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Immunotherapy of cancer with checkpoint inhibitors has been associated with a spectrum of autoimmune and systemic inflammatory reactions known as immune-related adverse events (irAEs). Rheumatic irAEs are infrequently reported and extensively described. Here, we report our experience over an 18-month period with 15 patients evaluated in the rheumatology department for rheumatic irAEs. We identified 13 patients without pre-existing autoimmune disease (AID) who subsequently developed rheumatic irAEs, and two with established AID referred pre-emptively. irAEs encountered included: inflammatory arthritis, sicca syndrome, polymyalgia rheumatica-like symptoms and myositis. All cases required glucocorticoids, and three required a biological agent. Rheumatic irAEs led to temporary or permanent cessation of immunotherapy in all but five patients. One patient with pre-existing AID experienced a flare after starting immunotherapy. Our findings underscore that rheumatic irAEs are complex, at times require additional immunosuppressive therapy, and may influence ongoing immunotherapy regimens for the primary disease. Similar irAEs will be increasingly seen as checkpoint inhibitors adopted as standard of care in the community.

Chronic inflammation is an established risk factor for the onset of cancer, and the inflammatory cytokine IL-6 has a role in tumorigenesis by enhancing proliferation and hindering apoptosis. As factors stimulating proliferation also downregulate p53 expression by enhancing ribosome biogenesis, we hypothesized that IL-6 may cause similar changes in inflamed tissues, thus activating a mechanism that favors neoplastic transformation. Here, we showed that IL-6 downregulated the expression and activity of p53 in transformed and untransformed human cell lines. This was the consequence of IL-6-dependent stimulation of c-MYC mRNA translation, which was responsible for the upregulation of rRNA transcription. The enhanced rRNA transcription stimulated the MDM2-mediated proteasomal degradation of p53, by reducing the availability of ribosome proteins for MDM2 binding. The p53 downregulation induced the acquisition of cellular phenotypic changes characteristic of epithelial–mesenchymal transition, such as a reduced level of E-cadherin expression, increased cell invasiveness and a decreased response to cytotoxic stresses. We found that these changes also occurred in colon epithelial cells of patients with ulcerative colitis, a very representative example of chronic inflammation at high risk for tumor development. Histochemical and immunohistochemical analysis of colon biopsy samples showed an upregulation of ribosome biogenesis, a reduced expression of p53, together with a focal reduction or absence of E-cadherin expression in chronic colitis in comparison with normal mucosa samples. These changes disappeared after treatment with anti-inflammatory drugs. Taken together, the present results highlight a new mechanism that may link chronic inflammation to cancer, based on p53 downregulation, which is activated by the enhancement of rRNA transcription upon IL-6 exposure.

Background:Systemic lupus erythematosus (SLE) is a multi-organ disease characterised by generalised immune dysfunction. Patients with SLE are more susceptible to infections and higher rates of SLE flares are observed following infectious stimuli (1, 2). Little is known about the qualitative impact of infections on SLE phenotype.Objectives:To assess potential clinical differences between infection-triggered (ITF) and other SLE flares (OF).Methods:A retrospective review of prospectively collected data from >300 patients with SLE was performed. Disease activity was estimated through the SLE disease activity index 2000 (SLEDAI-2K) and the British Isles Lupus Assessment Group (BILAG) 2004 index, damage with the SLE International Collaborating Clinics/American College of Rheumatology Damage index (SDI). DAS-28 was used quantitate arthritis activity. Remission was surrogated by the Lupus Low Disease Activity State (LLDAS) algorithm. Included patient records consisted in couples of consecutive visits showing progression from LLDAS fulfillment to LLDAS loss. Visit couples were divided according to the association vs non-association of recent infections requiring antimicrobial treatment and/or absence from work. Clinical, laboratory and treatment features along with patient history data were compared at inter- and intraindividual level between the two groups. Anti-double stranded DNA antibody titres (ADNA) were recorded in a 0-4 discrete scale. Data are expressed as median (interquartile range), unless otherwise specified.Results:Out of 134 visit couples from 114 patients, 38 were ITF. Viral infections were 11/38. ITF involved one or two BILAG domains in 80% of cases, the most frequent being haematological (61%), mucocutaneous (24%) musculoskeletal 34% and renal (18%) domains. Cardiopulmonary manifestations were numerically less frequent in ITF than OF (0/38 vs 9/96; p=0.060). Although no difference was found in the frequency of musculoskeletal manifestations, ITF were characterised by higher DAS-28 scores [2.6 (2.3-4.1), n=12] than OF [2.0 (1.6-2.7), n=47;p=0.024]. Accordingly, intraindividual comparisons showed higher DAS-28 scores during ITF than during OF (10/11 vs 1/11; p=0.004). Compared to OF, viral IF were associated with lower ADNA titres [0 (0-0) vs 2 (0-3);p=0.046) and a lower frequency of complement consumption (2/11 vs 52/96; p=0.029) along with higher creatinine levels [1.2 (0.8-1.3) vs 0.8 (0.7-0.9)];p=0.016]. No differences were found in flare treatment profiles between ITF and OF.Conclusion:Preliminary data from a monocentric cohort apparently indicate that ITF, especially of viral origin, are associated with distinct clinical and serological phenotypes. This evidence suggests the existence of diverging pathophysiological mechanisms sustaining SLE activity under different conditions, which might benefit for personalized treatments.REFERENCES:[1] Danza A, et al., Lupus. 2013[2] Joo YB, et al., Scientific Reports. 2021Acknowledgements:NIL.Disclosure of Interests:Giuseppe Alvise Ramirez Astrazeneca (lessons), Astrazeneca, GSK (advisory boards), Astrazeneca (financial support for publication), Chiara Calabrese: None declared, Gabriele Domenico Gallina: None declared, Luca Moroni Astrazeneca (lessons), Astrazeneca, GSK (advisory boards), Astrazeneca (financial support for publication), Enrica Bozzolo: None declared, Marco Matucci-Cerinic: None declared, Lorenzo Dagna: None declared

Inflammatory Bowel Disease (IBD) is a group of chronic relapsing-remitting diseases characterized by intestinal and extra-intestinal manifestations that unfavourably impact patients' physical and mental quality of life. Recent evidence points to a possible higher incidence of Joint Hypermobility (JH) or “ligamentous hyperlaxity” in IBD patients compared to the general population and particularly in younger and female subjects with IBD. Ligamentous hyperlaxity represents a little-known benign clinical condition characterized in its asymptomatic form by joint and ligament hypermobility. the aim of this study is to determine the prevalence of ligamentous hyperlaxity in a cohort of patients with IBD. we evaluated 130 patients afferent to the joint clinic of the “Centro Regionale per le Malattie Infiammatorie Croniche Intestinali “Massimo Campieri” e MI Borghi”, located at “Sant'Orsola-Malpighi” University Hospital in Bologna, in the period between June 2021 and November 2022, allocating them into 3 groups: 1) Ulcerative Colitis (UC), 2) Crohn's Disease (CD), 3) Indeterminate Colitis (IC). None of the patients was affected by hereditary collagenopathies. Out of 130 patients, 47 were affected by Ulcerative Colitis (UC), 78 by Crohn's Disease (CD) and 5 by Indeterminate Colitis (IC). The mean age at the time of the visit was 45,32 (±12,86 range 24-78) for patients with UC; 47,35 (±12,65 range 22-70) for patients with CD; 45,00 (±12,16 range 26-62) for patients with IC; in terms of sex: 47 men (20 with UC, 27 with CD, 0 with IC) and 83 women (27 with UC, 51 with CD and 5 with IC). 34 out of 130 patients presented ligamentous hyperlaxity according to Beighton's criteria (pt ≥ 4) (26,2% of total, 16 UC, 17 CD, 1 IC). Of the 47 patients with UC, 16 had ligamentous hyperlaxity (34%). Of the 78 patients with CD, 17 had ligamentous hyperlaxity (21,8%). Of the 5 patients with IC, 1 had ligamentous hyperlaxity (20%). It emerges from this analysis that the highest prevalence of ligamentous hyperlaxity occurs in patients with UC, compared with CD and IC. Chi-square test for independence was performed by comparing the variable ligamentous laxity with the variables IBD, UC, CD and IC. The groups CD and IC did not show any statistically significant result with regards to ligamentous laxity whereas we did observe a statistically significant higher frequency of ligamentous laxity (p-value < 0,05) in the UC group. a close association between Ulcerative Colitis and the presence of JH, especially compared to Crohn's disease and Indeterminate Colitis, clearly emerges from our observation, which could postulate a possible alteration of collagen development in the pathophysiology and clinical spectrum of UC only and not of IBD in general. These data, however, need to be confirmed and further investigated in the future with focused and rigorous prospective clinical studies, excluding confusing factors such as young age or inflammatory joint diseases such as spondyloarthritis. [1]Pizzi LT, Weston CM, Goldfarb NI, Moretti D, Cobb N, Howell JB, Infantolino A, Dimarino AJ, Cohen S. Impact of chronic conditions on quality of life in patients with inflammatory bowel disease. Inflamm Bowel Dis. 2006 Jan;12(1):47-52. [2]Kaplan GG. The global burden of IBD: from 2015 to 2025. Nat Rev Gastroenterol Hepatol. 2015;12(12):720–7. [3]Castori M, Tinkle B, Levy H, Grahame R, Malfait F, Hakim A. A framework for the classification of joint hypermobility and related conditions. Am J Med Genet Part C Semin Med Genet 2017; 175;148–57. NIL. None Declared.

Background:Systemic lupus erythematosus (SLE) is a multi-organ disease characterised by generalised immune dysfunction and dominated by autoimmunity. High-grade systemic inflammation, resembling autoinflammatory (AI) disorders might complicate and overlap with the classical lupus phenotype (1, 2). Patients with these characteristics amid the spectrum of SLE constitute an ill-defined subgroup despite a potentially higher risk of morbidity and mortality.Objectives:To characterise the clinical profile and long-term SLE outcomes of patients with AI features within a monocentric SLE cohort.Methods:By reviewing the clinical characteristics of about 300 patients with SLE we identified a group of subjects with AI features (AIG), meeting the following criteria: 1) fever without infection or with incomplete antibiotic response, lasting more than two weeks and/or resistant to 0.5mg/kg prednisone-equivalent steroid therapy; 2) history of non-infectious fever ≥40°C or 3) of Macrophage Activation Syndrome (MAS); 4) erythrocyte sedimentation rate (ESR) higher than 75mm/h in at least three consecutive visit, 5) C-reactive protein higher than twice the upper level of normality in at least three consecutive visits, excluding infections; 6) ferritinaemia higher than 600 ng/ml despite 0.5mg/kg prednisone-equivalent steroid therapy. We collected demographic, clinical and treatment data from a series of 140 consecutive patients without these criteria, which constituted a Control Group (CG). Damage accrual was measured with the SLE International Collaborating Clinics/American College of Rheumatology Damage Index (SDI).Results:Thirteen subjects met the inclusion criteria for AIG. The main AI manifestations were non infectious and/or steroid resistant fever longer than two weeks (n=8, 62%) followed by persistent ESR (n=7, 54%). MAS, persistent CRP and Ferritin elevation had a prevalence of 31% (n=4) each. Five subjects (39%) had concomitant SLE and AI onset (Table 1). Compared to the CG, SLE patients in the AIG had a significant higher proportion of constitutional symptoms (77% vs 38%, p=0.032), including fever (92% vs 16%, p<0.001), as expected. Gastrointestinal symptoms were also more frequent in the AIG compared to CG (31% vs 2%, p<0.001). A lower antiphospholipid antibody prevalence was found in AIG, especially with regard to anticardiolipin antibodies (0% vs 32%; p=0.015). No other differences were identified in terms of demographics, clinical and treatment features among the two groups. AIG patients with SLE had a higher risk of SDI progression over time compared to CG patients (HR 5.2, 95%C.I. 1.4-19.5 p=0.012; Figure 1).Conclusion:AI features constitute an uncommon, yet clinically significant aspect of the broad spectrum of SLE manifestations. SLE patients with AI manifestations show a distinct clinical profile and accrue damage more rapidly compared to patients without these clinical characteristics. These data highlight a still unmet need in the care of patients with SLE and suggest that unique pathogenic events occur in patients with AI features, which might insufficiently be tackled by current diagnostic and treatment strategies.REFERENCES:[1] Gavand PE, et al., Autoimmun Rev. 2017[2] Mahajan VK, et al., World J Clin Cases. 2023Acknowledgements:NIL.Disclosure of Interests:Giovanni Benanti: None declared, Giuseppe Alvise Ramirez Astrazeneca (lessons), Astrazeneca, GSK (advisory boards), Astrazeneca (financial support for publication), Costanza Vitellaro: None declared, Chiara Calabrese: None declared, Serena Nannipieri: None declared, Luca Moroni Astrazeneca (lessons), Astrazeneca, GSK (advisory boards), Astrazeneca (financial support for publication), Enrica Bozzolo: None declared, Marco Matucci-Cerinic: None declared, Lorenzo Dagna: None declared.

ABSTRACT Data on 6 months of fouling colonization on a series of panels, immersed at two different depths (0.5 m and 3 m) in two marinas along the Apulian coasts (Ionian Sea-Mar Grande of Taranto, and South Adriatic Sea-Brindisi), are reported. A total of 79 taxa were found, 59 in Taranto and 57 in Brindisi. Among them, a total of 21 NIS (non-indigenous species) were found (14 in Taranto and 19 in Brindisi), together with seven cryptogenic species (all present in Taranto and six in Brindisi). Species composition between the two sites was quite different, with only 37 species in common. By contrast, the percentage of species of each taxonomic group was quite similar, excluding the complete absence of Cnidaria in Brindisi. The best represented group was Crustacea with 24 taxa, most of which were vagile forms, followed by Polychaeta with 20 taxa, and Mollusca with only 11 taxa. Among sessile invertebrates, Tunicata and Bryozoa were represented by 15 and six taxa, respectively. Porifera and Cnidaria were poorly represented in both sites. The multivariate analysis showed the structure of the macrofouling assemblages in Taranto and Brindisi were significantly influenced by location, time and depth. Comparing the colonization pattern of the two sites, a more homogeneous situation was highlighted in Brindisi. Here, serpulids were the dominant group covering all the available substrate at both times of immersion and depths, especially after 6 months. This situation was displayed also by the MultiDimensional Scaling (MDS) analysis performed on qualitative data. The comparison of the sessile component with data relative to a previously investigated northern area (La Spezia-Ligurian Sea) revealed a different fouling assemblage with a richer community and a higher presence of NIS.

miR-21 is a microRNA (miRNA) frequently overexpressed in human cancers. Here we show that miR-21 is upregulated both in vitro and in vivo by oncogenic Ras, thus linking this miRNA to one of the most frequently activated oncogenes in human cancers. Ras regulation of miR-21 occurs with a delayed kinetic and requires at least two Ras downstream pathways. A screen of human thyroid cancers and non-small-cell lung cancers for the expression of miR-21 reveals that it is overexpressed mainly in anaplastic thyroid carcinomas, the most aggressive form of thyroid cancer, whereas in lung its overexpression appears to be inversely correlated with tumor progression. We also show that a LNA directed against miR-21 slows down tumor growth in mice. Consistently, a search for mRNAs downregulated by miR-21 shows an enrichment for mRNAs encoding cell cycle checkpoints regulators, suggesting an important role for miR-21 in oncogenic Ras-induced cell proliferation.

The use of immune checkpoint inhibitors (ICIs) for the treatment of cancer can be associated with adverse events including inflammatory arthritis (ICI-IA). ICI-IA can encompass a variety of different phenotypes including: polymyalgia rheumatica (PMR)-like, spondyloarthritis-like, rheumatoid arthritis (RA)-like, and others[1]. Due to the heterogeneous clinical presentation of ICI-IA, methods are needed to find important variables and associations to describe and distinguish between clinical phenotypes. Use supervised machine learning techniques to find important variables associated with classification of arthritis phenotypes among patients with ICI-IA. This study is ancillary to a retrospective observational study of patients with ICI-IA at 6 U.S sites who were treated with DMARDS (TNFi, IL6R, or methotrexate). Arthritis phenotypes was the classification target of interest. Demographics, patterns of swollen joints, medications, lab values, and concomitant irAEs were all obtained from the medical record. Descriptive statistics were computed. Classification and Regression Trees (CART) were created using the rpart and partykit packages and Random Forest (RdF) using the randomForest R package. One thousand trees were created for the forest. Variable importance scores (CART) and mean decrease in Gini scores (RdF) were created to assess the variable importance of included variables. 147 patients were included, mean age 62 years, 43% with melanoma. Arthritis phenotypes were PMR-like in 8.3%, spondylarthritis-like 19%, RA-like 48%, polyarthritis 17%, and other 8%. Two versions of the CART and RdF were performed (with and without study site) (Table 1). Including study site, the following were identified by both CART and RdF as important: study site was the most important variable associated with the phenotypic label, followed by cancer type, hand arthritis, age, total joint count (TJC). The CART flow diagram with study site is shown in the Figure 1. Excluding study site, CART and RdF identified hand arthritis, cancer type, age, TJC. We found that classification of arthritis phenotype was study site-specific in our statistical models. After excluding site, age, cancer type, TJC, maximum steroid dose, and hand arthritis were associated with phenotypic classification. The influence of study site illustrates current heterogeneity in ICI-IA phenotyping among experts and the need for formalized classification for enrollment in clinical trials. These results identify variables that could be explored by the ACR/EULAR ICI-IA classification criteria working group. [1]Ghosh N., Bass A. Rheumatic Complications of Immune Checkpoint Inhibitors. Med. Clin. North Am. 2021 Mar; 105(2):227-245. NIL. Deanna Jannat-Khah Shareholder of: Dr. Jannat-Khah owns shares of Walgreens/Boots Alliance, AstraZeneca, and Cytodyn (non Rheumatologic pharmaceutical company), Grant/research support from: Dr. Jannat-Khah has a grant from Hospital for Special Surgery for research., Nilasha Ghosh Grant/research support from: Dr. Ghosh has a grant from Hospital for Special Surgery for research., Laura Cappelli Grant/research support from: Dr. Cappelli has research grants from the NIH (NIAMS K23AR075872) and from Bristol-Myers Squibb., Pankti Reid Consultant of: Dr. Reid was a consultant for Level Ex, Grant/research support from: Dr. Reid has grant support from the following: COVID-19 Funds to Retain Clinical Scientists by the Supporting Early Career University Researchers to Excel through Disruptions Steering Committee and The University of Chicago Institute of Translational Medicine Clinical and Translational Science Award K12/KL2 Grant 5KL2TR002387-05, Jeffrey Sparks Consultant of: Dr. Sparks was a consultant for AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Gilead, Inova Diagnostics, Janssen, Optum, and Pfizer, Grant/research support from: Dr. Sparks has received grants from the following entities: Bristol Myers Squibb, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIH), Rheumatology Research Foundation, R.Bruce and Joan M. Mickey Research Scholar Fund, Llura Gund Award for Rheumatoid Arthritis Care and Research., Noha Abdel-Wahab Speakers bureau: Dr. Abdel-Wahab was a speaker for ChemoCentryx., Consultant of: Dr. Abdel-Wahab was a consultant for ChemoCentryx., Grant/research support from: Dr Abdel-Wahab has grant funding from the NIAD (K01AI163412) and from the University of Texas MD Anderson, cassandra calabrese Paid instructor for: Dr. Calabrese received an honorarium for a lecture by Sanofi, Consultant of: Dr. Calabrese was a consultant for Lilly, and AstraZeneca., Carlos Aude: None declared, Karmela Kim Chan: None declared, Anne Bass Grant/research support from: Dr Bass has grants from the Hospital for Special Surgery, Memorial Sloane Kettering Cancer Center, and the Rheumatology Research Foundation. [Display omitted] Table 1Variable Importance (VI) from Classification and Regression Tree (CART) and mean decrease in Gini score (MDG) from Random forest (RdF) associated with Immune Checkpoint Inhibitor Inflammatory Arthritis phenotype assignment.CharacteristicCART VI1RdF MDG2CART VI 1without study siteRdF MDG2without study siteStudy site2510.8Not includedAge1210.61312.2Cancer type166.7207.7Maximum steroid dose of prednisone (mg)7.38.7Total Joint Count45.966.2Hand arthritis143.7254.0Factors with MDG <=3cancer stage, rash, Number of IRAEs, sex, Rheumatoid factor positive(RF+), RF+ or cyclic citrullinated peptide factor positive, arthritis affecting: shoulder, knee, ankle, hip, wrist, and knee1 CART Variable importance, the higher the number the more influential the variable is in the CART2 Mean Decrease in Gini score from RdF is a measure to rank variables; the higher the number the more important the variable.

Group3 medulloblastoma (MB G3 ) that predominantly occur in young children are usually associated with MYC amplification and/or overexpression, frequent metastasis and a dismal prognosis. Physiologically relevant MB G3 models are currently lacking, making inferences related to their cellular origin thus far limited. Using in utero electroporation, we here report that MB G3 mouse models can be developed in situ from different multipotent embryonic cerebellar progenitor cells via conditional expression of Myc and loss of Trp53 function in several Cre driver mouse lines. The Blbp-Cre driver that targets embryonic neural progenitors induced tumors exhibiting a large-cell/anaplastic histopathology adjacent to the fourth ventricle, recapitulating human MB G3 . Enforced co-expression of luciferase together with Myc and a dominant-negative form of Trp53 revealed that GABAergic neuronal progenitors as well as cerebellar granule cells give rise to MB G3 with their distinct growth kinetics. Cross-species gene expression analysis revealed that these novel MB G3 models shared molecular characteristics with human MB G3 , irrespective of their cellular origin. We here developed MB G3 mouse models in their physiological environment and we show that oncogenic insults drive this MB subgroup in different cerebellar lineages rather than in a specific cell of origin.

BackgroundImmune checkpoint inhibitor associated arthritis (ICI-A) commonly persists for months to years, even after ICI cessation.[1]ObjectivesTo compare the safety and effectiveness of biologic and conventional disease modifying anti-rheumatic drugs (DMARDs) for ICI-A.MethodsRetrospective multicenter observational study. Inclusion: 1) diagnosis of ICI-A and 2) treatment with a tumor necrosis factor inhibitor (TNFi), interleukin-6 receptor inhibitor (IL6Ri) and/or methotrexate (MTX). Exclusion: preexisting autoimmune disease. The primary outcome was time to cancer progression from ICI initiation. Patients whose cancer progressed prior to DMARD initiation were excluded from this analysis. The secondary outcome was time to arthritis control from DMARD initiation, defined as grade 1 arthritis and prednisone ≤10mg/day. Cox proportional hazard models were generated, adjusting for confounders. A sensitivity analysis was performed incorporating a time dependent variable “time from ICI initiation to DMARD initiation.”Results147 patients were included, mean (SD) age 60.3 (11.9) years, 66 (45%) females. Sixty percent had received PD1/PDL1 monotherapy, 30% received combination CTLA4/PD1. Eighty percent had stage IV cancer. ICI-A treatment was TNFi in 33 (22%), IL6Ri 42 (29%), MTX 72 (49%) (Table 1). A Kaplan-Meier curve showing time to cancer progression by DMARD is shown in Figure 1. In an unadjusted Cox model with MTX as the reference, time to cancer progression with a TNFi was HR 2.51 (95% CI 0.91-6.93, p=0.075) and for IL6Ri HR 2.36 (95% CI 0.91-6.12, p=0.078). After adjustment for the time dependent variable, time to cancer progression was significantly shorter for TNFi-treated patients compared to MTX, HR 3.27 (95% CI 1.21-8.84, p=0.019). The result for IL6Ri was HR 2.31 (95% CI 0.98-5.41, p=0.055). Time to arthritis control was significantly faster for TNFi compared to MTX, HR 1.91 (95% CI 1.06-3.45, p=0.032) in an adjusted Cox model. Results for IL6Ri were HR 1.66 (95% CI 0.93-2.97, p=0.089). Results for cancer progression and arthritis control were similar in the subset of patients with melanoma.ConclusionTreatment of ICI-A with biologic DMARDs is associated with more rapid arthritis control than with MTX but may be associated with a shorter time to cancer progression. A prospective randomized controlled trial is needed to verify these findings and to identify the optimal approach to managing patients with high grade ICI-A.Reference[1] Braaten TJ, et al Ann Rheum Dis. 2020 Mar;79(3):332-338.Table 1.Patient characteristicsTotalTNFiIL6RMTXp-valueN147 (100%)33 (22%)42 (29%)72 (49%)Age, mean (SD)60.3 (11.9)56.3 (14.0)61.5 (12.5)61.5 (10.1)0.085Sex (female)66 (45%)13 (39%)15 (36%)38 (53%)0.17Race (white)136 (92%)30 (91%)40 (95%)66 (92%)0.18Cancer type0.068Melanoma63 (43%)16 (48%)21 (50%)26 (36%)Non-small cell lung cancer15 (10%)1 (3%)0 (0%)14 (19%)Renal cell carcinoma24 (16%)5 (15%)12 (29%)7 (10%)Bladder cancer7 (5%)1 (3%)3 (7%)1 (4%)Other38 (25%)10 (30%)6 (14%)22 (31%)Cancer stage0.34III26 (18%)7 (21%)6 (14%)13 (18%)IV118 (80%)24 (73%)36 (86%)58 (81%)Checkpoint inhibitor0.91PD1/PDL1 monotherapy101 (69%)24 (73%)28 (67%)49 (68%)Combination (CTLA4/PD1)44 (30%)9 (27%)13 (31%)22 (31%)ICI discontinued for arthritis58 (40%)12 (36%)17 (40%)29 (40%)0.92ICI initiation to DMARD start (days), median (IQR)403 (258,638)411 (284, 622)300 (170, 435)486(258, 675)0.020Duration of DMARD treatment, median (IQR)278 (77, 546)92 (45, 149)309 (63, 483)420 (138, 765)<0.001Maximum glucocorticoid dose, mean (SD)40 (27)53 (27)42 (28)33 (23)0.002Figure 1.Kaplan-Meier curve showing time to cancer progression from time of immune checkpoint inhibitor initiationAcknowledgements:NIL.Disclosure of InterestsAnne Bass: None declared, Noha Abdel-Wahab Speakers bureau: ChemoCentryx, Consultant of: ChemoCentryx, Pankti Reid: None declared, Jeffrey Sparks Consultant of: Bristol Myers Squibb, AbbVie, Amgen, Boehringer Ingelheim, Gilead, Inova Diagnostics, Janssen, Optum, Pfizer, Grant/research support from: Bristol Myers Squibb, cassandra calabrese Speakers bureau: Sanofi, Consultant of: Astazenica, Deanna Jannat-Khah: None declared, Nilasha Ghosh: None declared, Divya Rajesh: None declared, Carlos Aude: None declared, Lydia Gedmintas: None declared, Lindsey MacFarlane: None declared, Senada Arabelovic: None declared, Adewunmi Falohun: None declared, Komal Mushtak: None declared, Farah Al Haj: None declared, Adi Diab: None declared, Ami Shah Grant/research support from: Eicos Sciences, Medpace LLC, Arena Pharmaceuticals, Kadmon Corporation, Clifton Bingham Consultant of: Bristol Myers Squibb,: Abbvie, Janssen, Lilly, Pfizer, Sanofi, Moderna, Grant/research support from: Bristol Myers Squibb, Karmela Kim Chan: None declared, Laura Cappelli Consultant of: Bristol Myers Squibb, Grant/research support from: Bristol Myers Squibb.