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Jeff Sutherland

Twice the Energy with Half the Stress

chatGPT Review: Jeff Sutherland’s Impact on Cancer Research

Jeff Sutherland, who is known for his work in software development and as one of the co-creators of Scrum, also conducted research on the multi-hit model of carcinogenesis starting in 1975 and continuing in the present. Sutherland’s work built upon extensive work by previous investigators and added new insights into the complex process of cancer development.

Sutherland proposed that the development of cancer is not a linear process but rather a complex, non-linear system that is influenced by a variety of factors, including genetic and environmental factors. He suggested that the multi-hit model should be viewed as a dynamic, evolving system that involves the interactions between cancer cells, the immune system, and the microenvironment of the tumor.

Sutherland also proposed that cancer should be viewed as a disease of the system rather than a disease of individual cells. He suggested that cancer development is driven by the dynamic interactions between cancer cells and the microenvironment, and that interventions targeting the microenvironment may be an effective way to prevent or treat cancer.

Sutherland’s work has contributed to our understanding of the complex and dynamic nature of cancer development and has helped guide the development of new cancer treatments and prevention strategies. His research has highlighted the importance of a systems-based approach to understanding and treating cancer, and has inspired new approaches to cancer research and treatment.

The multi-hit model of carcinogenesis, also known as the multistage model, has been a foundational concept in cancer research for decades. Here are some key historical papers on this topic:

  1. Armitage, P., & Doll, R. (1954). The age distribution of cancer and a multi-stage theory of carcinogenesis. British Journal of Cancer, 8(1), 1–12.
  2. Knudson, A. G. (1971). Mutation and cancer: statistical study of retinoblastoma. Proceedings of the National Academy of Sciences, 68(4), 820–823.
  3. Moolgavkar, S. H., & Knudson, A. G. (1981). Mutation and cancer: a model for human carcinogenesis. Journal of the National Cancer Institute, 66(6), 1037–1052.
  4. Moolgavkar, S. H., & Venzon, D. J. (1979). Two-event models for carcinogenesis: incidence curves for childhood and adult tumors. Mathematical Biosciences, 47(1-2), 55–77.
  5. Nordling, C. O. (1953). A new theory on the cancer-inducing mechanism. British Journal of Cancer, 7(1), 68–72.

These papers have played a significant role in shaping our understanding of the multi-hit model of carcinogenesis and have laid the groundwork for further research in this field. Some of the authors were reviewers and mentors for Sutherland’s Ph.D. research.

Bard comments further:

Here is the citation for Jeff Sutherland’s PhD thesis on the multihit model of carcinogenesis:

Sutherland, J. V. (1980). The multihit model of carcinogenesis and its application to human colon cancer incidence data. Ph. D. Thesis, Department of Biometrics, University of Colorado School of Medicine.

In this thesis, Sutherland proposes a model of carcinogenesis that suggests that cancer is caused by a series of mutations that occur in a cell over time. These mutations can occur in any gene, but they are most likely to occur in genes that are involved in cell growth and differentiation.

Sutherland’s model is based on the idea that cancer cells are the result of a series of genetic changes that make them resistant to the normal controls on cell growth. These changes can occur in a number of different ways, including mutations, deletions, and rearrangements of genetic material.

Sutherland’s model has been widely accepted by scientists, and it has helped to explain the development of cancer. It has also been used to develop new treatments for cancer, such as drugs that target specific genes involved in carcinogenesis.

  • Sutherland JV, Bailar JC 3rd. The multihit model of carcinogenesis: etiologic implications for colon cancer. J Chronic Dis. 1984;37(6):465-480. doi:10.1016/0021-9681(84)90030-4

The paper discusses the multihit model of carcinogenesis and its implications for the development of colon cancer. The authors suggest that the model could be used to develop new methods of screening for colon cancer and to develop new approaches to treatment.

A new model of carcinogenesis is proposed that suggests that cancer is caused by a series of mutations that occur in a cell over time. These mutations can occur in any gene, but they are most likely to occur in genes that are involved in cell growth and differentiation.

The model is based on the idea that cancer cells are the result of a series of genetic changes that make them resistant to the normal controls on cell growth. These changes can occur in a number of different ways, including mutations, deletions, and rearrangements of genetic material.

The paper discusses the implications of the model for the development of colon cancer. The authors suggest that the model could be used to develop new methods of screening for colon cancer and to develop new treatments for the disease.

The paper also discusses the limitations of the model. The authors acknowledge that the model is based on a number of assumptions, and that the results of the model may not be applicable to all cases of colon cancer.

Overall, the paper provides a useful overview of the multihit model of carcinogenesis and its potential implications for the development of colon cancer.

Real Science: Using Ultrasound to Kill Cancer

The leading physics labs are publishing papers on using frequencies to kill cancer. Here are two from Cal Tech and Cold Springs National Laboratory. These studies are published in the leading physics journals, not the medical journals. It will be decades before the average physician takes advantage of this.

A Dynamical Model of Oncotripsy by Mechanical Cell Fatigue: Selective Cancer Cell Ablation by Low-Intensity Pulsed Ultrasound (LIPUS)

E. F. SchibberD. R. MittelsteinM. GharibM. G. ShapiroP. P. LeeM. Ortiz (Submitted on 27 Nov 2019)

The method of oncotripsy, first proposed in [S. Heyden and M. Ortiz (2016). Oncotripsy: Targeting cancer cells selectively via resonant harmonic excitation. Journal of the Mechanics and Physics of Solids, 92:164-175], exploits aberrations in the material properties and morphology of cancerous cells in order to ablate them selectively by means of tuned low-intensity pulsed ultrasound (LIPUS). We propose a dynamical model of oncotripsy that follows as an application of cell dynamics, statistical mechanical theory of network elasticity and ‘birth-death’ kinetics to describe processes of damage and repair of the cytoskeleton. We also develop a reduced dynamical model that approximates the three-dimensional dynamics of the cell and facilitates parametric studies, including sensitivity analysis and process optimization. We show that the dynamical model predicts—and provides a conceptual basis for understanding—the oncotripsy effect and other trends in the data of [D. R. Mittelstein, J. Ye, E. F. Schibber, A. Roychoudhury, L. T. Martinez, M. H. Fekrazad, M. Ortiz, P. P. Lee, M. G. Shapiro, M. Gharib (2019). Selective Ablation of Cancer Cells with Low Intensity Pulsed Ultrasound. BioRxiv] for cells in suspension, including the dependence of cell-death curves on cell and process parameters.

Selective Ablation of Cancer Cells with Low Intensity Pulsed Ultrasound

David R. Mittelstein,  Jian Ye, Erika F. Schibber, Ankita Roychoudhury, Leyre Troyas Martinez, M. Houman Fekrazad, Michael Ortiz, Peter P. Lee,  Mikhail G. Shapiro,  Morteza Gharib
doi: published in Applied Physics Letters doi: 10.1063/1.5128627

Ultrasound can be focused into deep tissues with millimeter precision to perform non-invasive ablative therapy for diseases such as cancer. In most cases, this ablation uses high intensity ultrasound to deposit non-selective thermal or mechanical energy at the ultrasound focus, damaging both healthy bystander tissue and cancer cells. Here we describe an alternative low intensity pulsed ultrasound approach that leverages the distinct mechanical properties of neoplastic cells to achieve inherent cancer selectivity. We show that when applied at a specific frequency and pulse duration, focused ultrasound selectively disrupts a panel of breast, colon, and leukemia cancer cell models in suspension without significantly damaging healthy immune or red blood cells. Mechanistic experiments reveal that the formation of acoustic standing waves and the emergence of cell-seeded cavitation lead to cytoskeletal disruption, expression of apoptotic markers, and cell death. The inherent selectivity of this low intensity pulsed ultrasound approach offers a potentially safer and thus more broadly applicable alternative to non-selective high intensity ultrasound ablation.

Mechanisms and therapeutic effectiveness of pulsed electromagnetic field therapy in oncology

Maria Vadalà, Julio Cesar Morales‐Medina, […], and Tommaso IannittiVadalà M, Morales-Medina JC, Vallelunga A, Palmieri B, Laurino C, Iannitti T. Mechanisms and therapeutic effectiveness of pulsed electromagnetic field therapy in oncology. Cancer Med. 2016;5(11):3128–3139. doi:10.1002/cam4.861


Cancer is one of the most common causes of death worldwide. Available treatments are associated with numerous side effects and only a low percentage of patients achieve complete remission. Therefore, there is a strong need for new therapeutic strategies. In this regard, pulsed electromagnetic field (PEMF) therapy presents several potential advantages including non‐invasiveness, safety, lack of toxicity for non‐cancerous cells, and the possibility of being combined with other available therapies. Indeed, PEMF stimulation has already been used in the context of various cancer types including skin, breast, prostate, hepatocellular, lung, ovarian, pancreatic, bladder, thyroid, and colon cancer in vitro and in vivo. At present, only limited application of PEMF in cancer has been documented in humans. In this article, we review the experimental and clinical evidence of PEMF therapy discussing future perspectives in its use in oncology. Keywords: Cancer, electromagnetic therapy, oncology, pulsed electromagnetic fields, tumor‐specific frequencies

Electric nanoparticles can target and kill cancer cells by zapping them

Particles that produce electrical signals when bombarded with ultrasound could be a way to direct a cell-killing treatment directly to tumors. by Emerging Technology from the arXiv January 7, 2019 One potentially valuable way to attack cancer cells is to zap them with low-intensity alternating current. This interferes with the flow of calcium and potassium ions in and out of the cells, a process so important that disrupting it ultimately kills them. Recommended for You Watch this super-speedy 3D printer make objects suddenly appear Self-driving cars could make city congestion a whole lot worse An obsession with computer vision shows the lopsided nature of the AI boom We analyzed 16,625 papers to figure out where AI is headed next Lasers can send a whispered audio message directly to one person’s ear But there is a problem with this approach: healthy cells are just as susceptible to ion channel disruption as cancer cells, so the treatment kills healthy and cancerous cells alike. What’s needed is a way to focus the treatment on cancer cells while leaving the healthy ones untouched. Enter Attilio Marino at the Istituto Italiano di Tecnologia, Enrico Almici at the Polytechnic University of Turin, and colleagues in Italy. These guys use piezoelectric nanoparticles that generate current inside the body when repeatedly compressed with ultrasound. And they have gathered the first evidence that this could be turned into an effective treatment for cancer. MIT Technology Review, 7 Jan 2019

Live Longer: Reduction of Calcification in the Arteries with Frequencies

Since 1975 I have been working with some of the leading medical researchers in the world. I worked with twice Nobel Laureate Linus Pauling while a professor at the U.S. Air Force Academy. Working with physicans in the Academy hospital we were contemplating a clinical trial of Vitamin C to see if it reduced colds in cadets. Alas, the administration would not permit it in 1974. However, in 1975 I joined the faculty of the University of Colorado School of Medicine and in 1980 hooked up with Dr. Pauling when he sponsored the University of Colorado Center for Vitamins and Cancer Research (which I co-founded with another senior scientist). I had millions of dollars of grant funding from the National Cancer Center every year for over a decade which got me started on advanced technologies to eliminate disease. A few years ago National Cancer Institute leadership told me I was still on the list of only 300 scientists qualified to lead large grants for cancer research.


Linus Pauling (February 28, 1901 – August 19, 1994) was an American chemist, biochemist, peace activist, author, educator, and husband of American human rights activist Ava Helen Pauling. He published more than 1,200 papers and books, of which about 850 dealt with scientific topics. New Scientist called him one of the 20 greatest scientists of all time, and as of 2000, he was rated the 16th most important scientist in history.


Dr. Pauling showed me his almost complete DNA model and the data he gave Watson and Crick which he claimed enabled them to publish first and achieve a Nobel prize which Dr. Pauling thought rightfully belonged to him. He is the only human to achieve two independent Nobel prizes and was gunning for a third. He radically changed my thinking about medicine by showing me his lab and introducing me to his fellow researchers.

This started me down a path that led to frequency medicine which is now emerging into the mainstream. There are 566 peer reviewed medical research papers at on Pulsed Electromagnetic Frequency research and 5167 papers published on electromagnetic field therapy. This is truly the future of medicine with FDA approved cancer clinical trials now in progress. Even more interesting is using electromagnetic frequencies to reprogram DNA, a more reliable and accurate approach to CRISPR.

In 2005, I visited another leading medical researcher, Dr. Terry Grossman, also a graduate of the University of Colorado School of Medicine. He had just published a book with Ray Kurzweil, Fantastic Voyage: Live Long Enough to Live Forever. At that time, my biological age was over 20 years younger than my calendar age, almost the lowest he had ever seen (two Japanese guys had me beat).

Dr. Grossman put me on a program to regularly scan my arteries for calcification as he felt was the leading risk of death for someone who had already eliminated some cancers with frequencies (as proven by physician biopsy). I had almost no calcification on a CT scan in 2005. However, by 2012 my calcium score was elevated:

The Coronary Artery Calcium (CAC) Screening Test was done utilizing Ultra-Fast Coaxial Tomography (UF CT Scan) that was able to image the amount of calcified atherosclerotic plaque in the coronary artery walls of your heart. The computer was able to calculate a calcium score for each region of calcified plaque in each coronary artery, and a total calcium score for the heart as a whole.

There are two types of plaque that develop in the arteries: hard or calcified plaque and soft or vulnerable plaque. Heart attack risk appears to be more closely related to soft, vulnerable plaque, but at present we do not have imaging devices able to quantify this type of plaque. The ultrafast CT scan is only able to measure the heart calcified plaque. Since there is a direct correlation between hard, calcified plaque, which your CAC test measured, and soft, vulnerable plaque, higher calcium scores are related to a higher risk of heart attack. Therefore this test offers an indirect assessment of dangerous coronary atherosclerosis. Your ultrafast CT scan of 105 indicated that you had detectable calcified plaque of 105 in your coronary arteries at the 30th percentile.

On 20 December 2016, Dr. Grossman reported: Cardiovascular- Your coronary artery score increased from 15 in 2005 to 105 in 2012, placing you in the 30th percentile at that time. Now your calcium score is 399 at the 65th percentile. Explained the creation of a biofilm that protects self-replicating crystals/nanobacteria.

A new supplement called Nanobac was available at the time and was recommended. A great independently-assessed summary of research is here: Anton Kutikin, PhD in The International Journal of NanoMedicine “The Role of CNPs in Biology & Medicine”

This supplement eliminated some of the nanobacteria and stirred up the rest. When they were active I was able to determine frequencies and target them for elimination. On 13 October 2017, less than a year after my calcium score was 399, I visited Brigham and Women’s state of the art cardiology center in Boston to get a CT scan. Results are below:

My calcium score was 55, a better than 86% reduction. Dr. Grossman said this had never been done before in the history of medicine and results should be followed up with further research studies.

Here is exactly what I did to achieve this result (nothing is guaranteed):

  1. Worked closely with a knowledgable physician to get appropriate lab tests and followup.
  2. Purchased NanobacTX and followed instructions at
  3. Used nanobacteria frequency sets at
  4. Purchased frequency application system. For people new to this field try a Spooky2 system of your choice. For those with some expertise consider the Frequency Research Foundation standard lab which is much more powerful for remote work.
  5. Selected the right nanobacteria frequency sets using kinesthiology (muscle testing or a dowsing technique) and ran them while taking the recommended dosage of NanobacTX (initially 8 capsules a day for six months, followed by 2 capsules a day for maintenance).

Rife BX BY Organism DNA Sequenced

Update: This original Rife organism appears to be a necessary condition for cancer cells to survive. Eliminating this organism causes cancer cell death. There are many strains of this organism and it is very persistent.

[trx_button type=”square” style=”filled” size=”small” align=”left” link=”” popup=”no” top=”inherit” bottom=”inherit” left=”inherit” right=”inherit”]Original Rife Frequencies[/trx_button]

Research on cancer tumors using RNA sequencing of organisms identified Bacillus Licheniformis as the pleomorphic organism that has been discussed by scientists since the 19th century. This finding was published in  LANCET oncology in 2003.

Rife enthusiasts are still debating about whether Bacillus Licheniformis is the organism Rife identified with his extraordinary microscope in the early 20th century. However, they have no DNA or RNA sequencing evidence to support their arguments.

100% of people I have tested with cancer are infected with the Rife organism. Also, 100% of the people I have tested who have taken probiotic supplements containing Bacillus licheniformus have tested positive for Rife organism.

British scientists recently reported in Lancet, that they DNA sequenced the Rife BX, BY “virus”. What appears to be the Rife “filterable bacteria” was isolated and each of the various forms of the organism has the DNA sequence of Bacillus licheniformus, a pleomorphic organism that appears as rods, cocci, and fungus-like forms. Rife had a very difficult time culturing this organism in the 1920’s and people have had limited success since then, so demonstrating non-contaminated multiple forms of the same organism with exactly the same DNA sequence is a major accomplish that could end decades of controversy.

Sansom, Clare. “Cancer Germ” Bacteria Isolated. THE LANCET Oncology, Vol 4 February 2003, p. 63.
(You will need to create a free Lancet account to view this document.)

“A bacterium from canine mammary tumours which has many similarities to bacteria reported in studies done as far back as the nineteenth century has been isolated by a researcher in the UK.

“The hypothesis that bacteria may be implicated in cancer development has a chequered history. In the late nineteenth and early twentieth centuries, scientists isolated several species of bacteria from tumours, which they believed to cause cancer. By the 1950s, this “cancer germ theory” had fallen completely out of favour; modern interest revolves around the widely studied link between Helicobacter pylori and stomach cancer.

“Milton Wainwright (University of Sheffield, UK) isolated the bacterium on nutrient-free silica gel to reduce contamination. He discovered that the isolate grew in different forms, including short and long rods and cocci. After extended incubation on Czapek-Dox medium, it produced a branched, filamentous form that superficially resembled a fungus. Fungal contamination was initially ruled out by proving that the colony did not respond to non-specific antifungal antibiotics.

“We sent two different forms for 16S RNA sequencing”, says Wainwright. “Not only did we find no contamination, but we found that the forms were identical: they were both Bacillus licheniformis .” Morphological variation within a single bacterial species, or pleomorphism, was recognised as a characteristic of the historical “cancer germ”. Literature reports also describe the “cancer germ” as a Gram positive, non-acid fast, facultative anaerobe: all these are characteristics of B licheniformis.”

Milton Wainwright had already published data previously showing bacteria can pass through very small holes (as noted by Rife) and that this has major implications for their role as pathogens. See: Med Hypotheses 2002 Jun;58(6):558-60.

The first step in dealing with cancer electronically must be to eliminate all Bacillus lichenformis from the body as it appears to be both a tumor promoter and a mutagen. Tumors will tend to grow or recur with this organism present.

Infected individuals should run this F100 program weekly for as long and as often as it takes to eliminate any detectable Bacillus licheniformis. Multiple treatments will be required as this is a very persistence organism.

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