The Challenging Scenario of Cancer Treatment for People with HIV: Clinical Experience with Immune Checkpoint Inhibitors

Current Oncology, Journal Year: 2025, Volume and Issue: 32(3), P. 164 - 164

Published: March 13, 2025

Over the past decade, there has been a notable increase in utilization of immune checkpoint inhibitors cancer care, transforming therapeutic landscape for several types solid tumors. This development not only expanded indications treatment but also significantly influenced management strategies and prognostic outcomes specific subsets patients. In contrast to general population patients, individuals diagnosed with both HIV encounter significant differences approaches outcomes. Consequently, this demonstrates increased rate mortality common cancer. Recent studies have reported insights into use among patient group. However, data remain insufficient, are still recognized barriers limitations regarding these agents Real-world reports from clinical practice offer critical perspectives, enabling sharing experiences assisting navigating complex decisions. report outlines two cases patients concurrent who were administered ICIs diverse settings, highlighting necessity cooperation between oncologists specialists provide cutting-edge increasingly tailored options.

Language: Английский

---

Immune Deficiency/Dysregulation-Associated EBV-Positive Classic Hodgkin Lymphoma

Cancers, Journal Year: 2025, Volume and Issue: 17(9), P. 1433 - 1433

Published: April 25, 2025

Classic Hodgkin lymphoma (cHL) in patients with immune deficiency/dysregulation represents a critical unmet need hematology, demanding the appropriate revision of classification and therapeutic paradigms. Epstein–Barr virus (EBV) is pivotal driver lymphomagenesis this high-risk subset, where viral oncoproteins (e.g., LMP1/2A) exploit vulnerabilities to activate NF-κB, rewire tumor microenvironments (TME), evade surveillance. EBV-positive cHL, prevalent immunosuppressed populations, exhibits distinct molecular hallmarks, including reduced somatic mutations, unique HLA associations, profound PD-L1-mediated suppression, that diverge from EBV-negative cases reliant on genetic aberrations. Despite advances combined antiretroviral therapy, HIV co-infection exacerbates pathogenesis, M2 macrophage dominance, T-cell exhaustion, while links other viruses remain ambiguous. Current therapies fail adequately target these complexities, leaving poorer outcomes. This review synthesizes insights into EBV’s etiological role, contexture disparities, genetic–environmental interplay shaping cHL heterogeneity. The WHO highlights reclassify EBV-associated as integrating status biomarkers diagnostic frameworks. Urgent priorities include global epidemiological studies clarify causal mechanisms, development virus-targeted EBV-specific strategies, PD-1/CTLA-4 blockade), personalized regimens for immune-dysregulated cohorts.

Language: Английский

---

Managing HIV-Associated Hodgkin Lymphoma During the COVID-19 Pandemic: Case Report and Literature Review

Viruses, Journal Year: 2025, Volume and Issue: 17(3), P. 404 - 404

Published: March 12, 2025

The COVID-19 pandemic delayed the consultation of many patients with specialists. We present case a 57-year-old patient HIV infection, pneumonia, and Hodgkin lymphoma. Discordant immunohistochemistry results from biopsy samples hematological diagnosis initiation oncological therapy. late infection at stage severe immunosuppression, along advanced lymphoma co-infection, represents complex pathogenic triad that is challenging to manage. Healthcare-associated infections pose significant risk during for chronic requiring frequent hospital visits.

Language: Английский

---

Pathological Mechanisms Involved in HIV-Associated Lymphomagenesis: Novel Targeted Therapeutic Approaches

Cells, Journal Year: 2025, Volume and Issue: 14(10), P. 705 - 705

Published: May 13, 2025

The intricate interplay of direct and indirect mechanisms relating to immune dysfunction, chronic inflammation, viral proteins represents a key factor lymphomagenesis in HIV-infected patients. Indirect based on cytokine dysregulation, HIV-induced co-infections with oncogenic viruses induce B-cell activation generation prone environment for malignant transformation tumor growth. Direct arise from influences p17, Tat, Nef HIV proteins, which generate genomic instability, alteration cellular signaling, pathways. Vp17's implication angiogenesis, ensured by PAR1/EGFR/PI3K/Akt MEK/ERK1/2 pathways, emphasizes the critical need developing therapeutic strategies that target their signaling mechanisms. This review shows an insight into pathological involved individuals, focusing finding novel approaches directed at rehabilitation

Language: Английский

---