This essay lists my new or “not generally accepted” ideas about cancer. It updates my 4 July 2021 post.
How life arises
1. Human life is best understood through the framework of complexity science rather than reductionism. In complex systems, the behavior of the whole is greater than the sum of the behavior of its parts. The additional behaviors arise from the dynamic interactions between the parts, a phenomenon known as emergent behavior (Pernick 2017a). In contrast, reductionism holds that the behavior of the whole is merely the sum of the behavior of the parts, viewing life as a sophisticated machine that can be understood by breaking it down into increasingly smaller, discrete components, with no interactions between the parts other than those that are obvious (Pernick 2022d).
2. Life should be viewed as a complex biological system composed of interacting networks and not as a modular, reductionist system. Although reductionism is logical and easier to understand, our traditional reductionist approach has been inadequate to understand and successfully treat cancer.
3. The human genome encodes ~20,000 protein-coding genes, which form networks that regulate each other by turning genes on or off. These genes and the proteins they produce interact to generate and modify the biomolecules that guide the transformation of a fertilized egg into an embryo, fetus, infant, child, teenager and adult. These networks also respond to environmental challenges (infections, infestations, trauma, heat and cold) and enable human reproduction and evolution.
4. Proteins and genes have chemical structures that promote diverse interactions, some beneficial and some potentially harmful. Yet networks with these proteins and genes must remain “on track” because inappropriate interactions can lead to disease, including cancer. Over time, human evolution has reduced the risk of disease by creating redundant control systems that restrain harmful biomolecular activity. However, evolution, which may require up to 1 million years to occur, cannot keep pace with recent environmental and lifestyle factors that increase the risk of cancer. Moreover, natural selection primarily favors traits that enhance reproductive success, not necessarily those that extend life beyond the reproductive years.
5. Human life begins when a fertilized egg uses stored proteins and RNA transcripts to rapidly divide and develop into an embryo. As development continues, cells secrete morphogens (signaling molecules) that diffuse across the embryo and interact with each other, creating three dimensional concentration gradients that cause the activation of specific genes, ultimately leading to cell differentiation. Although almost all cells contain the same DNA, these spatial differences in gene activity produce different proteins and distinct cell types. The process is largely unidirectional and guided by principles of self-organization, similar to how proteins fold into their functional shapes.
6. Genetic networks may be organized into cascades, where the activation of one gene triggers a sequence of other genes. For example, during embryonic development, activation of homeobox genes, which are key transcription factors, initiates the formation of body structures and axes through coordinated cascades of downstream genes.
How cancer arises - general overview
7. Cancer is best understood by examining the behavior of large numbers of biological networks rather than isolated pathways. Textbooks often depict biological pathways as linear sequences, similar to assembly lines, with clear starting and end points. In reality, however, each pathway is deeply influenced by many others, forming a complex, interconnected web. Disruptions in one pathway can often be bypassed through alternate routes within this web. This suggests that shifts in the overall behavior of these networks may be more informative than focusing solely on specific genetic mutations (Pernick 2022a).
8. Complex networks share universal properties, regardless of their specific components. These include:
Emergence: New and often unexpected properties or behaviors arise from interactions among simpler components. These emergent properties do not exist within the individual parts themselves but result from their collective dynamics.
Self-organization: The process by which biological order arises spontaneously from local interactions among parts of an initially disordered system. Self-organization may be the root source of order, upon which evolution then acts (Kauffman 1993).
Self-organized criticality: Small, incremental changes can accumulate silently until they reach a tipping point, triggering a sudden burst of reorganization and major transformation (Pernick 2023a). This concept helps explain sudden catastrophic events such as earthquakes and stock market crashes, as well as malignant transformation in cells. It is nature's way of making large changes based on individual factors thought too trivial to consider (Bak 1999). Human life has properties of self-organized criticality, which means that minor disturbances to biological networks typically cause network changes that have only a minor impact but rarely propagate throughout our bodies to cause catastrophic network failures. This has been analogized to adding grains of sand to a sandpile. Each grain causes internal structural changes to the sandpile, although this may not be readily apparent. Ultimately, one unremarkable grain of sand will cause the sandpile to collapse.
Hierarchies: These are systems in which a combination of agents (genes, proteins, pathways) at one level become single units or “agents” at the next, creating a pyramid-like structure (Pernick 2023c, Pernick 2023d). Hierarchies help explain why biological change tends to occur through bursts of activity rather than gradually; alterations at low levels can percolate upwards to produce larger systemic changes.
Human biology consists of complex hierarchical systems with many levels of anatomical organization that interrelate with each other to form networks of growing complexity (Grizzi 2005). Attractors: Networks often settle into stable patterns of activity, which helps maintain biological order. In adults, biological networks are typically constrained by interactions with many other networks, preventing rapid change. This concept explains why our estimated 30 trillion cells, despite small differences in network activity, organize into roughly 200 cell types with consistent functions and microscopic appearances. Attractors can be visualized as valleys on a topographic diagram, regions of low energy that tend to remain stable against common disruptions. This stability is augmented by biological control systems that maintain resistance against change (Pernick 2017a). Normal, premalignant and malignant cells may each occupy relatively stable attractor states.
9. Living systems are designed to reuse existing networks in different ways. Our evolutionary history began as a single celled organism whose main function was to reproduce rapidly and continuously, while subject to controls that halted reproduction under adverse conditions. In essence, these cells had toolkits of genes and adaptations important for the survival of the organism (Davies 2011). Since the toolkit for cell division was so reliable, we evolved to become larger and more sophisticated in part by reusing that toolkit in different ways (Mireles 2018). The toolkit for cell division is triggered not only during embryogenesis (Brantley 2021) but during fetal and childhood growth, to repair damaged tissue and to replace cells with short lifespans in the bone marrow and gastrointestinal tract (Richardson 2014).
10. The process of malignant transformation differs fundamentally from the normal, highly coordinated regulation of cellular networks. Complex biological processes such as embryogenesis, cell migration and inflammation depend on tightly controlled interactions among multiple networks. These processes are typically initiated by specific triggers and conclude through defined termination phases (Pernick 2021a). Embryogenesis involves rapid cell division that eventually halts through programmed cell cycle regulation and differentiation (Pernick 2023e). Cell migration occurs in both embryonic and adult tissues but only when triggered, and it typically stops through physiological mechanisms, although the details remain incompletely understood (Pernick 2024c, Pernick 2024d). In physiological inflammation, the signals that initiate the inflammatory response help coordinate its resolution (Pernick 2023c).
In contrast, cancer risk factors activate these embryonic, migratory and inflammatory pathways in a disorganized, uncontrolled manner, lacking the coordinated regulation and programmed conclusion seen in healthy physiology. For example, carcinogens from burnt tobacco leaves induce mutations in KRAS, leading to uncontrolled cell proliferation (Pernick 2023e). Additional mutations can disrupt DNA repair mechanisms or apoptosis pathways, causing network level changes that the body cannot physiologically correct.
11. Malignant transformation appears to occur not through gradual, stepwise progression but through bursts of network activity, consistent with the concept of self-organized criticality. Risk factors or random genetic events alter patterns of network behavior that accumulate over time, eventually manifesting as identifiable premalignant conditions, such as colonic adenomas (polyps) (Pernick 2024a). Some precursors may remain relatively stable at the molecular level, exhibiting no visible microscopic changes, and instead exist as altered patterns of gene expression (Pernick 2018a). Both visible and molecular precursors can evolve further, eventually giving rise to overt malignancy.
12. Networks often destabilize other networks through their interactions. Even networks seemingly unrelated to cancer, such as those involved in oxygen sensing, can influence malignant transformation because of the interconnectedness of biological systems.
13. Normal cells have physiologic processes that may be "hijacked" during malignant transformation (Pernick 2023c). This includes:
Cell division: occurs during embryogenesis and later in life for tissue growth, repair and replacement.
Cell migration: is necessary for embryonic development, wound healing and inflammation.
Inflammation: supports cell migration, stimulates blood vessel formation to nourish tissues and promotes network plasticity and instability.
Stem cells: may be the source of malignant cells due to their capacity for self-renewal and plasticity.
14. Cancer arises from the misappropriation and dysregulation of existing physiological mechanisms. Over evolutionary time, multicellular organisms developed sophisticated control systems to determine when these mechanisms should occur. Chronic exposure to cancer risk factors and random mutations undermines these controls, allowing their inappropriate activation and leading to malignancy.
15. Cancer is an unavoidable consequence of human biology, rooted in the tradeoffs required to maintain critical states that support embryonic development, enable inflammatory responses to injury and infection and allow our species to adapt and evolve. Cancer will always exist - it is a type of catastrophic systemic failure within these essential processes (Pernick 2023c). We can lower its incidence, detect it earlier and improve treatment outcomes, but achieving a “world without cancer” is not possible (Pernick 2022e).
16. New cancer cases are inevitable due to behaviors that increase cancer risk, such as tobacco use and obesity, as well as from longer lifespans and random biological events (Pernick 2022c).
17. Chronic cellular stress is the fundamental cause of most cancers. This ongoing stress, driven by risk factors or random events, disrupts the delicate balance within our interconnected cellular networks between forces that stimulate and those that restrain. In the right context, it pushes susceptible stem or progenitor cells into dysregulated and unstable network trajectories that can propagate within the cell, to nearby tissues and throughout the body (Pernick 2011). These disturbances may give rise to cancer attractors, which are cells with malignant traits maintained by mutually reinforcing gene networks that create a new, stable state that is resistant to change (Huang 2009).
While some chronic stressors are known to contribute to cancer, it remains unpredictable which specific stressors will have the greatest impact, where cancers will arise and what their molecular and microscopic characteristics will be (Pernick 2017a).
18. We initially identified nine chronic cellular stressors that promote cancer (Pernick 2017a):
Chronic inflammation from infection, infestation, autoimmune disorders, obesity or trauma
Exposure to carcinogens
Reproductive hormones
Western diet, characterized by high fat, low fiber and limited intake of vegetables and fruit
Aging
Radiation
Immune system dysfunction
Germline genetic changes
Random chronic stress, sometimes described as “bad luck”.
19. We subsequently condensed this list to 5 “superpromoters”: chronic inflammation (due to diet, aging and some aspects of carcinogen exposure), DNA alterations (due to carcinogen exposure, radiation, germline changes and a component of aging), immune system dysfunction (individual or societal), hormonal effects and random chronic stress (Pernick 2021a).
20. Chronic inflammation promotes malignancy through multiple mechanisms, including by producing reactive oxygen and nitrogen species that damage DNA, releasing cytokines and other growth factors that stimulate cell proliferation, creating a local microenvironment that supports malignant transformation and harming the immune system. It can arise from different disease processes that are site specific. For example, in the stomach, atrophic gastritis or autoimmune gastritis can cause a reduction in acid production, which triggers compensatory G (gastrin) cell hyperplasia (particularly pronounced in autoimmune gastritis) and leads to overproduction of gastrin (hypergastrinemia). This overproduction causes enterochromaffin-like cell hyperplasia, a known precursor to neuroendocrine tumors. Some patients with hypergastrinemia develop neuroendocrine tumors due to chronic proton pump inhibitor use, even when no other lesions are found.
21. DNA alterations disrupt network structure so they no longer function as intended. These changes can be germline (present before birth), somatic (arising after birth), random or related to other forms of “network rewiring” such as epigenetic modifications or changes in mRNA. Early on, these network alterations may have little impact because other regulatory systems can keep them in check. As additional networks become altered and control systems weaken, these changes play a greater role in driving malignant transformation (Pernick 2025b).
22. Cancer may develop through changes in the immune system as the malignancy evolves. The immune system operates as a complex biological web rather than a simple linear pathway (Pernick 2021a). Thus, targeting a single immune related abnormality may be inadequate treatment because compensatory mechanisms can bypass blocked pathways. In some lymphomas, such as classical Hodgkin lymphoma or nodular lymphocyte predominant Hodgkin lymphoma, a “runaway” immune system may exist in which dysregulation allows immune cells to proliferate or survive for prolonged periods and become malignant (Pernick 2020).
23. Prolonged exposure to hormones promotes continuous division of epithelial cells, increasing the chance that DNA alterations are passed to daughter cells and supporting malignant transformation.
24. Random chronic stress, also called bad luck, is a major cause of cancer death, particularly in nonsmokers who develop lung cancer (Pernick 2021c) or pancreatic cancer patients without identifiable risk factors (Pernick 2021a). These cases illustrate how stochastic cellular events, like random mutations that occur during normal cell division, can lead to malignancy (Pernick 2021b). We estimate that random chronic stress causes baseline rates of 2 cases per 100,000 people per year in the US for both lung and pancreatic cancer.
25. Advanced cancer usually begins with a small set of local biological changes. Over years or decades, these changes interact across multiple networks and eventually lead to systemic alterations known as an altered systems biology (Koutsogiannouli 2013).
Premalignant precursors
26. To date, we have identified 1216 distinct types of human cancer, based on WHO classifications and other well documented malignancies in the medical literature. This number does not include intraepithelial neoplasia, in situ or borderline lesions or benign locally aggressive lesions. To list each diagnosis only once, we exclude diagnoses that represent essentially the same entity outside of their usual locations, particularly for hematopoietic and soft tissue tumors. We exclude metastases at all sites.
27. Given this large number of unique malignancies, it is evident that no single treatment can address them all effectively. We should therefore move away from the notion of a “silver bullet for cancer.”
28. Although historically cancer precursors were thought to exist for every type of malignancy (Caporaso 2013), our recent work shows that only 15 percent of malignancies have a known premalignant precursor, with rates varying by subspecialty (Pernick 2025a). Many nonepithelial malignancies, including those in neuropathology, bone and soft tissue and hematopathology, rarely have identifiable precursors (Pernick 2024b). Some hematological malignancies have precursors defined only by clinical findings. For example, MGUS serves as a precursor to myeloma, and B cell monoclonal lymphocytosis is a precursor to CLL or SLL, but these precursors share the same morphology as the malignancy itself; the distinction lies only in clinical parameters.
29. Many epithelial malignancies, such as those arising in the thoracic organs, breast, genitourinary tract, gastrointestinal tract, gynecologic organs, head and neck and skin, often show identifiable intraepithelial precursor lesions (dysplasia). This appears to result from the influence of cell–cell interactions, cell–extracellular matrix interactions and basement membranes in epithelial tissues. These structures limit uncontrolled cell division and often require epithelial malignancies to pass through an intraepithelial neoplasia stage before acquiring fully malignant behavior. By comparison, nonepithelial cells can proliferate and expand without these intermediate steps.
30. Although melanoma arises from melanocytes, which are not epithelial cells, melanocytes are situated within a network of epithelial keratinocytes. This microenvironment may constrain melanocytic malignant transformation and require progression through identifiable precursor stages, such as acral nevus, dysplastic nevus, giant congenital nevus, lentigo maligna and melanoma in situ, similar to the intraepithelial neoplasia process seen in epithelial malignancies.
31. Many epithelial malignancies, in contrast to nonepithelial malignancies, have well documented risk factors that drive changes in molecular pathways leading to intraepithelial neoplasia and ultimately result in invasive malignancy.
32. In some lymphomas, persistent antigen driven lymphoproliferation plays a central role in malignant transformation. For example, Helicobacter pylori and Hepatitis C virus promote chronic activation of lymphocytes, which are intrinsically genetically unstable and may ultimately transform.
33. Malignancies without identifiable precursors may develop from a mutation or genetic alteration in a single stem or progenitor cell that then proliferates and acquires additional malignant features. In these cases, there are no recognizable morphological precursors, only groups of cells that display increasing malignant behavior. For example, in BRCA1 related cancers, malignant transformation may begin with the slow accumulation of mutations that do not cause observable microscopic changes in the early cells or their progeny. Over time, as mutations build up, a tipping point is reached where a critical number of dysfunctional proteins triggers an avalanche of rapid malignant changes, without the appearance of identifiable precursor lesions.
34. Malignant transformation often results from multiple, parallel and genetically distinct pathways (Wang 2024), rather than a simple stepwise progression from premalignant lesions to low grade, intermediate grade and eventually high grade disease. In fact, some high grade lesions appear to arise de novo as high grade malignancies rather than evolving from lower grade counterparts.
35. Malignancies may arise from benign tumors, but this may be difficult to determine. Benign tumors can transform into malignancies when their stem or progenitor cells acquire additional mutations that disrupt normal cell cycle control. This leads to excessive cell division and the development of invasive behavior. However, normal cells on the path to malignancy may also develop histologic features that resemble a benign tumor, even though the benign tumor itself never truly existed (Pernick 2025c).
36. Some tumors display distinct histologic features not usually linked to malignancy, such as the accumulation of glycogen, lipids, oncocytes or sebaceous cells (Pernick 2025e). Transformation pathways may coincidentally activate these metabolic or differentiation pathways alongside traditional malignant pathways because of the complex, interconnected nature of cellular networks:
Disturbances in the VHL gene, which affects oxygen sensing, may cause clear cell renal cell carcinoma.
The upregulation of nutrient transporters may contribute to the malignant potential of invasive micropapillary carcinoma cells.
Glycogen metabolism pathways may be hijacked during the malignant transformation of glycogen rich carcinoma.
In lipid rich breast carcinoma, transformation may select the best metabolic program to sustain tumor progression by lipid rich carcinoma cells.
Features of different types of cancer
37. Malignancies that arise from different sites or are driven by different molecular alterations may nonetheless appear similar due to the attractor concept: the idea that cells with thousands of distinct features are funneled into a limited number of phenotypic cancer types. For example, acinic cell carcinoma of the breast resembles its salivary gland counterpart, despite originating through different molecular pathways.
38. The histologic features of cancer reflect the complex interplay of various biological changes. These features include:
Metaplasia: May serve as a premalignant precursor in some contexts or become part of the malignant process itself, as seen in salivary gland tumors of the breast.
Phenotypic mimicry: Some tumors, such as epithelioid angiosarcoma, display an epithelial-like (epithelioid) appearance despite lacking true epithelial lineage differentiation. This reflects mimicry rather than actual transdifferentiation.
Cell adhesion alterations: Disruptions in adhesion molecules can influence tumor morphology and metastatic potential.
Divergent differentiation: Stem or progenitor cells may differentiate into unusual lineages, such as neuroendocrine tumors of the breast.
Neoantigens: Medullary carcinoma of the breast often has an increased burden of neoantigens - novel surface proteins arising from tumor specific somatic mutations, which can stimulate an immune response. This phenomenon is associated with BRCA1 mutations and basal-like breast cancers, including medullary carcinoma.
39. Identical risk factors may produce tumors with differing histologic features. For example, mucinous carcinoma of the breast is linked to prolonged estrogen exposure, similar to other ER+ and PR+ low-grade tumors, yet it lacks the characteristic genetic changes of those tumors. Instead, it may arise from the hijacking of mucin production as part of malignant transformation, analogous to glycogen-rich carcinoma.
40. Histologic variability can also result from epigenetic modifications or mutations in noncoding regions that influence gene expression.
41. Some widely used “classifications” can be misleading. For example, triple negative breast cancer encompasses at least 22 distinct histologic subtypes, although many are uncommon. Histologic type is generally a better predictor of tumor behavior than the triple negative label alone. The lack of ER, PR and HER2 expression does not define a unique gross or microscopic appearance, nor does it directly determine clinical behavior.
42. Biomarkers and histologic features may vary in prognostic significance in different malignancies. While HER2 overexpression is typically linked to aggressive tumors, most triple negative breast cancers are clinically aggressive but HER2 negative, underscoring the need to interpret biomarkers within the broader histologic and molecular context. The presence of abundant mucin can be associated with a favorable prognosis (in breast and pancreatic malignancies) or a poor prognosis (in ovarian and appendiceal malignancies), depending on tumor context.
Treatment strategies
43. To substantially reduce cancer deaths in the United States, which have plateaued at 600,000 per year, we must implement a strategic plan that specifies both what should be done now and what areas require further study. We must be willing to “dare greatly” (The Man in the Arena 1910), acknowledging that we must focus on some steps even though we don’t know what to do. Success will require monitoring of outcomes and continuous refinement of the plan in response to new evidence.
44. Our target goal is to reduce cancer deaths to 100,000 per year, an ambitious but not unprecedented 83% reduction, similar to the dramatic improvements already achieved in survival rates for many childhood cancers.
45. This strategic plan must incorporate every available treatment and public health intervention that can meaningfully impact cancer mortality (Pernick 2022b). Focusing on a “miracle cure” is unlikely to succeed since no single therapy can eliminate most adult cancer cells or fully restore order to the complex networks disrupted in malignancy (Pernick 2025d). Instead, success will most likely come from the cumulative effect of many incremental improvements over time, with occasional major advances (Pernick 2021f).
46. Cancer deaths cannot be reduced to zero. Even with optimal therapy, some patients will inevitably die due to treatment refusal, noncompliance, comorbid conditions that limit treatment options, medical errors, unexplained therapeutic failure or the development of secondary cancers (Pernick 2025d).
47. Effective treatment for adult cancer, as with childhood cancer, will likely depend on combinations of therapies, each aimed at distinct aspects of the malignant process. These distinct aspects include:
Cell growth, DNA repair, apoptosis and related networks: Targeting multiple molecules within these pathways helps prevent resistance (Barabási 2011). Here, the primary goal is to destroy as many cancer cells as possible.
Tumor microenvironment: Vasculature, inflammatory cells and their products and the extracellular matrix create a “fertile soil” that supports cancer cells at both primary and metastatic sites (Fidler 2003).
Chronic inflammation: Driven by underlying cancer risk factors and contributes to tumor initiation and progression.
Hormonal drivers: Estrogens in breast and endometrial cancers and androgens in prostate cancer stimulate malignant cell proliferation.
Dysfunctional immune networks: Undermine the body’s capacity to control cancer or, in rare cases, become malignant themselves.
Germline genetic mutations: Increase the susceptibility to cancer development.
Reprogramming surviving cancer cells: Redirecting them into less aggressive networks may be a treatment strategy (Pernick 2022b).
Other networks: We may want to target networks specific to each cancer type that contribute to transformation and progression.
48. Targeting multiple pathways within each network is essential because biological processes are interconnected (weblike), not linear. This allows cancer cells to bypass important steps blocked by treatment (Pernick 2022b). Additionally, the inherent heterogeneity of cancer cell populations means that no single therapy is likely to eradicate all malignant cells (Plana 2022). Effectively disrupting a single malignant process may require combinations of 3–5 therapies (Mukherjee 2011).
49. We speculate that for each cancer type, even the most aggressive, we may be able to develop combinations of 10 – 15 therapies that individually might have only modest effects but together could be curative (Pernick 2023b). This might consist of combinations of combinations of therapies to address several aspects simultaneously.
50. We cannot target every aspect of cancer because patients can only tolerate a limited number of therapies. Although disseminated cancer is a systemic disease, we speculate that successfully targeting key malignant networks will restore balance to the remaining networks disrupted during the malignant process.
51. We may need to develop 30 or more partially effective therapies to choose from to find the most effective combinations of 10 - 15 therapies noted above (Pernick 2021g). We can then use machine learning, cell lines, mathematical models, animal models and ultimately clinical trials to test the huge number of potential combinations.
52. Accelerating this process will require a significant increase in patient enrollment in clinical trials, allowing physicians to learn and adapt quickly (Pernick 2021e). Currently, only 7% of adult cancer patients participate in clinical trials (Unger 2024), compared to over 60% of children with cancer (Children’s Oncology Group). Clinical trials remain the most reliable method for determining whether treatment combinations are both effective and tolerable across diverse patient populations.
53. Achieving long term survival requires reducing the risk factors that contributed to the original cancer (Pernick 2017a), as these factors will persist and continue to drive malignancy unless actively mitigated.
54. To maximize the reduction in cancer deaths, we should prioritize treatments for lung and pancreatic cancers, as well as advanced colon and breast cancers, which are responsible for the highest number of cancer related deaths.
55. We should focus on reducing age related cancer deaths. The incidence of most cancers increases exponentially with age during adulthood; more than two thirds of invasive cancers occur at age 60 years or older (White 2019). Advancing age is the most important risk factor for cancer overall and for many individual cancer types (Pernick 2017a). As the U.S. population grows and ages, cancer incidence is projected to increase by nearly 50%, making cancer risk reduction an urgent priority (Weir 2021).
56. We should reduce cancer deaths that occur shortly after diagnosis, often caused by treatment side effects, infections or important disruptions to vital physiological networks (Pernick 2022f). Equally important is addressing deaths driven by a sense of futility, which may result from inaccurate information.
57. We can prolong the lifespan of patients with cancer and increase treatment options by achieving marginal gains at all steps of the disease process (Powell-Brett 2021) and by respecting patient therapeutic preferences (Balogh 2011, Tsvitman 2021). We should also promote overall patient health to improve the efficacy of treatment and allow patients to tolerate more treatment options.
Public health / prevention strategies
58. Over the long term, cancer deaths could be reduced by 30% to 40% through effective prevention and enhanced screening efforts.
59. To achieve these goals, we must prioritize healthy living at the national level and strengthen public health and prevention programs, particularly among children and young adults. This includes promoting evidence based guidelines such as the American Code Against Cancer and encouraging healthier lifestyles by:
Dramatically reducing tobacco use to 5% of the population and excess weight to 10% of the population.
Promoting plant based diets with more nonstarchy vegetables, fruits, fiber and whole grains and less fat, sugar and processed foods.
Reducing alcohol consumption, especially heavy, long term use (LoConte 2017).
Increasing HPV and Hepatitis B vaccination rates
Treating infections and infestations linked to cancer (Plummer 2016, de Martel 2020, Ferrara 2020, Nguyen 2020, Gredner 2018, Pernick 2021d)
Addressing other risk factors and implementing proven, evidence based prevention strategies (World Health Organization, accessed 6July2025, GBD 2019 Cancer Risk Factors Collaborators 2022).
60. Reducing even a single risk factor may have a disproportionate impact because a combination of multiple risk factors is typically needed to sufficiently disturb biological networks to overcome redundant controls and promote the malignant process. In addition, improving one factor (e.g., quitting smoking) often leads to broader health improvements, such as better diet, increased physical activity and reduced alcohol use.
62. At the societal level, public health and healthcare systems act as a “behavioral immune system” (Pernick 2021a) that helps reduce cancer risk factors and reduce cancer incidence. For example, “nonuse of screening” is a major risk factor for colorectal cancer (Pernick 2023f). We should also optimize access to medical care that reduces cancer deaths. This includes providing care to all patient populations and reducing disparities based on race or ethnicity, region of residence and socioeconomic status (Li 2024, Islami 2024), ensuring universal access to high quality healthcare for all Americans.
63. We should prioritize screening programs with the highest potential to reduce mortality. This includes:
Regular physical exams that incorporate screening for high mortality cancers when early detection improves outcomes.
Identifying and monitoring premalignant or malignant lesions in high risk individuals, including those with a history of cancer.
64. Investigating whether testing or treating chronic inflammation linked to cancer is beneficial (Pernick 2021e).
65. We should educate the public to:
Seek accurate, science based medical information from trusted governmental or academic sources and avoid medical misinformation.
Become proactive and organized in managing their health and medical care.
Receive regular physical exams for early detection, prevention discussions and appropriate testing, screenings and vaccinations.
Support policies that promote cancer prevention and early detection at the local, state and national levels.
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Thank you, Nat. I love being able to come to our blog bc I feel confident in my takeaways.
Great Article. What are the latest studies and tests to determine pancreatic cancer in early stages? I've lost 6 female relatives and 1 male in 3 years. All were on my maternal side. They were diagnosed with Diverticulitis, Chrohns and IBS. Drs refused to do any further testing after initial diagnosis. There's been an uptick in Pancreatic Cancer but it seems like it's diagnosed in Stage 3 or 4. A little of my background I was an RN-BSN specializing in High Risk Obstetrics for 18 years, I left during the tumultuous years when patients became a number and it all tied back to their wallet. When I left I studied with a Naturopath for quite a few years in Florida as well as 4 years with a Board Certified Homeopath, 5 years with a Master in Chinese Medicine. Retired now.