Clinical research in private hospitals: a perspective

Journal of Translational Medicine · 2026-01-08

The expansion of clinical research beyond academic hospitals into private hospitals is reshaping the way new therapies are tested and implemented. Traditionally, university and public hospitals have been the primary drivers of clinical research, yet private hospitals are increasingly positioned to contribute meaningfully to this landscape. This perspective explores the opportunities and complexities of establishing a clinical trial unit within a private setting, highlighting strategies to conduct innovative studies and deliver high-quality, patient-centered research. While private hospitals may face initial challenges related to infrastructure, regulatory compliance, and quality assurance, they offer important advantages, including more rapid decision-making, streamlined administrative pathways, and efficiency in initiating and conducting studies, all while adhering to the same regulatory requirements. By positioning themselves as complementary partners to academic institutions, private hospitals can provide efficient and fast paced environments for industry-sponsored trials, ultimately enriching the broader research ecosystem. Most importantly, these developments enable the realization of personalized medicine, where cutting-edge, individualized therapies, particularly in oncology, can be directly tailored and delivered to patients, transforming the promise of precision medicine into real clinical outcomes.

Figure S3 from PLT012, a Humanized CD36-Blocking Antibody, Is Effective for Unleashing Antitumor Immunity Against Liver Cancer and Liver Metastasis

2025-08-04

<p>Characterization for TILs population and gene signatures in liver cancer mouse models following PLT012 treatment.</p>

Figure S7 from PLT012, a Humanized CD36-Blocking Antibody, Is Effective for Unleashing Antitumor Immunity Against Liver Cancer and Liver Metastasis

2025-08-04

<p>Gating Strategy employed to assess the immune profile in human HCC tumor tissue.</p>

Table S1 from PLT012, a Humanized CD36-Blocking Antibody, Is Effective for Unleashing Antitumor Immunity Against Liver Cancer and Liver Metastasis

2025-08-04

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Supplementary Figure S1 from Bevacizumab, Atezolizumab, and Acetylsalicylic Acid in Recurrent, Platinum-Resistant Ovarian Cancer: The EORTC 1508-GCG Phase II Study

2025-06-03

<p>Study design including schematic representation of samples collection for translational research.</p>

Figure S2 from PLT012, a Humanized CD36-Blocking Antibody, Is Effective for Unleashing Antitumor Immunity Against Liver Cancer and Liver Metastasis

2025-08-04

<p>In vivo distribution assay for PLT012 treatment in HCC mouse model.</p>

Abstract 6077: PLT012, a humanized CD36-blocking antibody, is effective for unleashing anti-tumor immunity and against liver metastasis

Cancer Research · 2025-04-21

Abstract Tumor cells employ various mechanisms to evade immune surveillance, including metabolic modulation of the tumor microenvironment (TME). Lipid metabolic stress in the TME leads to upregulation of CD36 in tumor-infiltrating immune cells, impairing anti-tumor immunity by enhancing the survival and suppressive activity of regulatory T cells (Tregs) and promoting ferroptosis and exhaustion in CD8+ T cells. Here, we developed PLT012, a humanized anti-CD36 IgG4 antibody targeting the lipid-binding domain of CD36, with a remarkable safety profile and favorable pharmacokinetics demonstrated in cynomolgus monkey models. Moreover, PLT012 significantly reduces tumor growth and reprograms the immune landscape, enhancing CD8+ T cell effector functions while reducing Treg-mediated suppression. In both immunotherapy-sensitive and resistant hepatocellular carcinoma (HCC) models, PLT012 alone or in combination with PD-L1 blockade induces robust anti-tumor immunity. Importantly, in a syngeneic liver metastasis model, PLT012 decreases immunosuppressive populations, enhances effector T cell responses, and reduces ICI resistance. Notably, ex vivo studies with human HCC samples further confirm PLT012’s capacity to remodel the immune microenvironment. Taken together, these findings position PLT012 as a first-in-class immunotherapy targeting CD36, addressing critical challenges in HCC and liver metastasis treatment. Citation Format: Yi-Ru Yu, Sheue-Fen Tzeng, Zheng Meng, Jaeoh Park, Lana Kandalaft, Yun-Han Lin, Chin-Hsien Tsai, Ping-Chih Ho. PLT012, a humanized CD36-blocking antibody, is effective for unleashing anti-tumor immunity and against liver metastasis [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 6077.

Retrospective comprehensive analysis of regional lymph node recurrence in breast cancer patients (REASON study)

Journal of Cancer Research and Clinical Oncology · 2025-05-29

BACKGROUND: Randomized trials have progressively enabled the de-escalation of axillary surgery in breast cancer (BC) patients, reducing adverse events without compromising survival. Despite a not negligible rate of residual disease in the axilla after sentinel lymph node (SLN) procedure, the risk of regional lymph node recurrence (RLNR) is very low, due probably to multimodal adjuvant treatments. The characteristics of the small number of patients with RLNR remain poorly characterized and warrant further investigation, especially given their poor prognosis and the current context of ongoing studies exploring further de-escalation of axillary surgery. METHODS: In this retrospective and single institution study, we analyzed thoroughly a cohort of patients who experienced RLNR as first event between 2009 and 2020. MammaPrint and BluePrint analysis (MB) was performed in available primary invasive cancer tissues. RESULTS: Forty patients, median age of 52, were analyzed. Disease-free interval was 8.7 years. Most of the patients (65%) had no special type BC. Majority (73%) had hormone receptor positive-HER2 negative (HR + /HER2-) BC, 13% triple negative (TNBC), 6% HER2 + , 8% ductal carcinoma in situ and 3% unknown. The median size of the primary tumor was 1.8 cm (range 0.3-7.0) and 57% had no initial LN involvement. Forty five percent had primary SLN procedure and 53% axillary LN dissection (ALND) of the patients received neo-/adjuvant chemotherapy, 63% endocrine therapy and 68% radiotherapy (50% only in breast). Sixty three percent had only RLNR and 38% had concomitant distant metastases. Among irradiated patients, 63% had some relapse in the radiation field. The MB analysis classified 70% of the analyzed cancers as low-risk luminal A (82% in HR + /HER2-), 15% high-risk luminal B, 10% high-risk basal type, and 5% high-risk HER2 type. CONCLUSION: Our study confirms that patients treated with SLN do not show a higher risk of LRNR compared to ALND. LRNR is often diagnosed incidentally. Younger age, residual disease post-NAC, no regional radiation, stage II, and initial LN involvement were more represented, as well as patients with endocrine sensitive disease classified as low-risk luminal A by MB. Ongoing trials, including SOUND, INSEMA, and BOOG 2013-08, are further exploring axillary surgery de-escalation.

Data from Bevacizumab, Atezolizumab, and Acetylsalicylic Acid in Recurrent, Platinum-Resistant Ovarian Cancer: The EORTC 1508-GCG Phase II Study

2025-06-03

<div>AbstractPurpose:<p>Treatment options for patients with platinum-resistant ovarian cancer (PROC) are limited, and new therapeutic strategies are urgently needed. This phase II, randomized, multicentre trial evaluated the safety and activity of the anti–PD-L1 antibody atezolizumab (atezo) combined with the VEGF inhibitor bevacizumab (bev) and the irreversible cyclooxygenase 1/2 inhibitor aspirin [acetylsalicylic acid (ASA)] in PROC.</p>Patients and Methods:<p>Patients were randomized to bev monotherapy 15 mg/kg (arm 1), atezo 1,200 mg plus placebo (pbo; arm 2), atezo 1,200 mg plus ASA 320 mg/daily (arm 3), bev 15 mg/kg plus atezo 1,200 mg plus pbo (arm 4), or bev 15 mg/kg plus atezo 1,200 mg plus ASA 320 mg/daily (arm 5). Primary endpoint was progression-free survival at 6 months (PFS-6) according to RECIST v1.1 assessed by a local investigator. Secondary objectives included overall survival, PFS, second PFS (PFS2), and tolerability. Time to first subsequent therapy (TFST) was evaluated in a post hoc analysis.</p>Results:<p>In arms 1 (bev), 4 (bev–atezo–pbo), and 5 (bev–atezo–ASA), there were 7/32 [21.9%, 70% confidence interval (CI), 14.0–32.0], 8/32 (25.0%, 70% CI, 16.6–35.3), and 8/32 (25.0%, 70% CI, 16.6–35.3) patients alive and progression-free at 6 months. The primary objective was not reached in any arm. Median PFS and response rates were 2.3 for bev monotherapy, 4.1 for bev–atezo–pbo, and 4.0 months for bev–atezo–ASA and 10%, 19%, and 15%, respectively. Two patients achieved an ongoing complete response lasting for more than 5 years from randomization (1 in bev–atezo–pbo and 1 in bev–atezo–ASA). A post hoc analysis of TFST suggested benefit of adding bev to atezo–ASA (<i>P</i> < 0.001). Tumor-infiltrating lymphocytes (TIL) increased in the atezo-containing arms after the first two cycles, and increased TIL were associated with a significantly longer TFST.</p>Conclusions:<p>The addition of ASA to bev plus atezo was well-tolerated but did not improve efficacy in PROC. Relative to bev alone, the bev plus atezo combination numerically improved PFS. Exploratory translational analyses suggest clinical benefit in a subgroup of patients characterized by high TIL infiltration and PD-L1–positive tumors at baseline.</p></div>

Data from PLT012, a Humanized CD36-Blocking Antibody, Is Effective for Unleashing Antitumor Immunity Against Liver Cancer and Liver Metastasis

2025-08-04

<div>Abstract<p>Tumor cells develop various strategies to evade immune surveillance, one of which involves altering the metabolic state of the tumor microenvironment. In response to metabolic stress in the tumor microenvironment, several tumor-infiltrating immune subsets upregulate CD36 to take up lipids. This leads to impaired antitumor immunity, as intratumoral regulatory T cells exhibit increased survival and suppressive activity, whereas CD8<sup>+</sup> T cells become more susceptible to ferroptosis and exhaustion. In this study, we develop a humanized anti-CD36 IgG4 antibody, PLT012, against the lipid-binding domain of CD36 with excellent safety and favorable pharmacokinetic features in mice and cynomolgus monkeys. PLT012 alone or in combination with PD-L1 blockade or standard-of-care immunotherapy results in robust antitumor immunity in both immunotherapy-sensitive and -resistant hepatocellular carcinomas (HCC). Notably, PLT012 also reprograms the immune landscape of human HCC <i>ex vivo</i>. Our findings provide proof-of-concept evidence that PLT012 reprograms antitumor immunity in HCC, positioning it as a first-in-class immunotherapy targeting CD36.</p>Significance:<p>Despite the success of cancer immunotherapies, like immune checkpoint inhibitors, many patients still fail to demonstrate significant responses because of metabolic constraints in tumors. PLT012 rejuvenates antitumor immunity by targeting metabolic pathways to reprogram the immune landscape of liver cancer and liver metastasis, with potential to influence future HCC immunotherapy.</p></div>