This is a single center prospective observational study to characterize the immune landscape of newly diagnosed epithelial ovarian cancer (OC).
Patients with newly diagnosed epithelial OC will be enrolled in 4 different cohorts: A) Newly diagnosed high grade serous or endometroid OC undergoing primary debulking surgery; B) Newly diagnosed high grade serous or endometroid OC undergoing neoadjuvant chemotherapy (NACT) followed by interval debulking surgery; C) Rare subtypes of epithelial OC (low grade serous, low grade endometrioid, clear cell, mucinous or carcinosarcoma) undergoing primary debulking surgery; D) Rare subtypes of epithelial OC (low grade serous, low grade endometrioid, clear cell, mucinous or carcinosarcoma) undergoing NACT followed by interval debulking surgery. A cohort of women undergoing adnexectomy for benign pathology will be enrolled (cohort E) for comparative analysis.
Enrolled patients will be asked to provide the following biological samples at specified time points: archival and fresh tumor tissue, peripheral blood samples, rectal and vaginal swabs, ascites (when present).
The main aim of the study is to characterize the immune landscape of epithelial OC in tumor tissue and peripheral blood and correlate the presence of myeloid-derived suppressive cells (MDSCs) and other immune infiltrates and of the systemic immune response with progression free interval (PFI) in epithelial OC.

开始日期2022-12-20

申办/合作机构

Institute of Oncology Research

NCT04456049

/ Terminated临床2期IIT

COVID_ENZA Trial: Randomized Open Label Phase II Study to Evaluate the Efficacy of Enzalutamide in High Risk Male Outpatients With COVID-1

High risk outpatient adult males with a confirmed SARS-CoV-2 infection will be included in the study.
Patients will be randomized to receive Enzalutamide with standard of care (SOC) or SOC alone. Enzalutamide will be administered daily p.o. from Day 1 to Day 28 or until confirmed negativization of Nasopharyngeal swap (NPS) Polymerase chain reaction (PCR) (2 consecutive negative samples), whichever occurs first.

开始日期2020-08-24

申办/合作机构

Ente Ospedaliero Cantonale

[+1]

NCT04516850

/ CompletedN/AIIT

An Exploratory Analysis of the Expression of Receptors and Activating Proteases Mediating SARS-CoV-2 Entry and the Association Between HSD3B1 Gene Polymorphisms With Outcomes in SARS-CoV-2 Infected Patients

The study includes 2 sub-projects.
Sub-project 1: The aim is to evaluate the expression of receptors and activating proteases mediating SARS-CoV-2 entry and spreading in the local population of Ticino.
Sub-project 2: The aim is to investigate the association between the HSD3B1 gene variations and outcome of COVID-19 in the local population of Ticino.

开始日期2020-06-08

申办/合作机构

Institute of Oncology Research

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0 项与 Institute of Oncology Research 相关的专利（医药）

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517

项与 Institute of Oncology Research 相关的文献（医药）

2025-04-21·Cancer Research

Abstract 314: Improved tumor penetration and cytotoxic payload release with TD001, a novel PSMA-targeting ADC with optimized linker-payload composition, in PSMA-expressing CRPC CDX castrated mouse models

作者: Balla, Atik ; Mosole, Simone ; Cvitkovic, Esteban ; Rosenberg, Morris ; Deleglise, Bérangère ; Storelli, Elisa ; D'Incalci, Maurizio ; Morosi, Lavinia ; Jauk, Federico ; Impellizzieri, Daniela ; Catapano, Carlo V. ; Frapolli, Roberta ; Houacine, Jemila ; Dongilli, Cristina

AbstractProstate-specific membrane antigen (PSMA), a type II transmembrane glycoprotein belonging to the folate receptor family, is highly expressed in metastatic castration-resistant prostate cancer (mCRPC), and increases following androgen deprivation therapy (ADT). PSMA is a validated diagnostic and therapeutic target for radioligands and antibody-drug conjugates (ADCs). TD001 is a novel ADC composed of a deimmunized anti-PSMA IgG1 monoclonal antibody (HuJ591) conjugated to a highly stable protease-cleavable proprietary linker and the potent Topo I inhibitor exatecan payload. The LD038 linker-payload leverages exatecan’s ability to stabilize Topo I-DNA complexes and induce DNA damage and cell death. We tested TD001 in 2D and 3D cell cultures and in vivo in human CRPC xenograft models with different levels of PSMA expression. We evaluated cell internalization, payload release, and drug activity by flow cytometry, immunohistochemistry, and immunofluorescence microscopy. Free payload levels were measured 24 h post treatment in plasma and tumors by LC-MS/MS. TD001 showed efficient binding and rapid internalization within 1-3 h followed by lysosomal localization and payload release in PSMA-expressing cells. Due to the quick and effective payload release, TD001 exhibited selective and potent activity with the induction of Topo I-mediated DNA damage (gamma-H2AX) and apoptosis (cleaved caspase 3). TD001 had no effect on PSMA-negative cells. This was supported by 3D cell culture models, which demonstrated rapid diffusion into the extracellular matrix, and rapid internalization of TD001 into PSMA-expressing tumor cells. TD001 was evaluated in vivo in three CRPC xenograft models with different PSMA expression patterns: the high/homogenous (∼104 ligands/cell) PSMA-expressing LNCaP-abl cell line-derived xenograft (CDX) castrated mouse model, the intermediate/heterogeneous (∼102-104 ligands/cell) PSMA-expressing 22Rv1 CDX castrated mouse model, and the AR-positive, high/homogenous (∼105 ligands/cell)-PSMA-expressing patient-derived xenograft (PDX) C5 mouse model. The LD038 linker-payload in TD001 resulted in high free payload release within tumor tissue, triggering DNA damage, cell death, and growth arrest. Notably, tumor uptake and a very high tumor/plasma ratio (70-100 fold) of exatecan were similar 24 h after IV administration in all three in vivo models despite substantial differences in PSMA expression and heterogeneity. These findings highlight the ability of TD001 to deliver effectively and selectively the payload exatecan to PSMA-positive prostate tumors, resulting in potent antitumor activity in different CRPC models, including those with intermediate and heterogenous PSMA expression.Citation Format:Daniela Impellizzieri, Elisa Storelli, Atik Balla, Simone Mosole, Cristina Dongilli, Federico Jauk, Roberta Frapolli, Lavinia Morosi, Maurizio D'Incalci, Jemila Houacine, Morris Rosenberg, Bérangère Deleglise, Esteban Cvitkovic, Carlo V. Catapano. Improved tumor penetration and cytotoxic payload release with TD001, a novel PSMA-targeting ADC with optimized linker-payload composition, in PSMA-expressing CRPC CDX castrated mouse models [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 314.

2025-04-21·Cancer Research

Abstract 311: Long-term tumor growth inhibition and extended survival with TD001, a novel optimized PSMA-targeting ADC, in PSMA-expressing CRPC CDX castrated mouse models

作者: Balla, Atik ; Mosole, Simone ; Cvitkovic, Esteban ; Rosenberg, Morris ; Bekradda, Mohamed ; Storelli, Elisa ; D'Incalci, Maurizio ; Morosi, Lavinia ; Impellizzieri, Daniela ; Jauk, Federico ; Catapano, Carlo V. ; Frapolli, Roberta ; Houacine, Jemila ; Dongilli, Cristina

AbstractPatients with metastatic castration-resistant prostate cancer (mCRPC) who progress on androgen deprivation therapy (ADT) have limited therapeutic options. Prostate-specific membrane antigen (PSMA) is a type II transmembrane glycoprotein highly expressed in mCRPC and is a validated target for precision medicine approaches. TD001 is a novel antibody-drug conjugate (ADC) composed of a deimmunized anti-PSMA IgG1 monoclonal antibody (HuJ591) conjugated to a highly stable protease-cleavable topoisomerase I inhibitor (exatecan) proprietary linker-payload (LD038) with a drug-to-antibody ratio (DAR) of 8. TD001 was evaluated in vivo in human cell line-derived xenograft (CDX) models with high PSMA expression (LNCaP-abl; ∼104 ligands/cell) or intermediate/heterogeneous PSMA expression (22Rv1; ∼102-104 ligands/cell) in castrated NRG mice, and in the high PSMA-expressing (∼105 ligands/cell) patient-derived xenograft (PDX) model C5 in non-castrated NRG mice. Of note, PSMA expression increased upon castration in both CDX models, mimicking the clinical condition of the target patient population. After single IV administration across a wide range of doses (up to 20 mg/kg), TD001 achieved dose-dependent, potent tumor growth inhibition (TGI) not only in the high-PSMA LNCaP-abl CDX and C5 PDX models but also in the intermediate-PSMA 22Rv1 CDX model. Rapid responses and high TGI (>90%) after a single administration at optimal doses were seen across all models. Upon tumor regrowth, PSMA expression was unchanged between treated and vehicle control groups, indicating no impact on target expression. Recurrent tumors remained similarly responsive to rechallenge with TD001. Of note, fractionation of a single TD001 dose into 2 or 3 doses administered every 10 days resulted in persistent tumor regression (TGI ≥90% for 60-70 days) and extended survival compared to the equivalent higher single dose. TD001 was well tolerated with no body weight loss or other signs of toxicity, nor mortality at all doses after single and repeated dosing regimens. Alternative dosing schedules, dose response, and tumor/plasma ratio result in a 2-3 fold increase in therapeutic index (TGI ≥90% for up to 60 days). TD001 appears as a best-in-class anti-PSMA ADC with its novel linker-payload (LD038) and exhibits potent antitumor activity in preclinical models with a broad range of PSMA expression, representing a highly promising treatment for PSMA-expressing CRPC patients. The efficacy of TD001 in preclinical in vivo castrated CDX and PDX models supports further investigation in clinical settings.Citation Format:Daniela Impellizzieri, Elisa Storelli, Atik Balla, Simone Mosole, Cristina Dongilli, Federico Jauk, Roberta Frapolli, Lavinia Morosi, Maurizio D'Incalci, Jemila Houacine, Morris Rosenberg, Mohamed Bekradda, Esteban Cvitkovic, Carlo V. Catapano. Long-term tumor growth inhibition and extended survival with TD001, a novel optimized PSMA-targeting ADC, in PSMA-expressing CRPC CDX castrated mouse models [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 311.

2025-04-21·Cancer Research

Abstract 315: Dose-response and tumor size at time of treatment with TD001, a novel ADC against PSMA, drive potent tumor growth inhibition in a CRPC CDX castrated mouse model

作者: Morosi, Lavinia ; Catapano, Carlo V. ; Storelli, Elisa ; Cvitkovic, Esteban ; Houacine, Jemila ; D'Incalci, Maurizio ; Impellizzieri, Daniela ; Bello, Ezia ; Meroni, Marina ; Frapolli, Roberta

AbstractProstate-specific membrane antigen (PSMA), a type II transmembrane glycoprotein belonging to the folate receptor family, is highly expressed in metastatic castrate-resistant prostate cancer (CRPC), and increases following androgen deprivation therapy. TD001 is a novel antibody-drug conjugate (ADC) composed of a deimmunized anti-PSMA IgG1 monoclonal antibody (HuJ591), which binds to the extracellular domain of PSMA, conjugated to a proprietary cleavable topoisomerase I inhibitor exatecan linker-payload (LD038), with a drug-to-antibody ratio (DAR) of 8. Flow cytometry and immunofluorescence microscopy show TD001 is internalized and cleaved rapidly, colocalizing with lysosomes in PSMA-expressing tumor cells. TD001 (10-20 mg/kg IV) was evaluated in a human CRPC cell line-derived xenograft (CDX) model, LNCaP-abl with high PSMA expression, in castrated NSG mice, with a range of tumor sizes (from 150 to 700 mm3) at the time of treatment. TD001 gave dose-dependent and sustained potent activity (tumor growth inhibition [TGI] >80%) with single dosing. Sustained inhibition of regrowth for 20 days was observed after TD001 10 mg/kg even in large tumors up to 400 mm3. Strong antitumoral activity of a single dose of TD001 10 mg/kg was also observed even in tumors >400 mm3 at the time of treatment. Tumor regrowth was faster in larger tumors (mean volume ∼300-400 mm3) compared to smaller tumors (mean volume ∼200 mm3). PSMA expression was unchanged in tumor regrowth between treated and vehicle control in the CDX castrated mouse model after treatment with TD001 up to 20 mg/kg, indicating no impact on target expression. Fractionation of a single TD001 dose into 2 or 3 doses administered every 10 days resulted in a 2-3 fold higher therapeutic index (TGI >90%) compared to the equivalent higher single isodose. No mortality or weight loss was reported. Pharmacokinetics/pharmacodynamic correlations of TD001 are described separately. TD001 appears as a best-in-class anti-PSMA Topo I inhibitor ADC (exatecan payload), and exhibited potent and sustained antitumor activity, including in large tumors, and represents a promising new treatment for PSMA-expressing CRPC patients.Citation Format:Roberta Frapolli, Ezia Bello, Marina Meroni, Daniela Impellizzieri, Elisa Storelli, Carlo V. Catapano, Lavinia Morosi, Maurizio D'Incalci, Jemila Houacine, Esteban Cvitkovic. Dose-response and tumor size at time of treatment with TD001, a novel ADC against PSMA, drive potent tumor growth inhibition in a CRPC CDX castrated mouse model [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 315.

项与 Institute of Oncology Research 相关的新闻（医药）

2025-04-18

·奇点网

《免疫》：反复横跳！科学家发现，衰老癌细胞释放的线粒体DNA，会通过激活cGAS-STING通路，发挥免疫抑制作用

*仅供医学专业人士阅读参考“老而不死是为贼”，大伙都听过吧？那有多少朋友知道，这句攻击性拉满的话，出自孔子他老人家之口呢？当然攻击性高也没毛病，有些人有些事就该猛猛抨击，比如人体内一些不好好接受衰老命运，反而要转变成衰老相关分泌表型（SASPs），通过分泌各种东西促进衰老和癌症等疾病发展的细胞。而进入衰老状态的癌细胞，现在也模仿这一招来搞鬼了。近日，瑞士肿瘤研究所（IOR）团队在Immunity期刊发表的研究成果[1]就显示，被抗癌治疗诱导衰老的癌细胞，可将自身的线粒体DNA（mtDNA）装进囊泡释放到细胞外，随后这些囊泡会被肿瘤微环境中的多形核髓系来源免疫抑制细胞（PMN-MDSCs）摄取，使mtDNA激活cGAS-STING-NF-κB信号，增强PMN-MDSCs的免疫抑制性。只能说，老而不死的癌细胞也太阴险了，针对性阻断mtDNA释放的关键通道，才有望逆转免疫抑制。一图总结论文主要发现其实从分类来说，mtDNA此前更多是被划分到细胞释放的损伤相关分子模式（DAMPs）之中，全身各处的免疫细胞可通过cGAS等感受器感知到游离mtDNA，进而激活与创伤、炎症性疾病乃至癌症对应的免疫应答[2]；2023年登上《自然》的一项研究[3]还显示，凋亡应激可促使衰老细胞将mtDNA释放到细胞外驱动SASP进程，算是“机制共享”了。而化疗、靶向治疗等常用抗癌治疗手段，也经常会诱导癌细胞进入衰老状态，这些衰老癌细胞会不会也通过释放mtDNA造成负面影响呢？本次瑞士研究者们的探索就基于上述猜想展开，研究者们首先在多个不同细胞衰老模型中证实，衰老细胞释放mtDNA是普遍现象，且被多西他赛化疗或CDK4/6抑制剂治疗诱导衰老的癌细胞（前列腺癌细胞）也是如此。在相应的前列腺癌肿瘤模型中，示踪实验也表明主要负责摄取mtDNA的正是PMN-MDSCs，且mtDNA是被装在胞外囊泡（EVs）内被衰老癌细胞释放出去，再被PMN-MDSCs吞噬进胞内的；随后，PMN-MDSCs的多个免疫抑制功能相关基因（如编码PD-L1的Cd274）表达就开始显著上调，NF-κB、IL-6-STAT3等促癌信号通路也被激活，直接用mtDNA处理PMN-MDSCs也有相同效果，实锤了mtDNA可诱导免疫抑制。衰老癌细胞可将mtDNA包在EVs内释放，诱导PMN-MDSCs增强免疫抑制作用而细胞内能够感知mtDNA等核酸的，就是cGAS及Toll样受体9（TLR9）等经典感受器，实验显示敲除PMN-MDSCs的cGAS，才能使mtDNA无法诱导免疫抑制增强；而cGAS感受到mtDNA后，主要会激活STING而非I型干扰素信号（IRF3-IFN轴），再由STING介导PKR样内质网激酶（PERK）来放大NF-κB通路信号（PERK-eIF2α通路可抑制NF-κB p65抑制蛋白IκBα的翻译），完成对免疫抑制性增强的调控。回过头来说上游mtDNA的来路，导致它们被释放出来的直接原因，是癌细胞进入衰老状态时线粒体功能异常，生成了更多线粒体活性氧（mtROS），它们一方面会使mtDNA被释放到胞浆，再经由电压依赖性阴离子通道（VDACs）排到细胞以外，另一方面还会使核酸内切酶G（EndoG）发生核转位，避免它们去降解mtDNA；而要逆转mtDNA诱导的免疫抑制，最好的干预目标就是现阶段恰好有药物可用的VDAC（在研抑制剂VBIT-4），实验也证实抑制VDAC可通过增强抗肿瘤免疫应答，改善CDK4/6抑制剂的疗效。衰老癌细胞经由VDAC将线粒体释放到细胞外参考文献：[1]Lai P, Liu L, Bancaro N, et al. Mitochondrial DNA released by senescent tumor cells enhances PMN-MDSC-driven immunosuppression through the cGAS-STING pathway[J]. Immunity, 2025, 58(4): 811-25.e7.[2]Lin M, Liu N, Qin Z, et al. Mitochondrial-derived damage-associated molecular patterns amplify neuroinflammation in neurodegenerative diseases[J]. Acta Pharmacologica Sinica, 2022, 43(10): 2439-2447.[3]Victorelli S, Salmonowicz H, Chapman J, et al. Apoptotic stress causes mtDNA release during senescence and drives the SASP[J]. Nature, 2023, 622(7983): 627-636.本文作者丨谭硕

临床1期免疫疗法临床终止

2024-06-19

·Firstwordpharma

Macomics teams up with the Swiss cancer institute to develop macrophage therapies

Macomics partnered with the Institute of Oncology Research (IOR) to test the former’s macrophage-targeted therapies in the latter’s mouse models of prostate cancer. “Macrophages are key to multiple diseases of high unmet medical need, including as key mediators of solid tumour immunosuppression,” Macomics CEO Stephen Myatt said. “This collaboration enhances further our ability to explore and exploit macrophage biology for the development of novel therapeutic approaches.” IOR’s mouse models of prostate cancer are specifically designed to feature the fundamental role of myeloid cells in tumour progression and are based on the institute’s “deep understanding of molecular mechanisms in cancer development,” said Andrea Alimonti, the director of IOR. The partners will test and characterise Macomic’s macrophage-targeting drug candidates, which feature novel mechanisms of action.Macrophage target discoveryMacomics’ pipeline of preclinical macrophage-targeting antibodies was built using its ENIGMAC platform, which combines patient datasets, macrophage cell models, and gene editing capabilities to discover new disease-specific macrophage targets.The biotech shared early mechanistic and in vivo data for its lead cancer programme, a ligand independent-pan-LILRB antibody, at the American Association for Cancer Research meeting earlier this year. The results suggest MACO-355 can mediate macrophage reprogramming under immunosuppressive conditions.Macomics is also working with the AIRC Institute of Molecular Oncology in Italy to characterise its macrophage-directed therapies with the research organisation’s ex vivo tumoroid models.Separately, Ono Pharmaceutical has an exclusive option to license from Macomics an immuno-oncology candidate directed against a novel macrophage target.

AACR会议

2024-06-19

·BioSpace

Macomics and the Institute of Oncology Research (IOR, Switzerland) Announce Macrophage Scientific Collaboration in Prostate Cancer Drug Development

Laboratory of Prof. Andrea Alimonti at IOR (Institute of Oncology Research, Bellinzona, Switzerland) and Macomics to bring together expertise on myeloid-derived suppressor cells in prostate cancer mouse model systems The collaboration will combine advanced in vivo models with new therapeutic approaches to support Macomics’ continued exploration of novel macrophage biology for precision oncology medicines EDINBURGH, United Kingdom and CAMBRIDGE, United Kingdom and BELLINZONA, Switzerland, June 19, 2024 (GLOBE NEWSWIRE) -- Macomics Ltd, a leader in macrophage drug discovery, announces that it has entered a scientific collaboration with Prof. Andrea Alimonti at IOR (Institute of Oncology Research), one of Switzerland’s leading research institutes. IOR is focused on the study of cancer formation and development at the molecular level. Prof. Alimonti’s laboratory is pioneering studies on prostate cancer. The collaboration will see Macomics work with Dr Bianca Calì in Prof. Alimonti’s lab to synergize this deep knowledge, particularly in the use of novel in vivo mouse models, with Macomics’ macrophage expertise. The goal is to explore new modes of action for macrophage-targeted therapies. Macomics is exploiting the potential of macrophage-targeted approaches to develop first-in-class medicines to address disease of high unmet medical need. The company’s ENIGMAC™ macrophage drug discovery platform allows access to previously hidden or inaccessible disease-specific macrophage targets: It integrates large volume human data sets, next generation human macrophage cell models, and proprietary macrophage gene editing capability to discover novel targets, unlock new disease biology, and de-risk clinical translation. Under the collaboration, the parties will explore together the potential for the use of novel in vivo prostate cancer models developed by the Alimonti lab in the characterisation of macrophage-targeted therapies, including testing of novel drug candidates with new modes of action discovered by Macomics in its complex human assay systems. Dr Luca Cassetta, VP Immunology and Founder of Macomics, said, “We are delighted to collaborate with Prof. Alimonti as he is a prostate cancer expert. This collaboration will allow us to optimise the design of our therapies by accessing novel prostate cancer mouse models in which myeloid cells play a fundamental role for tumor progression.” Prof. Andrea Alimonti, IOR director, said, “This collaboration represents an exciting opportunity to combine our pioneering research in prostate cancer with Macomics' expertise in macrophage-targeted therapies. By leveraging our deep understanding of molecular mechanisms in cancer development and utilizing our preclinical models, we aim to uncover innovative approaches for combating advanced prostate cancer, a disease for which a definitive cure remains an unmet clinical challenge.” Dr Stephen Myatt, CEO of Macomics, said, “This collaboration enhances further our ability to explore and exploit macrophage biology for the development of novel therapeutic approaches. Macrophages are key to multiple diseases of high unmet medical need, including as key mediators of solid tumour immunosuppression and pathological inflammation in chronic inflammatory disorders.” About Macomics – Macomics Ltd is a macrophage drug discovery company with a world-leading macrophage drug discovery platform, developing first-in-class medicines to deliver transformational impact for patients with macrophage-driven diseases: Macrophages are key to multiple diseases of high unmet medical need, including as key mediators of solid tumour immunosuppression and pathological inflammation in chronic inflammatory disorders. The company is progressing a diversified portfolio of therapies targeting disease specific macrophages towards the clinic. Its ENIGMAC macrophage drug discovery platform enables identification and validation of novel macrophage therapeutic targets and provides a translationally relevant path to clinic through the development of more physiologically relevant human macrophage models combined with proprietary gene editing technology. The company was co-founded in 2020 by Prof. Jeffrey Pollard and Dr Luca Cassetta, University of Edinburgh, internationally recognised leaders in macrophage biology. It has R&D and office facilities in Edinburgh and Cambridge, UK. The company’s financing was led by Epidarex Capital, and the company is backed by Scottish Enterprise, LifeLink Ventures and Caribou Property Limited. Follow us on LinkedIn and About IOR - The Institute of Oncology Research (IOR) is a not-for-profit research institute located in Bellinzona (Switzerland) affiliated with the Università della Svizzera italiana (USI) and directed by Prof. Andrea Alimonti. Established in 2003, the IOR research spans from basic research to translational and clinical research on various aspects of cancer biology, diagnosis and therapy. With eight active research groups, the IOR hosts researchers from all over the world performing basic and translational research in oncology, with a special focus on cancer biology, genomics, molecular oncology, and experimental therapeutics. With approximately 100 researchers (data updated in 2023), the IOR operates two main research programs: the "Tumor Biology and Experimental Therapeutics Research Program,” focusing on solid tumors, and the "Lymphoma and Genomics Research Program," addressing hematological neoplasias and lymphomas. Researchers at the IOR employ an interdisciplinary approach, integrating biological, genomics, and molecular methods with preclinical and translational studies. The Institute emphasizes collaboration and interaction among teams and programs to achieve common goals, such as understanding cancer mechanisms and developing new diagnostic and therapeutic strategies. Follow us on LinkedIn and For further information please contact: Macomics At the Company - Steve Myatt, CEO, Macomics E: myatt@macomics.com Media enquiries (for Macomics) - Sue Charles, Charles Consultants T: +44 (0)7968 726585 E:sue@charles-consultants.com Institute of Oncology Research At the Institute – Andrea Alimonti, Director, E:andrea.alimonti@ior.usi.ch Media enquiries (for IOR) – USI Institutional Communication Service, T: +41 58 666 47 92 E: press@usi.ch

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