez, Maria Isabel, additional, Romualdi, Chiara, additional, Sanjuan-Hidalgo, Juan, additional, Scotlandi, Katia, additional, Shankaraiah, Ram C., additional, Slaby, Ondrej, additional, Solé, Carla, additional, Soni, Dharmendra Kumar, additional, Sozzi, Gabriella, additional, Thakur, Anamika, additional, Veronese, Angelo, additional, Visone, Rosa, additional, Vychytilova-Faltejskova, Petra, additional, and Zhang, Cen, additional

Published
2022
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54. RNA delivery for cancer gene therapy

Author

Oncul, Selin, primary, Amero, Paola, additional, Rodriguez-Aguayo, Cristian, additional, Sood, Anil K., additional, Calin, George A., additional, and Lopez-Berestein, Gabriel, additional

Published
2022
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55. Contributors

Author

Alameh, Mohamad-Gabriel, primary, Alcantara, Marice, additional, Alluin, Jessica, additional, Amero, Paola, additional, Arechavala-Gomeza, Virginia, additional, Calin, George A., additional, Corey, David R., additional, Cramer, Hagen, additional, Dammes, Niels, additional, Drolet, Daniel W., additional, Frederiksen, James, additional, Gelinas, Amy D., additional, Habib, Nagy A., additional, Hazan-Halevy, Inbal, additional, Holm, Kevin, additional, Janjic, Nebojsa, additional, Johnson, Krystal C., additional, Johnson, Samantha T., additional, Kon, Edo, additional, Kortylewski, Marcin, additional, Landesman-Milo, Dalit, additional, Lemaitre, Marc M., additional, Lincoln, Christopher, additional, Lopez-Berestein, Gabriel, additional, Lynch, Sean A., additional, Oncul, Selin, additional, Ostroff, Rachel M., additional, Peer, Dan, additional, Rodriguez-Aguayo, Cristian, additional, Rohloff, John C., additional, Rossi, Daniel, additional, Rossi, John J., additional, Rupp, Thomas M., additional, Schneider, Daniel J., additional, Soblechero-Martín, Patricia, additional, Song, Min-Sun, additional, Sood, Anil K., additional, Su, Yu-Lin, additional, Sullenger, Bruce A., additional, Voutila, Jon, additional, Weissman, Drew, additional, Williams, Preston, additional, Yu, Chunsong, additional, Yu, Haixiang, additional, Zhang, Zhuoran, additional, and Zhou, Jiehua, additional

Published
2022
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59. Non-Coding RNAs in Peritoneal Carcinomatosis: From Bench to Bedside.

Author

Bohosova, Julia, Ashraf, Nida Sarosh, Slaby, Ondrej, and Calin, George A.

Subjects
HEALTH literacy, CANCER invasiveness, RNA, PERITONEAL cancer, QUALITY assurance, BIOMARKERS, OVERALL survival, DISEASE progression
Abstract

Simple Summary: Peritoneal carcinomatosis is a term for cancer cells spreading from tumors of internal organs and massively invading a large part of the membrane lining the abdomen and pelvis. For most patients, peritoneal carcinomatosis suggests only several months of life left. Current medicine can offer only alleviation of symptoms from this incurable disease. Researchers are intensely exploring some new therapeutic targets. Among promising candidates are non-coding RNAs, short molecules serving as important regulators in cells. When a disease such as cancer develops in the body, it is accompanied by typical changes in levels of non-coding RNAs. In this review, we provide an overview of current state of knowledge regarding the changes of non-coding RNA levels in peritoneal carcinomatosis. Deeper understanding of this topic could lead to the identification of non-coding RNAs as feasible specific biomarkers or novel therapeutic targets in the treatment of peritoneal carcinomatosis. Peritoneal carcinomatosis represents an advanced stage of tumors within the peritoneal cavity. Once considered an incurable terminal cancer metastasis, contemporary medicine is on the hunt for certain potentially curative options alongside the present day's palliative disease management. However, for most patients, peritoneal carcinomatosis continues to pose a fatal late-stage prognosis with a grim future outlook. Over the past two decades, non-coding RNAs have garnered significant attention due to their undeniable significance in regulating cellular processes across all levels. Disruption of the intricate regulation led by non-coding RNAs has been demonstrated to have a substantial impact on various human diseases, particularly in cancer, including solid tumors originating from the organs of the peritoneal cavity. This review aims to offer a comprehensive overview of the current state of knowledge in the under-researched field of peritoneal carcinomatosis, focusing specifically on the role of non-coding RNAs in the development of this condition and delineating potential avenues for future research. [ABSTRACT FROM AUTHOR]

Published
2024
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60. ALYREF, a novel factor involved in breast carcinogenesis, acts through transcriptional and post-transcriptional mechanisms selectively regulating the short NEAT1 isoform

Author

Klec, Christiane, Knutsen, Erik, Schwarzenbacher, Daniela, Jonas, Katharina, Pasculli, Barbara, Heitzer, Ellen, Rinner, Beate, Krajina, Katarina, Prinz, Felix, Gottschalk, Benjamin, Ulz, Peter, Deutsch, Alexander, Prokesch, Andreas, Jahn, Stephan W., Lellahi, S. Mohammad, Perander, Maria, Barbano, Raffaela, Graier, Wolfgang F., Parrella, Paola, Calin, George Adrian, and Pichler, Martin

Published
2022
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61. The Long Noncoding RNA CCAT2 Induces Chromosomal Instability Through BOP1-AURKB Signaling

Author

Chen, Baoqing, Dragomir, Mihnea P., Fabris, Linda, Bayraktar, Recep, Knutsen, Erik, Liu, Xu, Tang, Changyan, Li, Yongfeng, Shimura, Tadanobu, Ivkovic, Tina Catela, Cruz De los Santos, Mireia, Anfossi, Simone, Shimizu, Masayoshi, Shah, Maitri Y., Ling, Hui, Shen, Peng, Multani, Asha S., Pardini, Barbara, Burks, Jared K., Katayama, Hiroyuki, Reineke, Lucas C., Huo, Longfei, Syed, Muddassir, Song, Shumei, Ferracin, Manuela, Oki, Eiji, Fromm, Bastian, Ivan, Cristina, Bhuvaneshwar, Krithika, Gusev, Yuriy, Mimori, Koshi, Menter, David, Sen, Subrata, Matsuyama, Takatoshi, Uetake, Hiroyuki, Vasilescu, Catalin, Kopetz, Scott, Parker-Thornburg, Jan, Taguchi, Ayumu, Hanash, Samir M., Girnita, Leonard, Slaby, Ondrej, Goel, Ajay, Varani, Gabriele, Gagea, Mihai, Li, Chunlai, Ajani, Jaffer A., and Calin, George A.

Published
2020
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65. Translational modeling-based evidence for enhanced efficacy of standard-of-care drugs in combination with anti-microRNA-155 in non-small-cell lung cancer

Author

Dogra, Prashant, primary, Shinglot, Vrushaly, additional, Ruiz-Ramírez, Javier, additional, Cave, Joseph, additional, Butner, Joseph D., additional, Schiavone, Carmine, additional, Duda, Dan G., additional, Kaseb, Ahmed O., additional, Chung, Caroline, additional, Koay, Eugene J., additional, Cristini, Vittorio, additional, Ozpolat, Bulent, additional, Calin, George A., additional, and Wang, Zhihui, additional

Published
2024
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67. Ofatumumab and Lenalidomide for Patients with Relapsed or Refractory Chronic Lymphocytic Leukemia: Correlation between Responses and Immune Characteristics

Author

Vitale, Candida, Falchi, Lorenzo, Hacken, Elisa ten, Gao, Hui, Shaim, Hila, Van Roosbroeck, Katrien, Calin, George, O'Brien, Susan, Faderl, Stefan, Wang, Xuemei, Wierda, William G, Rezvani, Katayoun, Reuben, James M, Burger, Jan A, Keating, Michael J, and Ferrajoli, Alessandra

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Oncology and Carcinogenesis, Infectious Diseases, Cancer, Clinical Research, Orphan Drug, Rare Diseases, Lymphatic Research, Clinical Trials and Supportive Activities, Hematology, 6.1 Pharmaceuticals, Good Health and Well Being, Adult, Aged, Aged, 80 and over, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Disease-Free Survival, Female, Humans, Lenalidomide, Leukemia, Lymphocytic, Chronic, B-Cell, Male, Middle Aged, Neoplasm Recurrence, Local, Thalidomide, Treatment Outcome, Oncology & Carcinogenesis, Clinical sciences, Oncology and carcinogenesis
Abstract

PurposeWe evaluated efficacy and tolerability of the combination of ofatumumab and lenalidomide in patients with relapsed/refractory chronic lymphocytic leukemia (CLL), and explored whether immune system characteristics could influence the response to treatment.Experimental designThirty-four patients were enrolled in this phase II study. Ofatumumab was administered at a dose of 300 mg on day 1, 1,000 mg on days 8, 15, and 22 during course 1, 1,000 mg on day 1 during courses 3-6, and once every other course during courses 7-24 (28-day courses). Oral lenalidomide (10 mg daily) was started on day 9 and continued for as long as a clinical benefit was observed.ResultsThe overall response rate was 71%. Eight patients (24%) achieved a complete remission (CR) or CR with incomplete recovery of blood counts, including 9% with minimal residual disease-negative CR. The median progression-free survival was 16 months, and the estimated 5-year survival was 53%. The most common treatment-related toxicity was neutropenia (grade >2 in 18% of the 574 patient courses). The most frequent infectious complications were pneumonia and neutropenic fever (24% and 9% of patients, respectively). We observed that patients who achieved a CR had at baseline higher numbers and a better preserved function of T cells and natural killer cells compared with non-responders.ConclusionsThe combination of ofatumumab and lenalidomide is a well-tolerated regimen that induces durable responses in the majority of patients with relapsed/refractory CLL. Our correlative data suggest a role of competent immune system in supporting the efficacy of this treatment. Clin Cancer Res; 22(10); 2359-67. ©2016 AACR.

Published
2016

70. Single-cell dissection of intratumoral heterogeneity and lineage diversity in metastatic gastric adenocarcinoma

Author

Wang, Ruiping, Dang, Minghao, Harada, Kazuto, Han, Guangchun, Wang, Fang, Pool Pizzi, Melissa, Zhao, Meina, Tatlonghari, Ghia, Zhang, Shaojun, Hao, Dapeng, Lu, Yang, Zhao, Shuangtao, Badgwell, Brian D., Murphy, Mariela Blum, Shanbhag, Namita, Estrella, Jeannelyn S., Roy-Chowdhuri, Sinchita, Abdelhakeem, Ahmed Adel Fouad, Wang, Yuanxin, Peng, Guang, Hanash, Samir, Calin, George A., Song, Xingzhi, Chu, Yanshuo, Zhang, Jianhua, Li, Mingyao, Chen, Ken, Lazar, Alexander J., Futreal, Andrew, Song, Shumei, Ajani, Jaffer A., and Wang, Linghua

Subjects
Genetic aspects, Prognosis, Patient outcomes, Stomach cancer -- Prognosis -- Genetic aspects -- Patient outcomes, Adenocarcinoma -- Prognosis -- Genetic aspects -- Patient outcomes, Cancer metastasis -- Prognosis -- Genetic aspects -- Patient outcomes, Metastasis -- Prognosis -- Genetic aspects -- Patient outcomes
Abstract

Author(s): Ruiping Wang [sup.1] , Minghao Dang [sup.1] , Kazuto Harada [sup.2] [sup.12] , Guangchun Han [sup.1] , Fang Wang [sup.3] , Melissa Pool Pizzi [sup.2] , Meina Zhao [sup.2] [...], Intratumoral heterogeneity (ITH) is a fundamental property of cancer; however, the origins of ITH remain poorly understood. We performed single-cell transcriptome profiling of peritoneal carcinomatosis (PC) from 15 patients with gastric adenocarcinoma (GAC), constructed a map of 45,048 PC cells, profiled the transcriptome states of tumor cell populations, incisively explored ITH of malignant PC cells and identified significant correlates with patient survival. The links between tumor cell lineage/state compositions and ITH were illustrated at transcriptomic, genotypic, molecular and phenotypic levels. We uncovered the diversity in tumor cell lineage/state compositions in PC specimens and defined it as a key contributor to ITH. Single-cell analysis of ITH classified PC specimens into two subtypes that were prognostically independent of clinical variables, and a 12-gene prognostic signature was derived and validated in multiple large-scale GAC cohorts. The prognostic signature appears fundamental to GAC carcinogenesis and progression and could be practical for patient stratification. Single-cell analysis of gastric cancer samples tracks the cell of origin of metastatic lesions and identifies an independent prognostic signature of the clinical outcome.

Published
2021
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71. Corrigendum to Exosomal miRNA confers chemo resistance via targeting Cav1/p-gp/M2-type macrophage axis in ovarian cancer

Author

Kanlikilicer, Pinar, Bayraktar, Recep, Denizli, Merve, Rashed, Mohammed H., Ivan, Cristina, Aslan, Burcu, Mitra, Rahul, Karagoz, Kubra, Bayraktar, Emine, Zhang, Xinna, Rodriguez-Aguayo, Cristian, El-Arabey, Amr Ahmed, Kahraman, Nermin, Baydogan, Seyda, Ozkayar, Ozgur, Gatza, Michael L., Ozpolat, Bulent, Calin, George A., Sood, Anil K., and Lopez-Berestein, Gabriel

Published
2025
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72. miRNA Expression Assays

Author

Braicu, Cornelia, Gulei, Diana, de Melo Maia, Beatriz, Berindan-Neagoe, Ioana, Calin, George A., Netto, George Jabboure, editor, and Kaul, Karen L., editor

Published
2019
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74. PRUNE2 is a human prostate cancer suppressor regulated by the intronic long noncoding RNA PCA3

Author

Salameh, Ahmad, Lee, Alessandro K, Cardó-Vila, Marina, Nunes, Diana N, Efstathiou, Eleni, Staquicini, Fernanda I, Dobroff, Andrey S, Marchiò, Serena, Navone, Nora M, Hosoya, Hitomi, Lauer, Richard C, Wen, Sijin, Salmeron, Carolina C, Hoang, Anh, Newsham, Irene, Lima, Leandro A, Carraro, Dirce M, Oliviero, Salvatore, Kolonin, Mikhail G, Sidman, Richard L, Do, Kim-Anh, Troncoso, Patricia, Logothetis, Christopher J, Brentani, Ricardo R, Calin, George A, Cavenee, Webster K, Dias-Neto, Emmanuel, Pasqualini, Renata, and Arap, Wadih

Subjects
Aging, Genetics, Prostate Cancer, Biotechnology, Cancer, Urologic Diseases, 2.1 Biological and endogenous factors, Aetiology, Adenosine Deaminase, Animals, Antigens, Neoplasm, Cell Line, Tumor, Gene Expression Regulation, Neoplastic, HEK293 Cells, HeLa Cells, Humans, Immunoblotting, Introns, MCF-7 Cells, Male, Mice, SCID, Molecular Sequence Data, Neoplasm Proteins, Prostatic Neoplasms, Protein Binding, RNA Interference, RNA Precursors, RNA, Long Noncoding, Reverse Transcriptase Polymerase Chain Reaction, Tumor Suppressor Proteins, Xenograft Model Antitumor Assays, PRUNE2, PCA3, long noncoding RNA, ADAR, prostate cancer, Hela Cells
Abstract

Prostate cancer antigen 3 (PCA3) is the most specific prostate cancer biomarker but its function remains unknown. Here we identify PRUNE2, a target protein-coding gene variant, which harbors the PCA3 locus, thereby classifying PCA3 as an antisense intronic long noncoding (lnc)RNA. We show that PCA3 controls PRUNE2 levels via a unique regulatory mechanism involving formation of a PRUNE2/PCA3 double-stranded RNA that undergoes adenosine deaminase acting on RNA (ADAR)-dependent adenosine-to-inosine RNA editing. PRUNE2 expression or silencing in prostate cancer cells decreased and increased cell proliferation, respectively. Moreover, PRUNE2 and PCA3 elicited opposite effects on tumor growth in immunodeficient tumor-bearing mice. Coregulation and RNA editing of PRUNE2 and PCA3 were confirmed in human prostate cancer specimens, supporting the medical relevance of our findings. These results establish PCA3 as a dominant-negative oncogene and PRUNE2 as an unrecognized tumor suppressor gene in human prostate cancer, and their regulatory axis represents a unique molecular target for diagnostic and therapeutic intervention.

Published
2015

75. Targeting IL11 Receptor in Leukemia and Lymphoma: A Functional Ligand-Directed Study and Hematopathology Analysis of Patient-Derived Specimens

Author

Karjalainen, Katja, Jaalouk, Diana E, Bueso-Ramos, Carlos, Bover, Laura, Sun, Yan, Kuniyasu, Akihiko, Driessen, Wouter HP, Cardó-Vila, Marina, Rietz, Cecilia, Zurita, Amado J, O'Brien, Susan, Kantarjian, Hagop M, Cortes, Jorge E, Calin, George A, Koivunen, Erkki, Arap, Wadih, and Pasqualini, Renata

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Orphan Drug, Pediatric, Lymphoma, Prostate Cancer, Urologic Diseases, Clinical Research, Cancer, Pediatric Cancer, Rare Diseases, Hematology, Amino Acid Sequence, Antineoplastic Agents, Cell Line, Tumor, Cell Survival, Drug Screening Assays, Antitumor, Humans, Inhibitory Concentration 50, Leukemia, Ligands, Molecular Sequence Data, Peptides, Receptors, Interleukin-11, Oncology & Carcinogenesis, Clinical sciences, Oncology and carcinogenesis
Abstract

PurposeThe IL11 receptor (IL11R) is an established molecular target in primary tumors of bone, such as osteosarcoma, and in secondary bone metastases from solid tumors, such as prostate cancer. However, its potential role in management of hematopoietic malignancies has not yet been determined. Here, we evaluated the IL11R as a candidate therapeutic target in human leukemia and lymphoma.Experimental design and resultsFirst, we show that the IL11R protein is expressed in a variety of human leukemia- and lymphoma-derived cell lines and in a large panel of bone marrow samples from leukemia and lymphoma patients, whereas expression is absent from nonmalignant control bone marrow. Moreover, a targeted peptidomimetic prototype (termed BMTP-11), specifically bound to leukemia and lymphoma cell membranes, induced ligand-receptor internalization mediated by the IL11R, and resulted in a specific dose-dependent cell death induction in these cells. Finally, a pilot drug lead-optimization program yielded a new myristoylated BMTP-11 analogue with an apparent improved antileukemia cell profile.ConclusionsThese results indicate (i) that the IL11R is a suitable cell surface target for ligand-directed applications in human leukemia and lymphoma and (ii) that BMTP-11 and its derivatives have translational potential against this group of malignant diseases.

Published
2015

76. Epstein–Barr Virus MicroRNAs are Expressed in Patients with Chronic Lymphocytic Leukemia and Correlate with Overall Survival

Author

Ferrajoli, Alessandra, Ivan, Cristina, Ciccone, Maria, Shimizu, Masayoshi, Kita, Yoshiaki, Ohtsuka, Masahisha, D'Abundo, Lucilla, Qiang, Jun, Lerner, Susan, Nouraee, Nazila, Rabe, Kari G, Rassenti, Laura Z, Van Roosbroeck, Katrien, Manning, John T, Yuan, Yuan, Zhang, Xinna, Shanafelt, Tait D, Wierda, William G, Sabbioni, Silvia, Tarrand, Jeffrey J, Estrov, Zeev, Radovich, Milan, Liang, Han, Negrini, Massimo, Kipps, Thomas J, Kay, Neil E, Keating, Michael, and Calin, George A

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Clinical Research, Infectious Diseases, Lymphoma, Hematology, Cancer, Genetics, Lymphatic Research, Rare Diseases, Biotechnology, 2.1 Biological and endogenous factors, Infection, Disease-Free Survival, Epstein-Barr Virus Nuclear Antigens, Herpesvirus 4, Human, Humans, Leukemia, Lymphocytic, Chronic, B-Cell, MicroRNAs, RNA, Viral, Tumor Cells, Cultured, Tumor Suppressor Protein p53, Viral Matrix Proteins, Viral Proteins, beta 2-Microglobulin, miRNAs, Epstein-Barr Virus, Chronic lymphocytic leukemia, BHRF1-1, Overall survival, Epstein–Barr Virus, Clinical Sciences, Public Health and Health Services, Clinical sciences, Epidemiology
Abstract

Although numerous studies highlighted the role of Epstein-Barr Virus (EBV) in B-cell transformation, the involvement of EBV proteins or genome in the development of the most frequent adult leukemia, chronic lymphocytic leukemia (CLL), has not yet been defined. We hypothesized that EBV microRNAs contribute to progression of CLL and demonstrated the presence of EBV miRNAs in B-cells, in paraffin-embedded bone marrow biopsies and in the plasma of patients with CLL by using three different methods (small RNA-sequencing, quantitative reverse transcription PCR [q-RT-PCR] and miRNAs in situ hybridization [miRNA-ISH]). We found that EBV miRNA BHRF1-1 expression levels were significantly higher in the plasma of patients with CLL compared with healthy individuals (p

Published
2015

83. Vitamin D Deficiency in Both Oral and Systemic Manifestations in SARS-CoV-2 Infection: Updated Review

Author

Alin Constantin Pinzariu, Ivona Andreea Sova, Minela Aida Maranduca, Nina Filip, Ilie Cristian Drochioi, Calin George Vamesu, Andreea Clim, Loredana Liliana Hurjui, Mihaela Moscalu, Radu Petru Soroceanu, Dragomir Nicolae Serban, and Ionela Lacramioara Serban

Subjects
coronavirus, COVID-19, SARS-CoV-2, vitamin D, prevention, systemic manifestations, Medicine (General), R5-920
Abstract

The specialized literature emphasizes the fact that vitamin D has a potentially beneficial effect in the context of the current COVID-19 pandemic. The purpose of this article is to highlight the role of vitamin D, both prophylactic and curative, in the treatment of patients diagnosed with COVID-19. Even though its relevance is still unknown and causes various controversies, there is currently no specific treatment for patients diagnosed with COVID-19. There are various prevention strategies with new vaccination schedules, but additional randomized and clinical trials are still needed to combat this pandemic. In addition to the systemic manifestations of SARS-CoV-2 infection, oral manifestations of this disease have also been described in the literature. The etiology of oral manifestations associated with COVID-19 infection and vitamin D deficiency remains controversial. In the present studies, oral manifestations such as salivary gland infections, aphthae, erythema, gingivitis, ulcers, etc. have been reported. This is a new topic, and the prevalence of manifestations is described in only a few studies, which is inconsistent with the number of COVID-19 cases reported since the beginning of the pandemic. The clinical symptomatology in patients with current COVID-19 infection is polymorphic. Whether the oral manifestation is directly caused by SARS-CoV-2 or a secondary manifestation remains an important topic to analyze and discuss.

Published
2022
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84. The Extracellular RNA Communication Consortium: Establishing Foundational Knowledge and Technologies for Extracellular RNA Research

Author

Abdel-Mageed, Asim B., Adamidi, Catherine, Adelson, P. David, Akat, Kemal M., Alsop, Eric, Ansel, K. Mark, Arango, Jorge, Aronin, Neil, Avsaroglu, Seda Kilinc, Azizian, Azadeh, Balaj, Leonora, Ben-Dov, Iddo Z., Bertram, Karl, Bitzer, Markus, Blelloch, Robert, Bogardus, Kimberly A., Breakefield, Xandra Owens, Calin, George A., Carter, Bob S., Charest, Al, Chen, Clark C., Chitnis, Tanuja, Coffey, Robert J., Courtright-Lim, Amanda, Das, Saumya, Datta, Amrita, DeHoff, Peter, Diacovo, Thomas G., Erle, David J., Etheridge, Alton, Ferrer, Marc, Franklin, Jeffrey L., Freedman, Jane E., Galas, David J., Galeev, Timur, Gandhi, Roopali, Garcia, Aitor, Gerstein, Mark Bender, Ghai, Vikas, Ghiran, Ionita Calin, Giraldez, Maria D., Goga, Andrei, Gogakos, Tasos, Goilav, Beatrice, Gould, Stephen J., Guo, Peixuan, Gupta, Mihir, Hochberg, Fred, Huang, Bo, Huentelman, Matt, Hunter, Craig, Hutchins, Elizabeth, Jackson, Andrew R., Kalani, M. Yashar S., Kanlikilicer, Pinar, Karaszti, Reka Agnes, Van Keuren-Jensen, Kendall, Khvorova, Anastasia, Kim, Yong, Kim, Hogyoung, Kim, Taek Kyun, Kitchen, Robert, Kraig, Richard P., Krichevsky, Anna M., Kwong, Raymond Y., Laurent, Louise C., Lee, Minyoung, L’Etoile, Noelle, Levy, Shawn E., Li, Feng, Li, Jenny, Li, Xin, Lopez-Berestein, Gabriel, Lucero, Rocco, Mateescu, Bogdan, Matin, A.C., Max, Klaas E.A., McManus, Michael T., Mempel, Thorsten R., Meyer, Cindy, Milosavljevic, Aleksandar, Mondal, Debasis, Mukamal, Kenneth Jay, Murillo, Oscar D., Muthukumar, Thangamani, Nickerson, Deborah A., O’Donnell, Christopher J., Patel, Dinshaw J., Patel, Tushar, Patton, James G., Paul, Anu, Peskind, Elaine R., Phelps, Mitch A., Putterman, Chaim, Quesenberry, Peter J., Quinn, Joseph F., Raffai, Robert L., Ranabothu, Saritha, Rao, Shannon Jiang, Rodriguez-Aguayo, Cristian, Rosenzweig, Anthony, Roth, Matthew E., Rozowsky, Joel, Sabatine, Marc S., Sakhanenko, Nikita A., Saugstad, Julie Anne, Schmittgen, Thomas D., Shah, Neethu, Shah, Ravi, Shedden, Kerby, Shi, Jian, Sood, Anil K., Sopeyin, Anuoluwapo, Spengler, Ryan M., Spetzler, Robert, Srinivasan, Srimeenakshi, Subramanian, Sai Lakshmi, Suthanthiran, Manikkam, Tanriverdi, Kahraman, Teng, Yun, Tewari, Muneesh, Thistlethwaite, William, Tuschl, Thomas, Urbanowicz, Karolina Kaczor, Vickers, Kasey C., Voinnet, Olivier, Wang, Kai, Weaver, Alissa M., Wei, Zhiyun, Weiner, Howard L., Weiss, Zachary R., Williams, Zev, Wong, David T.W., Woodruff, Prescott G., Xiao, Xinshu, Yan, Irene K., Yeri, Ashish, Zhang, Bing, Zhang, Huang-Ge, Breakefield, Xandra O., Charest, Alain, Gerstein, Mark B., and Saugstad, Julie A.

Published
2019
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85. The Modulatory Role of MicroRNA-873 in the Progression of KRAS-Driven Cancers

Author

Mokhlis, Hamada A., Bayraktar, Recep, Kabil, Nashwa N., Caner, Ayse, Kahraman, Nermin, Rodriguez-Aguayo, Cristian, Zambalde, Erika P., Sheng, Jianting, Karagoz, Kübra, Kanlikilicer, Pinar, Abdel Aziz, Abdel Aziz H., Abdelghany, Tamer M., Ashour, Ahmed A., Wong, Stephen, Gatza, Michael L., Calin, George A., Lopez-Berestein, Gabriel, and Ozpolat, Bulent

Published
2019
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87. Apoptotic cell death in disease—Current understanding of the NCCD 2023

Author

Associazione Italiana per la Ricerca sul Cancro, Italian Institute for Genomic Medicine, Compagnia di San Paolo, Vitale, Ilio [0000-0002-5918-1841], Pietrocola, Federico [0000-0002-2930-234X], Guilbaud, Emma [0000-0001-5261-1944], Aaronson, Stuart A. [0000-0002-4643-0474], Dieter, Adam [0000-0002-5668-5032], Agostini, Massimiliano [0000-0003-3124-2072], Agostinis, Patrizia [0000-0003-1314-2115], Alnemri, Emad S. [0000-0002-7295-3383], Altucci, Lucia [0000-0002-7312-5387], Amelio, Ivano [0000-0002-9126-5391], Andrews, David W. [0000-0002-9266-7157], Aqeilan, Rami I. [0000-0002-6034-023X], Arama, Eli [0000-0001-5953-0629], Balachandran, Siddharth [0000-0003-2084-1803], Bano, Daniele [0000-0002-9617-5504], Bartek, Jiri [0000-0003-2013-7525], Bazan, Nicolas G. [0000-0002-9243-5444], Bernassola, Francesca [0000-0002-8883-8654], Bertrand, Mathieu J. M. [0000-0001-9000-0626], Bianchi, Marco Emilio [0000-0002-5329-6445], Blander, J. Magarian [0000-0001-9207-1700], Blandino, Giovanni [0000-0002-6970-2241], Blomgren, Klas [0000-0002-0476-7271], Bortner, Carl D. [0000-0002-5444-6628], Bove, Pierluigi [0000-0002-4788-2982], Boya, Patricia [0000-0003-3045-951X], Broz, Petr [0000-0002-2334-7790], Damgaard, Rune Busk [0000-0002-1709-6534], Calin, George A. [0000-0002-7427-0578], Campanella, Michelangelo [0000-0002-6948-4184], Candi, Eleonora [0000-0001-8332-4825], Carbone, Michele [0000-0001-8928-8474], Carmona-Gutierrez, Didac [0000-0001-7548-7771], Cecconi, Francesco [0000-0002-5614-4359], Chen, Guo‑Qiang [0000-0002-7226-1782], Cheng, Emily H. [0000-0002-3595-2648], Chipuk, Jerry E. [0000-0002-1337-842X], Cidlowski, John A. [0000-0003-1420-0516], Ciechanover, Aaron [0000-0001-9184-8944], Ciliberto, Gennaro [0000-0003-2851-8605], Conrad, Marcus [0000-0003-1140-5612], Czabotar, Peter E. [0000-0002-2594-496X], D’Angiolella, Vincenzo [0000-0001-8365-9094], Daugaard, Mads [0000-0001-8383-055X], Dawson, Valina L. [0000-0002-2915-3970], De Maria, Ruggero [0000-0003-2255-0583], Debatin, Klaus-Michael [0000-0002-8397-1886], Deberardinis, Ralph J. [0000-0002-2705-7432], Degterev, Alexei [0000-0002-8240-7132], Del Sal, Giannino [0000-0003-2185-6003], Deshmukh, Mohanish [0000-0002-2597-5862], Di Virgilio, Francesco [0000-0003-3566-1362], Diederich, Marc [0000-0003-0115-4725], Dixon, Scott J. [0000-0001-6230-8199], El-Deiry, Wafik S. [0000-0002-9577-8266], Elrod, John W. [0000-0003-3925-2224], Engeland, Kurt [0000-0003-3525-0440], Fimia, Gian María [0000-0003-4438-3325], Ganini, Carlo [0000-0002-5839-3965], García-Sáez, Ana J. [0000-0002-3894-5945], Garg, Abhishek D. [0000-0002-9976-9922], Garrido, Carmen [0000-0003-1368-1493], Gavathiotis, Evripidis [0000-0001-6319-8331], Ghosh, Sourav [0000-0001-5990-8708], Green, Douglas R. [0000-0002-7332-1417], Gronemeyer, Hinrich [0000-0001-9454-2449}, Häcker, Georg [0000-0003-1058-5746], Hajnóczky, György [0000-0003-3813-2570], Hardwick, J. Marie [0000-0002-4847-2045], Haupt, Ygal [0000-0001-5925-0096], He, Sudan [0000-0002-0846-1210], Heery, David M. [0000-0002-5035-2392], Hengartner, Michael O. [0000-0002-7584-596X], Hetz, Claudio [0000-0003-1120-7966], Hildeman, David A. [0000-0002-0421-8483], Ichijo, Hidenori [0000-0002-5005-6438], Jäättelä, Marja [0000-0001-5950-7111], Janic, Ana [0000-0002-4200-2560], Joseph, Bertrand [0000-0001-5655-9979], Jost, Philipp J. [0000-0003-2454-0362], Kanneganti, Thirumala-Devi [0000-0002-6395-6443], Karin, Michael [0000-0002-2758-6473], Kashkar, Hamid [0000-0003-2796-1429], Kaufmann, Thomas [0000-0001-9906-874X], Kelly, Gemma L. [0000-0002-6533-1201], Kepp, Oliver [0000-0002-6081-9558], Kimchi, Adi [0000-0002-8236-8989], Klionsky, Daniel J. [0000-0002-7828-8118], Kluck, Ruth [0000-0002-7101-1925], Krysko, Dmitri V. [0000-0002-9692-2047], Kulms, Dagmar [0000-0001-6874-0548], Kumar, Sharad [0000-0001-7126-9814], Lavandero, Sergio [0000-0003-4258-1483], Lavrik, Inna N. [0000-0002-9324-309X], Liccardi, Gianmaria [0000-0002-2662-1281], Linkermann, Andreas [0000-0001-6287-9725], Lipton, Stuart A. [0000-0002-3490-1259], Lockshin, Richard A. [0000-0002-4389-4898], López-Otín, Carlos [0000-0001-6964-1904], Luedde, Tom [0000-0002-6288-8821], MacFarlane, Marion [0000-0001-7886-1159], Madeo, Frank [0000-0002-5070-1329], Malorni, Walter [0000-0002-1223-7000], Manic, Gwenola [0000-0003-3759-8029], Marchi, Saverio [0000-0003-2708-1843], Marine, Jean-Christophe [0000-0003-2433-9837], Martin, Seamus J. [0000-0002-8539-3143], Martinou, Jean-Claude [0000-0002-9847-2051], Mastroberardino, Pier G. [0000-0003-2364-4258], Medema, Jan Paul [0000-0003-3045-2924], Mehlen, Patrick [0000-0003-1743-5417], Meier, Pascal [0000-0003-2760-6523], Melino, Gerry [0000-0001-9428-5972], Melino, Sonia [0000-0001-7694-5279], Miao, Edward A. [0000-0001-7295-3490], Moll, Ute M. [0000-0003-1908-7516], Muñoz-Pinedo, Cristina [0000-0002-9120-664X], Murphy, Daniel J. [0000-0002-5538-5468], Niklison-Chirou, Maria Victoria [0000-0002-2147-370X], Novelli, Flavia [0000-0002-3746-7478], Oberst, Andrew [0000-0002-9500-7912], Ofengeim, Dimitry [0000-0003-2348-3642], Opferman, Joseph T. [0000-0002-1147-5621], Oren, Moshe [0000-0003-4311-7172], Pagano, Michele [0000-0003-3210-2442], Panaretakis, Theocharis [0000-0001-5754-6950], Pasparakis, Manolis [0000-0002-9870-0966], Penninger, Josef M. [0000-0002-8194-3777], Pentimalli, Francesca [0000-0003-4740-6801], Pereira, David M. [0000-0003-0384-7592], Pervaiz, Shazib [0000-0002-4738-019X], Peter, Marcus E. [0000-0003-3216-036X], Pinton, Paolo [0000-0001-7108-6508], Porta, Giovanni [0000-0001-5260-2415], Puthalakath, Hamsa [0000-0001-5178-1175], Rabinovich, Gabriel A. [0000-0002-0947-8735], Rajalingam, Krishnaraj [0000-0002-4175-9633], Ravinchandran, Kodi S. [0000-0001-9049-1410], Rehm, Markus [0000-0001-6149-9261], Ricci, Jean-Ehrland [0000-0003-1585-8117], Rizzuto, Rosario [0000-0001-7044-5097], Robinson, Nirmal [0000-0002-7361-9491], Rotblat, Barak [0000-0003-2985-7115], Rothlin, Carla V. [0000-0002-5693-5572], Rubinsztein, David C. [0000-0001-5002-5263], Rufini, Alessandro [0000-0002-5855-655X], Ryan, Kevin M. [0000-0002-1059-9681], Sarosiek, Kristopher A. [0000-0002-4618-5085], Sawa, Akira [0000-0003-1401-3008], Sayan, Emre [0000-0002-5291-1485], Schroder, Kate [0000-0001-9261-3805], Scorrano, Luca [0000-0002-8515-8928], Sesti, Federico [0000-0002-2761-9693], Shi, Yufang [0000-0001-8964-319X], Sica, Giuseppe [0000-0002-7407-0584], Silke, John [0000-0002-7611-5774], Simon, Hans-Uwe [0000-0002-9404-7736], Sistigu, Antonella [0000-0002-2528-1238], Stockwell, Brent R. [0000-0002-3532-3868], Strappazzon, Flavie [0000-0003-0285-7449], Sun, Liming [0000-0002-0136-5605], Sun, Erwei [0000-0001-5664-513X], Szabadkai, G [0000-0002-3006-3577], Tait, Stephen W. G. [0000-0001-7697-132X], Tang, Daolin [0000-0002-1903-6180], Tavernarakis, Nektarios [0000-0002-5253-1466], Turk, Boris [0000-0002-9007-5764], Urbano, Nicoletta [0000-0003-1822-155X], Vandenabeele, Peter [0000-0002-6669-8822], Vanden Berghe, Tom [0000-0002-1633-0974], Vander Heiden, Matthew G. [0000-0002-6702-4192], Vanderluit, Jacqueline L. [0000-0002-4960-920X], Verkhratsky, A. [0000-0003-2592-9898], Villunger, Andreas [0000-0001-8259-4153], Von Karstedt, Silvia [0000-0002-7816-5919], Voss, Anne K. [0000-0002-3853-9381], Vucic, Domagoj [0000-0003-3614-8093], Vuri, Daniela [0000-0001-8693-3845], Wagner, Erwin F. [0000-0001-7872-0196], Walczak, Henning [0000-0002-6312-4591], Wallach, David [0000-0003-2724-9757], Wang, Ruoning [0000-0001-9798-8032], Weber, Achim [0000-0003-0073-3637], Yamazaki, Takahiro [0000-0002-7420-4394], Zakeri, Zahra [0000-0003-4386-8072], Zawacka-Pankau, Joanna E. [0000-0002-7415-2942], Zhivotovsky, Boris [0000-0002-2238-3482], Piacentini, Mauro [0000-0003-2919-1296], Kroemer, Guido [0000-0002-9334-4405], Galluzzi, Lorenzo [0000-0003-2257-8500 ], Vitale, Ilio, Pietrocola, Federico, Guilbaud, Emma, Aaronson, Stuart A., Abrams, John M., Dieter, Adam, Agostini, Massimiliano, Agostinis, Patrizia, Alnemri, Emad S., Altucci, Lucia, Amelio, Ivano, Andrews, David W., Aqeilan, Rami I., Arama, Eli, Baehrecke, Eric H., Balachandran, Siddharth, Bano, Daniele, Barlev, Nickolai A., Bartek, Jiri, Bazan, Nicolas G., Becker, Christoph, Bernassola, Francesca, Bertrand, Mathieu J. M., Bianchi, Marco Emilio, Blagosklonny, Mikhail V., Blander, J. Magarian, Blandino, Giovanni, Blomgren, Klas, Bomer, Christoph, Bortner, Carl D., Bove, Pierluigi, Boya, Patricia, Brenner, Catherine, Broz, Petr, Brunner, T., Damgaard, Rune Busk, Calin, George A., Campanella, Michelangelo, Candi, Eleonora, Carbone, Michele, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K.-M., Chen, Guo‑Qiang, Chen, Quan, Chen, Youhai H., Cheng, Emily H., Chipuk, Jerry E., Cidlowski, John A., Ciechanover, Aaron, Ciliberto, Gennaro, Conrad, Marcus, Cubillos-Ruiz, Juan R., Czabotar, Peter E., D’Angiolella, Vincenzo, Daugaard, Mads, Dawson, Ted M., Dawson, Valina L., De Maria, Ruggero, De Strooper, B., Debatin, Klaus-Michael, Deberardinis, Ralph J., Degterev, Alexei, Del Sal, Giannino, Deshmukh, Mohanish, Di Virgilio, Francesco, Diederich, Marc, Dixon, Scott J., Dynlacht, Brian D., El-Deiry, Wafik S., Elrod, John W., Engeland, Kurt, Fimia, Gian María, Galassi, Claudia, Ganini, Carlo, García-Sáez, Ana J., Garg, Abhishek D., Garrido, Carmen, Gavathiotis, Evripidis, Gerlic, Motti, Ghosh, Sourav, Green, Douglas R., Greene, Lloyd A., Gronemeyer, Hinrich, Häcker, Georg, Hajnóczky, György, Hardwick, J. Marie, Haupt, Ygal, He, Sudan, Heery, David M., Hengartner, Michael O., Hetz, Claudio, Hildeman, David A., Ichijo, Hidenori, Inoue, Satoshi, Jäättelä, Marja, Janic, Ana, Joseph, Bertrand, Jost, Philipp J., Kanneganti, Thirumala-Devi, Karin, Michael, Kashkar, Hamid, Kaufmann, Thomas, Kelly, Gemma L., Kepp, Oliver, Kimchi, Adi, Kitsis, Richard N., Klionsky, Daniel J., Kluck, Ruth, Krysko, Dmitri V., Kulms, Dagmar, Kumar, Sharad, Lavandero, Sergio, Lavrik, Inna N., Lemasters, John J., Liccardi, Gianmaria, Linkermann, Andreas, Lipton, Stuart A., Lockshin, Richard A., López-Otín, Carlos, Luedde, Tom, MacFarlane, Marion, Madeo, Frank, Malorni, Walter, Manic, Gwenola, Mantovani, Roberto, Marchi, Saverio, Marine, Jean-Christophe, Martin, Seamus J., Martinou, Jean-Claude, Mastroberardino, Pier G., Medema, Jan Paul, Mehlen, Patrick, Meier, Pascal, Melino, Gerry, Melino, Sonia, Miao, Edward A., Moll, Ute M., Muñoz-Pinedo, Cristina, Murphy, Daniel J., Niklison-Chirou, Maria Victoria, Novelli, Flavia, Núñez, Gabriel, Oberst, Andrew, Ofengeim, Dimitry, Opferman, Joseph T., Oren, Moshe, Pagano, Michele, Panaretakis, Theocharis, Pasparakis, Manolis, Penninger, Josef M., Pentimalli, Francesca, Pereira, David M., Pervaiz, Shazib, Peter, Marcus E., Pinton, Paolo, Porta, Giovanni, Prehn, Jochen H. M., Puthalakath, Hamsa, Rabinovich, Gabriel A., Rajalingam, Krishnaraj, Ravinchandran, Kodi S., Rehm, Markus, Ricci, Jean-Ehrland, Rizzuto, Rosario, Robinson, Nirmal, Rodrigues, Cecilia M. P., Rotblat, Barak, Rothlin, Carla V., Rubinsztein, David C., Rudel, Thomas, Rufini, Alessandro, Ryan, Kevin M., Sarosiek, Kristopher A., Sawa, Akira, Sayan, Emre, Schroder, Kate, Scorrano, Luca, Sesti, Federico, Shao, Feng, Shi, Yufang, Sica, Giuseppe, Silke, John, Simon, Hans-Uwe, Sistigu, Antonella, Stephanou, Anastasis, Stockwell, Brent R., Strappazzon, Flavie, Strasser, Andreas, Sun, Liming, Sun, Erwei, Sun, Qiang, Szabadkai, G, Tait, Stephen W. G., Tang, Daolin, Tavernarakis, Nektarios, Troy, Carol M., Turk, Boris, Urbano, Nicoletta, Vandenabeele, Peter, Vanden Berghe, Tom, Vander Heiden, Matthew G., Vanderluit, Jacqueline L., Verkhratsky, A., Villunger, Andreas, Von Karstedt, Silvia, Voss, Anne K., Vousden, Karen H., Vucic, Domagoj, Vuri, Daniela, Wagner, Erwin F., Walczak, Henning, Wallach, David, Wang, Ruoning, Wang, Ying, Weber, Achim, Wood, Will, Yamazaki, Takahiro, Yang, Zahra, Zakeri, Zahra, Zawacka-Pankau, Joanna E., Zhang, Lin, Zhang, Haibin, Zhivotovsky, Boris, Zhou, Wenzhao, Piacentini, Mauro, Kroemer, Guido, Galluzzi, Lorenzo, Associazione Italiana per la Ricerca sul Cancro, Italian Institute for Genomic Medicine, Compagnia di San Paolo, Vitale, Ilio [0000-0002-5918-1841], Pietrocola, Federico [0000-0002-2930-234X], Guilbaud, Emma [0000-0001-5261-1944], Aaronson, Stuart A. [0000-0002-4643-0474], Dieter, Adam [0000-0002-5668-5032], Agostini, Massimiliano [0000-0003-3124-2072], Agostinis, Patrizia [0000-0003-1314-2115], Alnemri, Emad S. [0000-0002-7295-3383], Altucci, Lucia [0000-0002-7312-5387], Amelio, Ivano [0000-0002-9126-5391], Andrews, David W. [0000-0002-9266-7157], Aqeilan, Rami I. [0000-0002-6034-023X], Arama, Eli [0000-0001-5953-0629], Balachandran, Siddharth [0000-0003-2084-1803], Bano, Daniele [0000-0002-9617-5504], Bartek, Jiri [0000-0003-2013-7525], Bazan, Nicolas G. [0000-0002-9243-5444], Bernassola, Francesca [0000-0002-8883-8654], Bertrand, Mathieu J. M. [0000-0001-9000-0626], Bianchi, Marco Emilio [0000-0002-5329-6445], Blander, J. Magarian [0000-0001-9207-1700], Blandino, Giovanni [0000-0002-6970-2241], Blomgren, Klas [0000-0002-0476-7271], Bortner, Carl D. [0000-0002-5444-6628], Bove, Pierluigi [0000-0002-4788-2982], Boya, Patricia [0000-0003-3045-951X], Broz, Petr [0000-0002-2334-7790], Damgaard, Rune Busk [0000-0002-1709-6534], Calin, George A. [0000-0002-7427-0578], Campanella, Michelangelo [0000-0002-6948-4184], Candi, Eleonora [0000-0001-8332-4825], Carbone, Michele [0000-0001-8928-8474], Carmona-Gutierrez, Didac [0000-0001-7548-7771], Cecconi, Francesco [0000-0002-5614-4359], Chen, Guo‑Qiang [0000-0002-7226-1782], Cheng, Emily H. [0000-0002-3595-2648], Chipuk, Jerry E. [0000-0002-1337-842X], Cidlowski, John A. [0000-0003-1420-0516], Ciechanover, Aaron [0000-0001-9184-8944], Ciliberto, Gennaro [0000-0003-2851-8605], Conrad, Marcus [0000-0003-1140-5612], Czabotar, Peter E. [0000-0002-2594-496X], D’Angiolella, Vincenzo [0000-0001-8365-9094], Daugaard, Mads [0000-0001-8383-055X], Dawson, Valina L. [0000-0002-2915-3970], De Maria, Ruggero [0000-0003-2255-0583], Debatin, Klaus-Michael [0000-0002-8397-1886], Deberardinis, Ralph J. [0000-0002-2705-7432], Degterev, Alexei [0000-0002-8240-7132], Del Sal, Giannino [0000-0003-2185-6003], Deshmukh, Mohanish [0000-0002-2597-5862], Di Virgilio, Francesco [0000-0003-3566-1362], Diederich, Marc [0000-0003-0115-4725], Dixon, Scott J. [0000-0001-6230-8199], El-Deiry, Wafik S. [0000-0002-9577-8266], Elrod, John W. [0000-0003-3925-2224], Engeland, Kurt [0000-0003-3525-0440], Fimia, Gian María [0000-0003-4438-3325], Ganini, Carlo [0000-0002-5839-3965], García-Sáez, Ana J. [0000-0002-3894-5945], Garg, Abhishek D. [0000-0002-9976-9922], Garrido, Carmen [0000-0003-1368-1493], Gavathiotis, Evripidis [0000-0001-6319-8331], Ghosh, Sourav [0000-0001-5990-8708], Green, Douglas R. [0000-0002-7332-1417], Gronemeyer, Hinrich [0000-0001-9454-2449}, Häcker, Georg [0000-0003-1058-5746], Hajnóczky, György [0000-0003-3813-2570], Hardwick, J. Marie [0000-0002-4847-2045], Haupt, Ygal [0000-0001-5925-0096], He, Sudan [0000-0002-0846-1210], Heery, David M. [0000-0002-5035-2392], Hengartner, Michael O. [0000-0002-7584-596X], Hetz, Claudio [0000-0003-1120-7966], Hildeman, David A. [0000-0002-0421-8483], Ichijo, Hidenori [0000-0002-5005-6438], Jäättelä, Marja [0000-0001-5950-7111], Janic, Ana [0000-0002-4200-2560], Joseph, Bertrand [0000-0001-5655-9979], Jost, Philipp J. [0000-0003-2454-0362], Kanneganti, Thirumala-Devi [0000-0002-6395-6443], Karin, Michael [0000-0002-2758-6473], Kashkar, Hamid [0000-0003-2796-1429], Kaufmann, Thomas [0000-0001-9906-874X], Kelly, Gemma L. [0000-0002-6533-1201], Kepp, Oliver [0000-0002-6081-9558], Kimchi, Adi [0000-0002-8236-8989], Klionsky, Daniel J. [0000-0002-7828-8118], Kluck, Ruth [0000-0002-7101-1925], Krysko, Dmitri V. [0000-0002-9692-2047], Kulms, Dagmar [0000-0001-6874-0548], Kumar, Sharad [0000-0001-7126-9814], Lavandero, Sergio [0000-0003-4258-1483], Lavrik, Inna N. [0000-0002-9324-309X], Liccardi, Gianmaria [0000-0002-2662-1281], Linkermann, Andreas [0000-0001-6287-9725], Lipton, Stuart A. [0000-0002-3490-1259], Lockshin, Richard A. [0000-0002-4389-4898], López-Otín, Carlos [0000-0001-6964-1904], Luedde, Tom [0000-0002-6288-8821], MacFarlane, Marion [0000-0001-7886-1159], Madeo, Frank [0000-0002-5070-1329], Malorni, Walter [0000-0002-1223-7000], Manic, Gwenola [0000-0003-3759-8029], Marchi, Saverio [0000-0003-2708-1843], Marine, Jean-Christophe [0000-0003-2433-9837], Martin, Seamus J. [0000-0002-8539-3143], Martinou, Jean-Claude [0000-0002-9847-2051], Mastroberardino, Pier G. [0000-0003-2364-4258], Medema, Jan Paul [0000-0003-3045-2924], Mehlen, Patrick [0000-0003-1743-5417], Meier, Pascal [0000-0003-2760-6523], Melino, Gerry [0000-0001-9428-5972], Melino, Sonia [0000-0001-7694-5279], Miao, Edward A. [0000-0001-7295-3490], Moll, Ute M. [0000-0003-1908-7516], Muñoz-Pinedo, Cristina [0000-0002-9120-664X], Murphy, Daniel J. [0000-0002-5538-5468], Niklison-Chirou, Maria Victoria [0000-0002-2147-370X], Novelli, Flavia [0000-0002-3746-7478], Oberst, Andrew [0000-0002-9500-7912], Ofengeim, Dimitry [0000-0003-2348-3642], Opferman, Joseph T. [0000-0002-1147-5621], Oren, Moshe [0000-0003-4311-7172], Pagano, Michele [0000-0003-3210-2442], Panaretakis, Theocharis [0000-0001-5754-6950], Pasparakis, Manolis [0000-0002-9870-0966], Penninger, Josef M. [0000-0002-8194-3777], Pentimalli, Francesca [0000-0003-4740-6801], Pereira, David M. [0000-0003-0384-7592], Pervaiz, Shazib [0000-0002-4738-019X], Peter, Marcus E. [0000-0003-3216-036X], Pinton, Paolo [0000-0001-7108-6508], Porta, Giovanni [0000-0001-5260-2415], Puthalakath, Hamsa [0000-0001-5178-1175], Rabinovich, Gabriel A. [0000-0002-0947-8735], Rajalingam, Krishnaraj [0000-0002-4175-9633], Ravinchandran, Kodi S. [0000-0001-9049-1410], Rehm, Markus [0000-0001-6149-9261], Ricci, Jean-Ehrland [0000-0003-1585-8117], Rizzuto, Rosario [0000-0001-7044-5097], Robinson, Nirmal [0000-0002-7361-9491], Rotblat, Barak [0000-0003-2985-7115], Rothlin, Carla V. [0000-0002-5693-5572], Rubinsztein, David C. [0000-0001-5002-5263], Rufini, Alessandro [0000-0002-5855-655X], Ryan, Kevin M. [0000-0002-1059-9681], Sarosiek, Kristopher A. [0000-0002-4618-5085], Sawa, Akira [0000-0003-1401-3008], Sayan, Emre [0000-0002-5291-1485], Schroder, Kate [0000-0001-9261-3805], Scorrano, Luca [0000-0002-8515-8928], Sesti, Federico [0000-0002-2761-9693], Shi, Yufang [0000-0001-8964-319X], Sica, Giuseppe [0000-0002-7407-0584], Silke, John [0000-0002-7611-5774], Simon, Hans-Uwe [0000-0002-9404-7736], Sistigu, Antonella [0000-0002-2528-1238], Stockwell, Brent R. [0000-0002-3532-3868], Strappazzon, Flavie [0000-0003-0285-7449], Sun, Liming [0000-0002-0136-5605], Sun, Erwei [0000-0001-5664-513X], Szabadkai, G [0000-0002-3006-3577], Tait, Stephen W. G. [0000-0001-7697-132X], Tang, Daolin [0000-0002-1903-6180], Tavernarakis, Nektarios [0000-0002-5253-1466], Turk, Boris [0000-0002-9007-5764], Urbano, Nicoletta [0000-0003-1822-155X], Vandenabeele, Peter [0000-0002-6669-8822], Vanden Berghe, Tom [0000-0002-1633-0974], Vander Heiden, Matthew G. [0000-0002-6702-4192], Vanderluit, Jacqueline L. [0000-0002-4960-920X], Verkhratsky, A. [0000-0003-2592-9898], Villunger, Andreas [0000-0001-8259-4153], Von Karstedt, Silvia [0000-0002-7816-5919], Voss, Anne K. [0000-0002-3853-9381], Vucic, Domagoj [0000-0003-3614-8093], Vuri, Daniela [0000-0001-8693-3845], Wagner, Erwin F. [0000-0001-7872-0196], Walczak, Henning [0000-0002-6312-4591], Wallach, David [0000-0003-2724-9757], Wang, Ruoning [0000-0001-9798-8032], Weber, Achim [0000-0003-0073-3637], Yamazaki, Takahiro [0000-0002-7420-4394], Zakeri, Zahra [0000-0003-4386-8072], Zawacka-Pankau, Joanna E. [0000-0002-7415-2942], Zhivotovsky, Boris [0000-0002-2238-3482], Piacentini, Mauro [0000-0003-2919-1296], Kroemer, Guido [0000-0002-9334-4405], Galluzzi, Lorenzo [0000-0003-2257-8500 ], Vitale, Ilio, Pietrocola, Federico, Guilbaud, Emma, Aaronson, Stuart A., Abrams, John M., Dieter, Adam, Agostini, Massimiliano, Agostinis, Patrizia, Alnemri, Emad S., Altucci, Lucia, Amelio, Ivano, Andrews, David W., Aqeilan, Rami I., Arama, Eli, Baehrecke, Eric H., Balachandran, Siddharth, Bano, Daniele, Barlev, Nickolai A., Bartek, Jiri, Bazan, Nicolas G., Becker, Christoph, Bernassola, Francesca, Bertrand, Mathieu J. M., Bianchi, Marco Emilio, Blagosklonny, Mikhail V., Blander, J. Magarian, Blandino, Giovanni, Blomgren, Klas, Bomer, Christoph, Bortner, Carl D., Bove, Pierluigi, Boya, Patricia, Brenner, Catherine, Broz, Petr, Brunner, T., Damgaard, Rune Busk, Calin, George A., Campanella, Michelangelo, Candi, Eleonora, Carbone, Michele, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K.-M., Chen, Guo‑Qiang, Chen, Quan, Chen, Youhai H., Cheng, Emily H., Chipuk, Jerry E., Cidlowski, John A., Ciechanover, Aaron, Ciliberto, Gennaro, Conrad, Marcus, Cubillos-Ruiz, Juan R., Czabotar, Peter E., D’Angiolella, Vincenzo, Daugaard, Mads, Dawson, Ted M., Dawson, Valina L., De Maria, Ruggero, De Strooper, B., Debatin, Klaus-Michael, Deberardinis, Ralph J., Degterev, Alexei, Del Sal, Giannino, Deshmukh, Mohanish, Di Virgilio, Francesco, Diederich, Marc, Dixon, Scott J., Dynlacht, Brian D., El-Deiry, Wafik S., Elrod, John W., Engeland, Kurt, Fimia, Gian María, Galassi, Claudia, Ganini, Carlo, García-Sáez, Ana J., Garg, Abhishek D., Garrido, Carmen, Gavathiotis, Evripidis, Gerlic, Motti, Ghosh, Sourav, Green, Douglas R., Greene, Lloyd A., Gronemeyer, Hinrich, Häcker, Georg, Hajnóczky, György, Hardwick, J. Marie, Haupt, Ygal, He, Sudan, Heery, David M., Hengartner, Michael O., Hetz, Claudio, Hildeman, David A., Ichijo, Hidenori, Inoue, Satoshi, Jäättelä, Marja, Janic, Ana, Joseph, Bertrand, Jost, Philipp J., Kanneganti, Thirumala-Devi, Karin, Michael, Kashkar, Hamid, Kaufmann, Thomas, Kelly, Gemma L., Kepp, Oliver, Kimchi, Adi, Kitsis, Richard N., Klionsky, Daniel J., Kluck, Ruth, Krysko, Dmitri V., Kulms, Dagmar, Kumar, Sharad, Lavandero, Sergio, Lavrik, Inna N., Lemasters, John J., Liccardi, Gianmaria, Linkermann, Andreas, Lipton, Stuart A., Lockshin, Richard A., López-Otín, Carlos, Luedde, Tom, MacFarlane, Marion, Madeo, Frank, Malorni, Walter, Manic, Gwenola, Mantovani, Roberto, Marchi, Saverio, Marine, Jean-Christophe, Martin, Seamus J., Martinou, Jean-Claude, Mastroberardino, Pier G., Medema, Jan Paul, Mehlen, Patrick, Meier, Pascal, Melino, Gerry, Melino, Sonia, Miao, Edward A., Moll, Ute M., Muñoz-Pinedo, Cristina, Murphy, Daniel J., Niklison-Chirou, Maria Victoria, Novelli, Flavia, Núñez, Gabriel, Oberst, Andrew, Ofengeim, Dimitry, Opferman, Joseph T., Oren, Moshe, Pagano, Michele, Panaretakis, Theocharis, Pasparakis, Manolis, Penninger, Josef M., Pentimalli, Francesca, Pereira, David M., Pervaiz, Shazib, Peter, Marcus E., Pinton, Paolo, Porta, Giovanni, Prehn, Jochen H. M., Puthalakath, Hamsa, Rabinovich, Gabriel A., Rajalingam, Krishnaraj, Ravinchandran, Kodi S., Rehm, Markus, Ricci, Jean-Ehrland, Rizzuto, Rosario, Robinson, Nirmal, Rodrigues, Cecilia M. P., Rotblat, Barak, Rothlin, Carla V., Rubinsztein, David C., Rudel, Thomas, Rufini, Alessandro, Ryan, Kevin M., Sarosiek, Kristopher A., Sawa, Akira, Sayan, Emre, Schroder, Kate, Scorrano, Luca, Sesti, Federico, Shao, Feng, Shi, Yufang, Sica, Giuseppe, Silke, John, Simon, Hans-Uwe, Sistigu, Antonella, Stephanou, Anastasis, Stockwell, Brent R., Strappazzon, Flavie, Strasser, Andreas, Sun, Liming, Sun, Erwei, Sun, Qiang, Szabadkai, G, Tait, Stephen W. G., Tang, Daolin, Tavernarakis, Nektarios, Troy, Carol M., Turk, Boris, Urbano, Nicoletta, Vandenabeele, Peter, Vanden Berghe, Tom, Vander Heiden, Matthew G., Vanderluit, Jacqueline L., Verkhratsky, A., Villunger, Andreas, Von Karstedt, Silvia, Voss, Anne K., Vousden, Karen H., Vucic, Domagoj, Vuri, Daniela, Wagner, Erwin F., Walczak, Henning, Wallach, David, Wang, Ruoning, Wang, Ying, Weber, Achim, Wood, Will, Yamazaki, Takahiro, Yang, Zahra, Zakeri, Zahra, Zawacka-Pankau, Joanna E., Zhang, Lin, Zhang, Haibin, Zhivotovsky, Boris, Zhou, Wenzhao, Piacentini, Mauro, Kroemer, Guido, and Galluzzi, Lorenzo

Abstract

Apoptosis is a form of regulated cell death (RCD) that involves proteases of the caspase family. Pharmacological and genetic strategies that experimentally inhibit or delay apoptosis in mammalian systems have elucidated the key contribution of this process not only to (post-)embryonic development and adult tissue homeostasis, but also to the etiology of multiple human disorders. Consistent with this notion, while defects in the molecular machinery for apoptotic cell death impair organismal development and promote oncogenesis, the unwarranted activation of apoptosis promotes cell loss and tissue damage in the context of various neurological, cardiovascular, renal, hepatic, infectious, neoplastic and inflammatory conditions. Here, the Nomenclature Committee on Cell Death (NCCD) gathered to critically summarize an abundant pre-clinical literature mechanistically linking the core apoptotic apparatus to organismal homeostasis in the context of disease.

Published
2023

90. The RAAS Axis and SARS-CoV-2: From Oral to Systemic Manifestations

Author

Minela Aida Maranduca, Calin George Vamesu, Daniela Maria Tanase, Andreea Clim, Ilie Cristian Drochioi, Alin Constantin Pinzariu, Nina Filip, Nicoleta Dima, Ionut Tudorancea, Dragomir Nicolae Serban, and Ionela Lacramioara Serban

Subjects
RAAS, ACE2, SARS-CoV-2, COVID-19, Medicine (General), R5-920
Abstract

One of the essential regulators of arterial blood pressure, the renin-angiotensin-aldosterone system (RAAS) seems to be one of the most complex mechanisms in the human body. Since the discovery of its key components and their actions, new substances and functions are still being unraveled. The main pathway begins with the secretion of renin in the kidney and culminates with the synthesis of angiotensin II (Ang II)—a strong vasoconstrictor—thanks to the angiotensin-converting enzyme (ACE). Research conducted in 2000 identified another enzyme, named ACE2, that converts Ang II into Ang-(1–7), a heptapeptide with opposing effects to those of Ang II: vasodilation and anti-inflammatory properties. This particular enzyme became of paramount importance during the last two decades, as a result of the confrontation of the human race with life-threatening epidemics. Multiple studies have been performed in order to uncover the link between ACE2 and human coronaviruses, the results of which we systemized in order to create an overview of the pathogenic mechanism. Human coronaviruses, such as SARS-CoV and SARS-CoV-2, attach to ACE2 via their spike proteins (S), causing the destruction of the enzyme. Because ACE2 limits the production of Ang II (by converting it into Ang-(1–7)), its destruction leads to a dysregulated inflammatory response. The purpose of this review is to decipher the complex pathophysiological mechanisms underlying the multiorgan complications (oral, cardiac, pulmonary, systemic) that appear as a result of the interaction of the SARS CoV-2 virus with the angiotensin-converting enzyme type 2.

Published
2022
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91. MicroRNAs, Regulatory Messengers Inside and Outside Cancer Cells

Author

Anfossi, Simone, Fu, Xiao, Nagvekar, Rahul, Calin, George A., COHEN, IRUN R., Series Editor, LAJTHA, ABEL, Series Editor, LAMBRIS, JOHN D., Series Editor, PAOLETTI, RODOLFO, Series Editor, REZAEI, NIMA, Series Editor, Mettinger, Karl L., editor, Rameshwar, Pranela, editor, and Kumar, Vinod, editor

Published
2018
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93. KRAS mutations as essential promoters of lymphangiogenesis via extracellular vesicles in pancreatic cancer

Author

Pirlog, Radu and Calin, George A.

Subjects
Health care industry
Abstract

Kirsten rat sarcoma virus (KRAS) gene mutations are present in more than 90% of pancreatic ductal adenocarcinomas (PDACs). [KRAS.sup.G12D] is the most frequent alteration, promoting preneoplastic lesions and associating with a more aggressive phenotype. These tumors possess increased intratumoral lymphatic networks and frequent lymph node (LN) metastases. In this issue of the JCI, Luo, Li, et al. explored the relationship between the presence of the [KRAS.sup.G12D] mutation and lymphangiogenesis in PDAC. The authors used in vitro and in vivo models and an elegant mechanistic approach to describe an alternative pathway for lymphangiogenesis promotion. [KRAS.sup.G12D] induced SUMOylation of heterogenous nuclear ribonucleoprotein A1 (hnRNPAI) via SAE1 and SUMO2 activation. SUMOylated hnRNPAI was loaded into extracellular vesicles (EVs) and internalized by human endothelial lymphatic cells (HLEC). Further, SUMOylated hnRNPAI promoted lymphangiogenesis and LN metastasis by stabilizing prospero homeodomain protein 1 (PROX1) mRNA. These data provide mechanistic insight into cancer lymphangiogenesis with the potential for developing biomarkers and RAS pathway therapeutics., KRAS mutations in pancreatic cancers Pancreatic cancer is the deadliest gastrointestinal malignancy, as the fourth leading cause of cancer-related death and with one of the lowest 5-year survival rates, at [...]

Published
2022
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94. SIK2 inhibition enhances PARP inhibitor activity synergistically in ovarian and triple-negative breast cancers

Author

Lu, Zhen, Mao, Weiqun, Yang, Hailing, Santiago-OFarrill, Janice M., Rask, Philip J., Mondal, Jayanta, Chen, Hu, Ivan, Cristina, Liu, Xiuping, Liu, Chang-Gong, Xi, Yuanxin, Masuda, Kenta, Carrami, Eli M., Chen, Meng, Tang, Yitao, Pang, Lan, Lakomy, David S., Calin, George A., Liang, Han, Ahmed, Ahmed A., Vankayalapati, Hariprasad, and Bast, Robert C., Jr.

Subjects
Drug synergism, Ovarian cancer -- Drug therapy -- Models, Health care industry
Abstract

Poly(ADP-ribose) polymerase inhibitors (PARP inhibitors) have had an increasing role in the treatment of ovarian and breast cancers. PARP inhibitors are selectively active in cells with homologous recombination DNA repair deficiency caused by mutations in BRCA1/2 and other DNA repair pathway genes. Cancers with homologous recombination DNA repair proficiency respond poorly to PARP inhibitors. Cancers that initially respond to PARP inhibitors eventually develop drug resistance. We have identified salt-inducible kinase 2 (SIK2) inhibitors, ARN3236 and ARN3261, which decreased DNA double-strand break (DSB) repair functions and produced synthetic lethality with multiple PARP inhibitors in both homologous recombination DNA repair deficiency and proficiency cancer cells. SIK2 is required for centrosome splitting and PI3K activation and regulates cancer cell proliferation, metastasis, and sensitivity to chemotherapy. Here, we showed that SIK2 inhibitors sensitized ovarian and triple-negative breast cancer (TNBC) cells and xenografts to PARP inhibitors. SIK2 inhibitors decreased PARP enzyme activity and phosphorylation of class-IIa histone deacetylases (HDAC4/5/7). Furthermore, SIK2 inhibitors abolished class-IIa HDAC4/5/7-associated transcriptional activity of myocyte enhancer factor-2D (MEF2D), decreasing MEF2D binding to regulatory regions with high chromatin accessibility in FANCD2, EXO1, and XRCC4 genes, resulting in repression of their functions in the DNA DSB repair pathway. The combination of PARP inhibitors and SIK2 inhibitors provides a therapeutic strategy to enhance PARP inhibitor sensitivity for ovarian cancer and TNBC., Introduction Recent studies indicate that DNA damage, aberrations in the DNA damage response, and defects in DNA repair machinery play a major role in ovarian cancer and triple-negative breast cancer [...]

Published
2022
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97. Loss of p53 drives neuron reprogramming in head and neck cancer

Author

Amit, Moran, Takahashi, Hideaki, Dragomir, Mihnea Paul, Lindemann, Antje, Gleber-Netto, Frederico O., Pickering, Curtis R., Anfossi, Simone, Osman, Abdullah A., Cai, Yu, Wang, Rong, Knutsen, Erik, Shimizu, Masayoshi, Ivan, Cristina, Rao, Xiayu, Wang, Jing, Silverman, Deborah A., Tam, Samantha, Zhao, Mei, Caulin, Carlos, Zinger, Assaf, Tasciotti, Ennio, Dougherty, Patrick M., El-Naggar, Adel, Calin, George A., and Myers, Jeffrey N.

Published
2020
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98. GLS2 is protumorigenic in breast cancers

Author

Dias, Marilia M., Adamoski, Douglas, dos Reis, Larissa M., Ascenção, Carolline F. R., de Oliveira, Krishina R. S., Mafra, Ana Carolina Paschoalini, da Silva Bastos, Alliny Cristiny, Quintero, Melissa, de G. Cassago, Carolina, Ferreira, Igor M., Fidelis, Carlos H. V., Rocco, Silvana A., Bajgelman, Marcio Chaim, Stine, Zachary, Berindan-Neagoe, Ioana, Calin, George A., Ambrosio, Andre Luis Berteli, and Dias, Sandra Martha Gomes

Published
2020
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99. Association Between Germline Mutations in BRF1, a Subunit of the RNA Polymerase III Transcription Complex, and Hereditary Colorectal Cancer

Author

Bellido, Fernando, Sowada, Nadine, Mur, Pilar, Lázaro, Conxi, Pons, Tirso, Valdés-Mas, Rafael, Pineda, Marta, Aiza, Gemma, Iglesias, Silvia, Soto, José Luís, Urioste, Miguel, Caldés, Trinidad, Balbín, Milagros, Blay, Pilar, Rueda, Daniel, Durán, Mercedes, Valencia, Alfonso, Moreno, Victor, Brunet, Joan, Blanco, Ignacio, Navarro, Matilde, Calin, George A., Borck, Guntram, Puente, Xose S., Capellá, Gabriel, and Valle, Laura

Published
2018
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