The Difference Between Killing Cancer and Changing The Environment
Please Keep Off the Grass
The difference between killing cancer and changing terrain is important because these are not always the same thing.
Killing a cancer cell is not particularly difficult in a laboratory dish. Many things can injure or destroy isolated cancer cells once they have been removed from the body, separated from their native environment, stripped of immune signaling, vascular influence, endocrine communication, stromal interaction, and the biologic complexity that exists inside a living human being. This does not make these observations meaningless. But it does mean they must be interpreted carefully and within context.
This is one of the places where oncology — especially (now) integrative oncology — is becoming overly reductionistic. We may become very focused on whether something kills a cell, suppresses a pathway, lowers a marker, or shrinks a tumor, while missing the larger biologic question:
What is happening to the person?
Because tumor reduction alone is not always synonymous with durable biologic recovery.
A scan may improve while the terrain continues to deteriorate. Tumor markers may decline while immune exhaustion deepens. A patient may show temporary response while simultaneously losing mitochondrial reserve, endocrine resilience, metabolic flexibility, neurologic stability, or physiologic adaptability.
Conversely, we sometimes see patients whose scans are relatively unchanged, yet pain decreases, function improves, inflammation stabilizes, sleep normalizes, energy returns, and overall resilience increases. Those changes matter biologically.
One of the more interesting historical demonstrations of this concept came from the work of Mintz and Illmensee in the 1970s. The experiment is often oversimplified as “placing a cancer nucleus into a healthy cell,” but that is not exactly what occurred. In reality, malignant teratocarcinoma cells were introduced into normal embryonic blastocysts. Rather than continuing to behave aggressively, many of those malignant cells became integrated into normal tissue development within the healthy embryologic environment.
The significance of this was profound. It suggested that malignant behavior is not determined solely by the cancer cell itself, but also by the biologic environment in which that cell exists. In other words, the terrain matters.
This does not mean mutations are irrelevant, nor does it suggest that cancer can simply be reversed through environment alone.
The biologic terrain directly influences whether cancer cells survive, adapt, evade, become dormant, or are recognized and eliminated. It influences how long responses last. It influences whether therapies are tolerated, whether the immune system can sustain pressure, whether detoxification pathways can keep pace with treatment burden, and whether the body has enough reserve to maintain repair while simultaneously fighting disease.
When we evaluate terrain, we are looking at multiple interconnected domains simultaneously.
This is why treatment cannot be evaluated only by asking whether a therapy kills cancer cells. We also have to ask what it is doing to the terrain of the person receiving it.
We can begin by looking at laboratory patterns and physiologic markers to understand how a patient’s terrain is functioning and adapting over time. We may start noticing that certain combinations, timing strategies, sequencing approaches, or therapeutic stacks appear to fit more appropriately for a particular patient and produce better overall outcomes biologically.
But equally important is what we observe in the patient themselves.
Are they declining rapidly despite “good” imaging? Is pain increasing? Is recovery becoming harder? Is inflammation escalating? Are they losing resilience faster than the disease appears to be progressing? Or are they stabilizing, regaining energy, sleeping better, thinking more clearly, tolerating therapy more effectively, and recovering faster between interventions?
Those observations are not separate from the biology. They are reflections of the biology.
And sometimes they tell us more about the direction of the terrain than the tumor alone ever could.
References & Citations
Mintz, B., & Illmensee, K. (1975). Normal genetically mosaic mice produced from malignant teratocarcinoma cells. Proceedings of the National Academy of Sciences, 72(9), 3585–3589.
https://doi.org/10.1073/pnas.72.9.3585
Hochedlinger, K., Blelloch, R., Brennan, C., Yamada, Y., Kim, M., Chin, L., & Jaenisch, R. (2004). Reprogramming of a melanoma genome by nuclear transplantation. Genes & Development, 18(15), 1875–1885.
https://doi.org/10.1101/gad.1213504
Li, L., Connelly, M. C., Wetmore, C., Curran, T., & Morgan, J. I. (2003). Mouse embryos cloned from brain tumors. Cancer Research, 63(11), 2733–2736.
Hanahan, D., & Weinberg, R. A. (2011). Hallmarks of cancer: The next generation. Cell, 144(5), 646–674.
https://doi.org/10.1016/j.cell.2011.02.013
Seyfried, T. N. (2012). Cancer as a Metabolic Disease: On the Origin, Management, and Prevention of Cancer. Wiley.
Bissell, M. J., & Hines, W. C. (2011). Why don’t we get more cancer? A proposed role of the microenvironment in restraining cancer progression. Nature Medicine, 17(3), 320–329.
https://doi.org/10.1038/nm.2328
Quail, D. F., & Joyce, J. A. (2013). Microenvironmental regulation of tumor progression and metastasis. Nature Medicine, 19(11), 1423–1437.
https://doi.org/10.1038/nm.3394
Pavlova, N. N., & Thompson, C. B. (2016). The emerging hallmarks of cancer metabolism. Cell Metabolism, 23(1), 27–47.
https://doi.org/10.1016/j.cmet.2015.12.006
