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Article: Case report: First evidence of impressive efficacy of modulated dose selpercatinib in a young Caucasian with ANK3-RET fusion-positive NSCLC.

De Carlo, Elisa / Bertoli, Elisa / Schiappacassi, Monica / Stanzione, Brigida / Del Conte, Alessandro / Doliana, Roberto / Spina, Michele / Bearz, Alessandra

Frontiers in oncology

2024 Volume 14, Page(s) 1307458

Abstract: Over the past decade, molecular characterization has led to change the management of advanced non-small cell lung cancer (NSCLC) harboring driver mutations. Rearranged during transfection ( ...

Abstract	Over the past decade, molecular characterization has led to change the management of advanced non-small cell lung cancer (NSCLC) harboring driver mutations. Rearranged during transfection (
Language	English
Publishing date	2024-02-07
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2024.1307458
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Article ; Online: Liquid Biopsy in NSCLC: An Investigation with Multiple Clinical Implications.

Bertoli, Elisa / De Carlo, Elisa / Basile, Debora / Zara, Diego / Stanzione, Brigida / Schiappacassi, Monica / Del Conte, Alessandro / Spina, Michele / Bearz, Alessandra

International journal of molecular sciences

2023 Volume 24, Issue 13

Abstract: Tissue biopsy is essential for NSCLC diagnosis and treatment management. Over the past decades, liquid biopsy has proven to be a powerful tool in clinical oncology, isolating tumor-derived entities from the blood. Liquid biopsy permits several advantages ...

Abstract	Tissue biopsy is essential for NSCLC diagnosis and treatment management. Over the past decades, liquid biopsy has proven to be a powerful tool in clinical oncology, isolating tumor-derived entities from the blood. Liquid biopsy permits several advantages over tissue biopsy: it is non-invasive, and it should provide a better view of tumor heterogeneity, gene alterations, and clonal evolution. Consequentially, liquid biopsy has gained attention as a cancer biomarker tool, with growing clinical applications in NSCLC. In the era of precision medicine based on molecular typing, non-invasive genotyping methods became increasingly important due to the great number of oncogene drivers and the small tissue specimen often available. In our work, we comprehensively reviewed established and emerging applications of liquid biopsy in NSCLC. We made an excursus on laboratory analysis methods and the applications of liquid biopsy either in early or metastatic NSCLC disease settings. We deeply reviewed current data and future perspectives regarding screening, minimal residual disease, micrometastasis detection, and their implication in adjuvant and neoadjuvant therapy management. Moreover, we reviewed liquid biopsy diagnostic utility in the absence of tissue biopsy and its role in monitoring treatment response and emerging resistance in metastatic NSCLC treated with target therapy and immuno-therapy.
MeSH term(s)	Humans ; Lung Neoplasms/diagnosis ; Lung Neoplasms/genetics ; Lung Neoplasms/drug therapy ; Carcinoma, Non-Small-Cell Lung/diagnosis ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/pathology ; Liquid Biopsy/methods ; Biopsy ; Precision Medicine/methods ; Biomarkers, Tumor/genetics
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2023-06-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241310803
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Article ; Online: Combination of Chemotherapy and ALK Inhibitors in ALK-Positive NSCLC.

De Carlo, Elisa / Schiappacassi, Monica / Del Conte, Alessandro / Stanzione, Brigida / Bearz, Alessandra

Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer

2021 Volume 16, Issue 5, Page(s) e31–e32

MeSH term(s)	Drug Therapy, Combination ; Humans ; Lung Neoplasms/drug therapy ; Pemetrexed/therapeutic use ; Platinum/therapeutic use ; Protein Kinase Inhibitors/therapeutic use ; Receptor Protein-Tyrosine Kinases/genetics
Chemical Substances	Protein Kinase Inhibitors ; Pemetrexed (04Q9AIZ7NO) ; Platinum (49DFR088MY) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	2021-03-31
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	2432037-7
ISSN	1556-1380 ; 1556-0864
ISSN (online)	1556-1380
ISSN	1556-0864
DOI	10.1016/j.jtho.2021.01.1612
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Article ; Online: Platinum-induced upregulation of ITGA6 promotes chemoresistance and spreading in ovarian cancer.

Gambelli, Alice / Nespolo, Anna / Rampioni Vinciguerra, Gian Luca / Pivetta, Eliana / Pellarin, Ilenia / Nicoloso, Milena S / Scapin, Chiara / Stefanatti, Linda / Segatto, Ilenia / Favero, Andrea / D'Andrea, Sara / Mucignat, Maria Teresa / Bartoletti, Michele / Lucia, Emilio / Schiappacassi, Monica / Spessotto, Paola / Canzonieri, Vincenzo / Giorda, Giorgio / Puglisi, Fabio /

Vecchione, Andrea / Belletti, Barbara / Sonego, Maura / Baldassarre, Gustavo

EMBO molecular medicine

2024

Abstract: Platinum (PT)-resistant Epithelial Ovarian Cancer (EOC) grows as a metastatic disease, disseminating in the abdomen and pelvis. Very few options are available for PT-resistant EOC patients, and little is known about how the acquisition of PT-resistance ... ...

Abstract	Platinum (PT)-resistant Epithelial Ovarian Cancer (EOC) grows as a metastatic disease, disseminating in the abdomen and pelvis. Very few options are available for PT-resistant EOC patients, and little is known about how the acquisition of PT-resistance mediates the increased spreading capabilities of EOC. Here, using isogenic PT-resistant cells, genetic and pharmacological approaches, and patient-derived models, we report that Integrin α6 (ITGA6) is overexpressed by PT-resistant cells and is necessary to sustain EOC metastatic ability and adhesion-dependent PT-resistance. Using in vitro approaches, we showed that PT induces a positive loop that, by stimulating ITGA6 transcription and secretion, contributes to the formation of a pre-metastatic niche enabling EOC cells to disseminate. At molecular level, ITGA6 engagement regulates the production and availability of insulin-like growth factors (IGFs), over-stimulating the IGF1R pathway and upregulating Snail expression. In vitro data were recapitulated using in vivo models in which the targeting of ITGA6 prevents PT-resistant EOC dissemination and improves PT-activity, supporting ITGA6 as a promising druggable target for EOC patients.
Language	English
Publishing date	2024-04-24
Publishing country	England
Document type	Journal Article
ZDB-ID	2467145-9
ISSN	1757-4684 ; 1757-4676
ISSN (online)	1757-4684
ISSN	1757-4676
DOI	10.1038/s44321-024-00069-3
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Article ; Online: Acquired BRAF V600E Mutation as Resistant Mechanism after Treatment with Third-Generation EGFR Tyrosine Kinase Inhibitor.

Bearz, Alessandra / De Carlo, Elisa / Doliana, Roberto / Schiappacassi, Monica

Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer

2017 Volume 12, Issue 11, Page(s) e181–e182

MeSH term(s)	Acrylamides ; Aniline Compounds ; ErbB Receptors/antagonists & inhibitors ; Humans ; Lung Neoplasms/genetics ; Mutation ; Piperazines ; Proto-Oncogene Proteins B-raf/antagonists & inhibitors
Chemical Substances	Acrylamides ; Aniline Compounds ; Piperazines ; osimertinib (3C06JJ0Z2O) ; EGFR protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1) ; BRAF protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1)
Language	English
Publishing date	2017-10-25
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	2432037-7
ISSN	1556-1380 ; 1556-0864
ISSN (online)	1556-1380
ISSN	1556-0864
DOI	10.1016/j.jtho.2017.07.017
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Article ; Online: Acquired EGFR C797G Mutation Detected by Liquid Biopsy as Resistance Mechanism After Treatment With Osimertinib: A Case Report.

DE Carlo, Elisa / Schiappacassi, Monica / Pelizzari, Giacomo / Baresic, Tania / Del Conte, Alessandro / Stanzione, Brigida / DA Ros, Valentina / Doliana, Roberto / Baldassarre, Gustavo / Bearz, Alessandra

In vivo (Athens, Greece)

2021 Volume 35, Issue 5, Page(s) 2941–2945

Abstract: Background: Osimertinib is a third-generation EGFR-tyrosine kinase inhibitor approved for the treatment of T790M-positive non-small-cell lung cancer. More recently, osimertinib demonstrated improved disease control compared to other EGFR-TKIs. Multiple ... ...

Abstract	Background: Osimertinib is a third-generation EGFR-tyrosine kinase inhibitor approved for the treatment of T790M-positive non-small-cell lung cancer. More recently, osimertinib demonstrated improved disease control compared to other EGFR-TKIs. Multiple mechanisms of resistance have been described in T790M-positive patients who experienced treatment failure with osimertinib. Case report: We report the case of a 78-year-old non-smoker woman with stage IV EGFR L858R-positive lung adenocarcinoma presented with T790M mutation after five years of treatment with gefitinib. The patient was started on osimertinib, but after two and a half years of treatment experienced disease progression. The analyses of circulating tumor DNA using next-generation sequencing showed, together with the pre-existing T790M and exon 21 L858R, the presence of the EGFR C797G resistance mutation. Conclusion: Our case report revealed a rare EGFR-dependent acquired resistance mutation to osimertinib in circulating tumor DNA. Liquid biopsy appears to be a promising resource to understand the biology of osimertinib resistance by clonal evolution monitoring and the identification of novel resistance mechanisms.
MeSH term(s)	Acrylamides ; Aged ; Aniline Compounds ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Drug Resistance, Neoplasm/genetics ; ErbB Receptors/genetics ; Female ; Humans ; Liquid Biopsy ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Mutation ; Protein Kinase Inhibitors/therapeutic use
Chemical Substances	Acrylamides ; Aniline Compounds ; Protein Kinase Inhibitors ; osimertinib (3C06JJ0Z2O) ; EGFR protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2021-08-19
Publishing country	Greece
Document type	Case Reports ; Journal Article
ZDB-ID	807031-3
ISSN	1791-7549 ; 0258-851X
ISSN (online)	1791-7549
ISSN	0258-851X
DOI	10.21873/invivo.12586
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Article ; Online: Identification and Characterization of a New Platinum-Induced TP53 Mutation in MDAH Ovarian Cancer Cells.

Lorenzon, Ilaria / Pellarin, Ilenia / Pellizzari, Ilenia / D'Andrea, Sara / Belletti, Barbara / Sonego, Maura / Baldassarre, Gustavo / Schiappacassi, Monica

Cells

2019 Volume 9, Issue 1

Abstract: Platinum-based chemotherapy is the therapy of choice for epithelial ovarian cancer (EOC). Acquired resistance to platinum (PT) is a frequent event that leads to disease progression and predicts poor prognosis. To understand possible mechanisms underlying ...

Abstract	Platinum-based chemotherapy is the therapy of choice for epithelial ovarian cancer (EOC). Acquired resistance to platinum (PT) is a frequent event that leads to disease progression and predicts poor prognosis. To understand possible mechanisms underlying acquired PT-resistance, we have recently generated and characterized three PT-resistant isogenic EOC cell lines. Here, we more deeply characterize several PT-resistant clones derived from MDAH-2774 cells. We show that, in these cells, the increased PT resistance was accompanied by the presence of a subpopulation of multinucleated giant cells. This phenotype was likely due to an altered progression through the M phase of the cell cycle and accompanied by the deregulated expression of genes involved in M phase progression known to be target of mutant TP53. Interestingly, we found that PT-resistant MDAH cells acquired in the TP53 gene a novel secondary mutation (i.e., S185G) that accompanied the R273H typical of MDAH cells. The double p53
MeSH term(s)	Antineoplastic Agents/pharmacology ; Carcinoma, Ovarian Epithelial/genetics ; Cell Cycle/drug effects ; Cell Line, Tumor ; Cell Survival/drug effects ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/genetics ; Female ; Humans ; Mitosis/genetics ; Mutation ; Ovarian Neoplasms/genetics ; Ovary/pathology ; Platinum/pharmacology ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Antineoplastic Agents ; TP53 protein, human ; Tumor Suppressor Protein p53 ; Platinum (49DFR088MY)
Language	English
Publishing date	2019-12-21
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/cells9010036
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Article ; Online: Splicing factor proline- and glutamine-rich (SFPQ) protein regulates platinum response in ovarian cancer-modulating SRSF2 activity.

Pellarin, Ilenia / Dall'Acqua, Alessandra / Gambelli, Alice / Pellizzari, Ilenia / D'Andrea, Sara / Sonego, Maura / Lorenzon, Ilaria / Schiappacassi, Monica / Belletti, Barbara / Baldassarre, Gustavo

Oncogene

2020 Volume 39, Issue 22, Page(s) 4390–4403

Abstract: In epithelial ovarian cancer (EOC), response to platinum (PT)-based chemotherapy dictates subsequent treatments and predicts patients' prognosis. Alternative splicing is often deregulated in human cancers and can be altered by chemotherapy. Whether and ... ...

Abstract	In epithelial ovarian cancer (EOC), response to platinum (PT)-based chemotherapy dictates subsequent treatments and predicts patients' prognosis. Alternative splicing is often deregulated in human cancers and can be altered by chemotherapy. Whether and how changes in alternative splicing regulation could impact on the response of EOC to PT-based chemotherapy is still not clarified. We identified the splicing factor proline and glutamine rich (SFPQ) as a critical mediator of response to PT in an unbiased functional genomic screening in EOC cells and, using a large cohort of primary and recurrent EOC samples, we observed that it is frequently overexpressed in recurrent PT-treated samples and that its overexpression correlates with PT resistance. At mechanistic level, we show that, under PT treatment, SFPQ, in complex with p54
MeSH term(s)	Animals ; Antineoplastic Agents, Alkylating/pharmacology ; Antineoplastic Agents, Alkylating/therapeutic use ; Apoptosis ; Caspase 8/metabolism ; Caspase 9/genetics ; Caspase 9/metabolism ; Caspase Inhibitors/pharmacology ; Cell Line, Tumor ; Cisplatin/pharmacology ; Cisplatin/therapeutic use ; DNA-Binding Proteins/antagonists & inhibitors ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/physiology ; Drug Resistance, Neoplasm/drug effects ; Female ; Gene Knockdown Techniques ; Humans ; Mice ; Neoplasm Proteins/physiology ; Ovarian Neoplasms/drug therapy ; Ovarian Neoplasms/metabolism ; PTB-Associated Splicing Factor/physiology ; RNA Splicing ; RNA, Messenger/metabolism ; RNA, Neoplasm/metabolism ; RNA-Binding Proteins/antagonists & inhibitors ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/physiology ; Recurrence ; Serine-Arginine Splicing Factors/physiology ; Spliceosomes/metabolism
Chemical Substances	Antineoplastic Agents, Alkylating ; Caspase Inhibitors ; DNA-Binding Proteins ; NONO protein, human ; Neoplasm Proteins ; PTB-Associated Splicing Factor ; RNA, Messenger ; RNA, Neoplasm ; RNA-Binding Proteins ; SRSF2 protein, human (147153-65-9) ; Serine-Arginine Splicing Factors (170974-22-8) ; CASP8 protein, human (EC 3.4.22.-) ; Caspase 8 (EC 3.4.22.-) ; Caspase 9 (EC 3.4.22.-) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2020-04-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-020-1292-6
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Article ; Online: Serum- and glucocorticoid- inducible kinase 2, SGK2, is a novel autophagy regulator and modulates platinum drugs response in cancer cells.

Ranzuglia, Valentina / Lorenzon, Ilaria / Pellarin, Ilenia / Sonego, Maura / Dall'Acqua, Alessandra / D'Andrea, Sara / Lovisa, Sara / Segatto, Ilenia / Coan, Michela / Polesel, Jerry / Serraino, Diego / Sabatelli, Patrizia / Spessotto, Paola / Belletti, Barbara / Baldassarre, Gustavo / Schiappacassi, Monica

Oncogene

2020 Volume 39, Issue 40, Page(s) 6370–6386

Abstract: For many tumor types chemotherapy still represents the therapy of choice and many standard treatments are based on the use of platinum (PT) drugs. However, de novo or acquired resistance to platinum is frequent and leads to disease progression. In ... ...

Abstract	For many tumor types chemotherapy still represents the therapy of choice and many standard treatments are based on the use of platinum (PT) drugs. However, de novo or acquired resistance to platinum is frequent and leads to disease progression. In Epithelial Ovarian Cancer (EOC) patients, PT-resistant recurrences are very common and improving the response to treatment still represents an unmet clinical need. To identify new modulators of PT-sensitivity, we performed a loss-of-function screening targeting 680 genes potentially involved in the response of EOC cells to platinum. We found that SGK2 (Serum-and Glucocorticoid-inducible kinase 2) plays a key role in PT-response. We show here that EOC cells relay on the induction of autophagy to escape PT-induced death and that SGK2 inhibition increases PT sensitivity inducing a block in the autophagy cascade due to the impairment of lysosomal acidification. Mechanistically we demonstrate that SGK2 controls autophagy in a kinase-dependent manner by binding and inhibiting the V-ATPase proton pump. Accordingly, SGK2 phosphorylates the subunit V1H (ATP6V1H) of V-ATPase and silencing or chemical inhibition of SGK2, affects the normal autophagic flux and sensitizes EOC cells to platinum. Hence, we identified a new pathway that links autophagy to the survival of cancer cells under platinum treatment in which the druggable kinase SGK2 plays a central role. Our data suggest that blocking autophagy via SGK2 inhibition could represent a novel therapeutic strategy to improve patients' response to platinum.
MeSH term(s)	Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Apoptosis/drug effects ; Autophagy/drug effects ; Benzoates/pharmacology ; Benzoates/therapeutic use ; Bridged Bicyclo Compounds, Heterocyclic/pharmacology ; Bridged Bicyclo Compounds, Heterocyclic/therapeutic use ; Carboplatin/pharmacology ; Carboplatin/therapeutic use ; Carcinoma, Ovarian Epithelial/drug therapy ; Carcinoma, Ovarian Epithelial/genetics ; Carcinoma, Ovarian Epithelial/pathology ; Cell Line, Tumor ; Cell Survival/drug effects ; Cisplatin/pharmacology ; Cisplatin/therapeutic use ; Drug Resistance, Neoplasm/drug effects ; Female ; Humans ; Immediate-Early Proteins/antagonists & inhibitors ; Immediate-Early Proteins/genetics ; Immediate-Early Proteins/metabolism ; Ovarian Neoplasms/drug therapy ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/pathology ; Paclitaxel/pharmacology ; Paclitaxel/therapeutic use ; Phosphorylation/drug effects ; Phosphorylation/genetics ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Protein Serine-Threonine Kinases/antagonists & inhibitors ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism ; RNA, Small Interfering/metabolism ; Vacuolar Proton-Translocating ATPases/metabolism
Chemical Substances	Benzoates ; Bridged Bicyclo Compounds, Heterocyclic ; Immediate-Early Proteins ; Protein Kinase Inhibitors ; RNA, Small Interfering ; 2-cyclopentyl-4-(5-phenyl-1H-pyrrolo(2,3-b)pyridin-3-yl)-benzoic acid (56887611DJ) ; Carboplatin (BG3F62OND5) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; serum-glucocorticoid regulated kinase (EC 2.7.11.1) ; ATP6V1H protein, human (EC 3.6.1.-) ; Vacuolar Proton-Translocating ATPases (EC 3.6.1.-) ; Paclitaxel (P88XT4IS4D) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2020-08-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-020-01433-6
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Article: Therapeutic decision based on molecular detection of resistance mechanism in an ALK-rearranged lung cancer patient: a case report.

De Carlo, Elisa / Schiappacassi, Monica / Urbani, Martina / Doliana, Roberto / Baldassarre, Gustavo / Da Ros, Valentina / Santarossa, Sandra / Chimienti, Emanuela / Berto, Eleonora / Fratino, Lucia / Bearz, Alessandra

OncoTargets and therapy

2018 Volume 11, Page(s) 8945–8950

Abstract: Background: The use of tyrosine kinase inhibitors (TKIs) of ALK is the therapy of choice for ALK-fusion patients. Unfortunately, all patients under this kind of treatment eventually develop acquired resistance through several well-known mechanisms, such ...

Abstract	Background: The use of tyrosine kinase inhibitors (TKIs) of ALK is the therapy of choice for ALK-fusion patients. Unfortunately, all patients under this kind of treatment eventually develop acquired resistance through several well-known mechanisms, such as acquisition of a secondary mutation within the kinase domain, activation of a bypass signaling pathway, or a histological change like small-cell lung cancer transformation. At the time of progression, a tissue re-biopsy may give important molecular and morphological information regarding the mechanisms driving resistance to ALK TKIs. However, this procedure is not always feasible and it may not reflect the tumor heterogeneity, and therefore gives incomplete information. To overcome these drawbacks, the analysis of circulating tumor DNA (ctDNA) isolated from plasma, the so-called liquid biopsy, is emerging as a noninvasive and useful tool for detecting resistance mutations. Secondary resistance mutations are common in second-generation TKIs resistant patients and among these, Gly1202Arg (p.G1202R) emerged as the most frequent mutation. Case presentation: We have treated an ALK-positive lung adenocarcinoma patient with a sequential strategy of ALK TKIs. Patient follow-up was performed combining clinical, radiological, and molecular profiling. ctDNA was isolated from plasma and by means of ultra-deep next generation sequencing; we searched for secondary ALK resistance mutations on exons 21-25. ALK mutation Gly1202Arg (G1202R) was detected. We have documented consistency between plasma levels of G1202R mutation and radiological progression or improvement. Conclusion: Liquid biopsy appears to be a promising tool to anticipate progression and to drive the therapeutic strategy based upon ALK resistance mutations.
Language	English
Publishing date	2018-12-10
Publishing country	New Zealand
Document type	Case Reports
ZDB-ID	2495130-4
ISSN	1178-6930
ISSN	1178-6930
DOI	10.2147/OTT.S184745
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