Lymphatics

Classic Hodgkin lymphoma in children is a malignant disease with a high cure rate. It is therefore evident that minimizing the acute and chronic toxic effects of the therapies used is a crucial issue in early ages. Radiotherapy has historically been a component of paediatric treatments for this lymphoma. At present, it is possible to cure this disease without using radiotherapy, the main cause of the most frequent long-term sequelae and complications. The evolution of treatment for paediatric Hodgkin lymphoma is discussed, highlighting the reported evidence of studies supporting a high survival rate without radiotherapy.

Cholesterol is increasingly recognized as a regulator of hematolymphoid malignancy biology, by influencing tumor proliferation, immune function, and therapeutic response. This review summarizes current evidence regarding the relationship between cholesterol metabolism and hematologic malignancies, integrating mechanistic studies with retrospective and emerging prospective clinical data. Cholesterol contributes to immune dysfunction by promoting CD8⁺ T-cell exhaustion within the tumor microenvironment. Clinical studies have reported associations between serum lipid profiles, statin use, and outcomes across multiple hematologic malignancies, although findings remain heterogeneous and are largely derived from retrospective analyses. Preclinical studies demonstrate that statins disrupt cholesterol-dependent signaling and inhibit tumor growth, whereas retrospective clinical studies generally support the safety of statin use and suggest possible therapeutic benefits in some lymphoma subtypes. Clinically, low high-density lipoprotein cholesterol (HDL) has been associated with advanced disease across multiple hematological malignancies. However, prospective, interventional data remain limited. Collectively, this review highlights the possible relationship between cholesterol metabolism and hematologic malignancy biology, with a focus on potential impacts on disease related outcomes.

Lymphedema is usually approached as a survivorship complication; yet, many of the injuries that produce lymphatic failure begin during cancer treatment planning. Regional nodal irradiation, chemoradiation, lymph-node surgery, systemic therapy, obesity, infection history, and baseline lymphatic reserve can converge to produce chronic swelling, fibrosis, cellulitis risk, functional limitation, and an impaired quality of life. Despite this, lymphatic drainage pathways are rarely contoured, constrained, or prospectively monitored as organs at risk in radiotherapy practice. This commentary argues that the lymphatic system should enter radiotherapy-planning discussions as a candidate toxicity structure, while cautioning against premature universal dose constraints. Evidence signals are clinically meaningful but not yet protocol-defining: in the MA.20 breast cancer trial, regional nodal irradiation increased lymphedema from 4.5% to 8.4%; in nasopharyngeal carcinoma, mean doses of approximately 58.7 Gy to level IV and 58.6 Gy to levels I–VII were proposed as thresholds associated with moderate/severe facial lymphedema; and gynecological cancer studies report wide lower-limb lymphedema incidence ranges, with radiotherapy, lymphadenectomy, number of nodes removed, and body mass index repeatedly implicated as risk factors. The immediate priority is not mandatory lymphatic sparing, but lymphatic-aware planning: a baseline risk assessment, reproducible candidate contours, dose–volume reporting, selective sparing where oncologically safe, and prospective toxicity monitoring. The author proposed a framework to reflect this argument. Making lymphatic toxicity visible, measurable, and modelled may help shift lymphedema from an accepted late effect to a potentially preventable planning endpoint.