DeCure for Reticulum cell sarcoma

In SJL/J mice, spontaneous reticulum cell sarcoma arose in mesenteric lymph nodes and Peyer's patches. Neoplastic reticulum cells grew in clusters resembling normal germinal centres; after proliferation most cells in a cluster died, and the site progressed through granuloma formation to dense fibrous tissue. The pleomorphic histology characteristic of the tumour came from the juxtaposition of proliferating clusters, granulomatous reaction with plasma cells and giant cells, and fibrous scar tissue. Tumour cell cytoplasmic folds clasped collagen fibres, which the authors suggested might explain the lack of massive dissemination.

In 52 cases of reticulum cell sarcoma of bone treated with bacterial toxin therapy alone or combined with surgery or radiotherapy, or with concurrent infection, the authors reported that the most important factors for prognosis were stage and extent of disease at start of toxin therapy, timing and dosage of radiotherapy, and technique of toxin administration. They stated that such adjuvant therapy yielded almost 50% better five-year survival rates than surgery or radiotherapy alone, but gave no absolute survival numbers or control group details. In 86 patients with reticulum-cell sarcoma evaluated three years after first treatment, prognosis was less favourable than in Hodgkin's disease, though occasional unexpectedly long survival with extensive disease and unpredictability of the disease course were noted. In 122 cases (58 nodal, 64 extranodal) treated with radiation, cumulative five-year survival rates for patients receiving 3000 rads to all known disease were: nodal Stage I and II, 46%; nodal Stage III, 34%; nodal Stage IV, 8%; extranodal Stage I, 53%; extranodal Stage II, 12%. Survival seemed more related to stage than location, and patterns of reactivation did not follow sequential spread.

Reticulum cell sarcoma was described as the least responsive to therapy among malignant lymphoreticular tumours, with a course of inexorable progression. Alkylating agents, vinblastine, and irradiation produced responses that were not frequent, often incomplete and transient. In six patients with far advanced disease resistant to other therapy, vincristine was given in low doses (as low as 5 µg/kg biweekly) in an attempt to avoid neurotoxicity while maintaining response. The abstract does not report outcomes for those six patients.

What is missing is any modern randomised trial comparing these older approaches to current standard therapy, prospective data on patient stratification by molecular or immune markers, and funding for such work. The bacterial toxin and low-dose vincristine reports are from small, uncontrolled series from the 1960s and 1970s, and no subsequent large-scale validation has been published.