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Recent Comments
Thank you for sharing!
This is very relevant for infection-induced forms of cancer, in particular - virus-induced forms of cancer. Viruses that form chronic forms of diseases usually replicate in monoclonal blood cells, including lymphocytes, which can affect the course of both the cancer itself and the outcome of chemotherapy.
So well said - this is absolutely an understudied part of cancer biology.
Continuation of the comment below.
That study published in 1971 involved 280 patients diagnosed at the U of Chicago btween 1931 and 1964, with 40 patients surviving ≥ 10 years.
Of the forty patients, twenty-nine have died. Eighteen of these patients· had postmortem examinations. In sixteen, histologic evidence of Hodgkin's disease was observed.
In the group of twenty-nine patients, the cause of death could be determined in twenty-one. Hodgkin's disease could be implicated as a significant contributory cause of death in fourteen. In seven patients, the cause of death could not be directly attributed to Hodgkin's disease but to causes such as disseminated breast carcinoma, malignant melanoma, coronary occlusion, enteritis, nephritis, and hepatitis secondary to radiation, pneumonia secondary to chemotherapy, and pulmonary fibrosis secondary to. radiation, and systemic coccidioidomycosis. In six of these, autopsies were performed, and in four, Hodgkin's disease was present. In the patients with systemic coccidioidomycosis and pulmonary fibrosis, no histologic evidence of Hodgkin's disease was found.
The conclusion presented in that publication from 54 years ago was that "The finding of persistent Hodgkin's disease in long-term survivors, especially in those dying from apparently unrelated causes, suggests that in some patients with Hodgkin's disease, clinical cure may in fact represent a state of equilibrium in which the host has come to terms with his disease."
My focus in oncology changed to prostate cancer in the early 1980s as a result of my collaboration with Fernand Labrie in treating metastatic disease with combination anti-androgen receptor blockade + LHRH-agonist (LHRH-A) therapy. Many of these patients went into a profound remission with a significant reduction in tumor burden based on a sustained decrease in ultrasensitive PSA levels to undetectable levels. Moreover, an appreciation of the many fuels used to sustain cancer growth allowed for interventions that were and continue to be an integrative approach to cancer patient management:
Cancer Fuels
1. High glycemic carbohydrates [check 2hr-PPBG] i.e., PPBG (post-prandial blood glucose)
2. LDL [check NMR LipoProfile] via LipoScience at http://www.lipoprofile.com/index.cfm
3. Omega 6 fatty acids [check Comprehensive Fatty Acid [CFA] profile] via Mayo Medical Labs at http://bit.ly/1AtZ7
4. Arginine, Copper [review supplements, diet]
5. Glutamates, aspartates, cysteine [review diet]
6. pro-inflammatory cytokines [check IL-1β, TNF-α, PLA2, Rx COX2 inhibitors]
7. bone-derived growth factors (BDGF) [check bone resorption markers DpD (deoxypyridinoline) on urine, CTX (C-Terminal Telopeptide, b-Crosslaps) on serum, TRAP5β only available in Europe
8. Hypoxia
9. Hypercoagulability [check coagulation panel], e.g., PT, PTT, fibrinogen, fibrin monomer, anti-thrombin III, platelet count
All of these, and likely more unidentified energy sources for the cancer cell population, became part of what was termed the SAIN (Systems Analysis & Integrity Networking) methodology in treating those with neoplastic disease. This multi-factorial view of the tumor microenvironment (TME) has allowed the prolonged survival of many men with prostate cancer. I would expect that if detailed autopsies were performed on this population, microscopic or very low tumor burdens would be found, similar to those in the HD study from 54 years ago.
Dr. Strum — thank you for sharing this remarkable perspective and history. Your 1971 study with Dr. Rappaport is a profound early demonstration of what we now call tumor dormancy: microscopic persistence even in patients who appeared clinically “cured.” The conclusion you drew then — that long-term remission may reflect a negotiated equilibrium rather than complete eradication — resonates deeply with the very questions Paget and Virchow set in motion, and it is also at the heart of my forthcoming book, Beyond the Cell, which explores how the tumor microenvironment governs cancer’s silences as much as its growth.
I’m struck by how your trajectory from Hodgkin’s disease to prostate cancer mirrors the broader shift in oncology — from focusing on the seed alone to recognizing the soil and the fuels that sustain it. Your SAIN methodology anticipates many of the modern integrative frameworks for understanding cancer as an ecological system, with multiple energy inputs and regulatory constraints.
Your comment beautifully underscores the continuity between past and present: the idea that “remission” may represent a state of containment, balance, or truce — not absence. I would love to hear more of your reflections on how today’s molecular and microenvironmental tools (spatial transcriptomics, immune profiling, metabolic assays) either confirm or challenge what you observed in the clinic decades ago.
Thank you again for taking the time to add this history. It enriches the cancer narrative immeasurably.