An Omega-3 That’s Poison for Cancer Tumors

[morganism]

hope this holds up, is a simple function.

The poison acts on tumor cells via a phenomenon called ferroptosis, a type of cell death linked to the peroxidation of certain fatty acids. The greater the amount of unsaturated fatty acids in the cell, the greater the risk of their oxidation. Normally, in the acidic compartment within tumors, cells store these fatty acids in lipid droplets, a kind of bundle in which fatty acids are protected from oxidation. But in the presence of a large amount of DHA, the tumor cell is overwhelmed and cannot store the DHA, which oxidizes and leads to cell death. By using a lipid metabolism inhibitor that prevents the formation of lipid droplets, researchers were able to observe that this phenomenon is further amplified, which confirms the identified mechanism and opens the door to combined treatment possibilities.

For their study, UCLouvain researchers used a 3D tumor cell culture system, called spheroids. In the presence of DHA, spheroids first grow and then implode. The team also administered a DHA-enriched diet to mice with tumors. The result: tumor development was significantly slowed compared to that in mice on a conventional diet.

This UCLouvain study shows the value of DHA in fighting cancer. “For an adult,” the UCLouvain researchers stated, “it’s recommended to consume at least 250 mg of DHA per day. But studies show that our diet provides on average only 50 to 100 mg per day. This is well below the minimum recommended intake.”

https://scitechdaily.com/an-omega-3-thats-poison-for-cancer-tumors/

Reference: 11 June 2021, Cell Metabolism.
DOI: 10.1016/j.cmet.2021.05.016

[Jim Hunt]

So just eat lots of fish?

Where to get at least 250 mg of DHA per day in your food if you're vegan/vegetarian?

[SteveMDFP]

So just eat lots of fish?

Where to get at least 250 mg of DHA per day in your food if you're vegan/vegetarian?

Hard to find, but algae oil.  Fish don't make their own DHA, they get it in the food chain.
If you don't mind eating tiny animals, krill oil would also do the trick.  That's more widely available.

If fish knew how healthy their flesh was for humans, I'm sure fish would volunteer to be eaten.

[WildFit]

So just eat lots of fish?

Where to get at least 250 mg of DHA per day in your food if you're vegan/vegetarian?

Nuts for one, wanna know more google is your friend but there are plenty of non-cadaverous sources. 


Of course you mostly have to scroll down a bit because fish and such are  usually on top.

[ivica]

This do not answers Jim's question, anyway - blog: Plant-Based Omega-3: What is ALA? | Fullscript

How to get omega-3 as a vegan or vegetarian
You can find omega-3 in land-based plants containing ALA or sea-based plants that contain EPA and DHA, but the latter must be consumed as extracts in supplemental format. (7) Examples of ALA-containing whole foods include flaxseeds and walnuts. (2) When ALA is consumed, it’s converted by enzymes in our bodies into eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).

i have to eat so i eat what i have , like purslane - showing up these days everywhere in garden, even in pots...

[nukefix]

ALA won't cut it but as mentioned EPA&DHA are available from vegan sources.

[SteveMDFP]

ALA won't cut it but as mentioned EPA&DHA are available from vegan sources.

Exactly.  Sources such as nuts, flax, and safflower oil may contain abundant ALA, but negligible EPA or DHA.  DHA was the original fatty acid under discussion.  The body can convert some ALA to DHA, but to a very limited extent.  See;

Can adults adequately convert alpha-linolenic acid (18:3n-3) to eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3)?
https://pubmed.ncbi.nlm.nih.gov/9637947/

"The parent fatty acid ALA (18:3n-3), found in vegetable oils such as flaxseed or rapeseed oil, is used by the human organism partly as a source of energy, partly as a precursor of the metabolites, but the degree of conversion appears to be unreliable and restricted. More specifically, most studies in humans have shown that whereas a certain, though restricted, conversion of high doses of ALA to EPA occurs, conversion to DHA is severely restricted. The use of ALA labelled with radioisotopes suggested that with a background diet high in saturated fat conversion to long-chain metabolites is approximately 6% for EPA and 3.8% for DHA. With a diet rich in n-6 PUFA, conversion is reduced by 40 to 50%."


So it really is fish oil for pescatarians, algae oil for vegans.

[WildFit]

So it really is fish oil for pescatarians, algae oil for vegans.

While thanking for the detailed explanations that are one of the best ever read in a few lines, one question as to the "Oils"

Why are oils that much promoted? I usually recommend to have the original, means olives instead of olive oil if possible, fish instad of fish oil and algea instead of algae oil. The original sources of any oil IMO have huge benefits themselves and then the energy to volume relation is somehow better for people who tend to eat greater volumes of food.

What do you think?

[SteveMDFP]

So it really is fish oil for pescatarians, algae oil for vegans.

While thanking for the detailed explanations that are one of the best ever read in a few lines, one question as to the "Oils"

Why are oils that much promoted? I usually recommend to have the original, means olives instead of olive oil if possible, fish instad of fish oil and algea instead of algae oil. The original sources of any oil IMO have huge benefits themselves and then the energy to volume relation is somehow better for people who tend to eat greater volumes of food.

What do you think?

Well, yes.  It's probably better to get these oils from actual food rather than supplements.  American Heart Association recommends eating fish for cardiac health, not supplements.  I believe the observational evidence is stronger for fish than for supplements.

This was more clearly seen with e.g. beta-carotene and cancer.  People with diets high in beta carotene were noted to have lower rates of cancer.  Under experimental protocols, however, beta carotene supplements did not decrease cancer rates.  See, for example:

Vitamins C and E and Beta Carotene Supplementation and Cancer Risk: A Randomized Controlled Trial
https://academic.oup.com/jnci/article/101/1/14/914826?login=true

There are a lot more components to real food than just a supplement or two will contain.  This reminds me to put more salmon and sardines on my shopping list.  And holy mackerel !

[be cause]

LOL .. just in from packing the sardines for a mini-holiday with mother (93); after enjoying salmon for lunch and kippers for tea . Holy mackerel will have to wait 'till we get to Bunagee .

[morganism]

good analysis folks, thanks.

Also, do not take beta carotene if you are a smoker. They had to stop a study on using for heart and cancer, and had to halt the study cause all the smokers started dieing.

[Rodius]

good analysis folks, thanks.

Also, do not take beta carotene if you are a smoker. They had to stop a study on using for heart and cancer, and had to halt the study cause all the smokers started dieing.

You would think it would be better to stop the smokers from smoking than to stop a study ....

[Human Habitat Index]

Prof. Thomas Seyfried - 'Cancer as a Metabolic Disease: Implications for Novel Therapies'

[morganism]

re-post of a study write up that got lost. will leave it here, so it can still show in a cancer search.

"Palmitic acid promotes cancer metastasis and leaves a more aggressive “memory” in tumour cells.

Researchers at IRB Barcelona publish in the journal Nature the mechanism by which dietary palmitic acid (and not oleic or linoleic acid) favours tumour expansion.

(authors) have described the mechanism by which a diet rich in palmitic acid makes tumour cells more aggressive, conferring them a greater capacity to metastasize.

The authors have identified several “memory” markers left in tumour cells after exposure to palmitic acid: a change that causes cells to conserve greater metastatic capacity, even months after exposure to the fatty acid and that it could be related to a greater capacity of these tumor cells to promote innervation.

“In 2017, we published a study indicating that palmitic acid correlates with increased risk of metastasis, but we didn’t know the mechanism responsible for this. In this study, we detail the process and reveal the involvement of a metastatic capacity “memory” factor and we point to a therapeutic approach to reverse it. This is promising,”

This work has been carried out using the latest single-cell RNA sequencing and positional RNA sequencing technologies, which have allowed detailed characterisation of the composition of the distinct cells that form the tumour. This is one of the first times that positional RNA-sequencing technology has been used to study the cell composition of metastases."

https://www.irbbarcelona.org/en/news/scientific/palmitic-acid-promotes-cancer-metastasis-and-leaves-more-aggressive-memory-tumour

Nature (2021) DOI: 10.1038/s41586-021-04075-0

[morganism]

Meet the plant virus that may help cure cancer
April 29, 2022

"Not all viruses are bad, and one in particular may have the power to stop cancer. Researchers at the University of California-San Diego are studying how a plant virus called cowpea mosaic virus stops cancer and prevents it from coming back. Their latest research shows that when the virus infects cancerous cells, it signals to the immune system and extends the anti-cancer response toward the tumor.

Cowpea mosaic virus is an infectious plant virus that commonly targets legumes. For the past seven years, however, study authors have been using animal models to determine its potential as a cancer immunotherapy treatment.

“This study helps validate the cowpea mosaic plant virus nanoparticle as our lead cancer immunotherapy candidate,” Nicole Steinmetz, a professor of nanoengineering at the UC San Diego Jacobs School of Engineering and the director of the Center for NanoImmunoEngineering, in a university release. “Now we have mechanistic data to explain why it is the most potent candidate, which further de-risks it for clinical translation.”
The perfect bait for fighting cancer?

The team has studied the cowpea mosaic virus in the form of nanoparticles. They injected the nanoparticles directly into the tumor to serve as bait for the immune system. Once the lure is set, immune cells detect the viral nanoparticles and send alarms to the rest of the immune system of a foreign invader in the body. While the immune cells build up to fight the virus, they start to eliminate the cancerous cells once they realize cowpea mosaic virus is inside a tumor.

Not only does the virus help get rid of the existing tumor, but Dr. Steinmetz notes that it also triggers a systemic immune response against any future tumors. While not studied in humans yet, they have observed this immune effect in canines and mouse models of various types of cancer. The cowpea mosaic virus is also unique in that it triggers an anti-cancer response that scientists don’t see in other plant viruses or virus-like particles.

“We’ve shown that it works, and now we need to show what makes it so special that it can induce this kind of response,” says lead author Veronique Beiss, a former postdoctoral researcher in Dr. Steinmetz’s lab. “That’s the knowledge gap we’re looking to fill.”
The virus triggers more disease-killing inflammation

To look at anti-tumor efficacy in similar plant viruses, the team compared the cowpea mosaic viruses with two plant viruses from the same family with similar shapes and sizes. The cowpea severe mosaic virus shared a similar RNA sequence and protein makeup. The other plant virus, the tobacco ringspot virus, only had a similar structure.

They then infected a melanoma tumor in mice with three doses of each virus-based nanoparticle immunotherapy given a week apart. Mice receiving the cowpea mosaic virus nanoparticles were more likely to survive and have the smallest tumors than those that did not. The tumor growth stopped about four days after the second dose.

Afterward, the researchers took immune cells from the spleen and lymph nodes from mice. They found that all plant viruses contain a protein shell to activate toll-like receptors that are on the surface of immune cells. However, the cowpea mosaic virus takes an extra step by using its RNA to activate an extra toll-like receptor. Activating additional toll-like receptors leads to more pro-inflammatory proteins called cytokines appearing and strengthening the immune response against cancer.

Another way the cowpea mosaic virus increases the immune response is by extending the cytokine response.

“We don’t see this with the other two plant viruses. The cytokine levels peak quickly, then go down and are gone,” explains Beiss. “This prolonged immune response is another key difference that sets cowpea mosaic virus apart.”

The study is published in the journal Molecular Pharmaceutics.

https://www.studyfinds.org/plant-virus-may-cure-cancer/


Cowpea Mosaic Virus Outperforms Other Members of the Secoviridae as In Situ Vaccine for Cancer Immunotherapy

In situ vaccination for cancer immunotherapy uses intratumoral administration of small molecules, proteins, nanoparticles, or viruses that activate pathogen recognition receptors (PRRs) to reprogram the tumor microenvironment and prime systemic antitumor immunity. Cowpea mosaic virus (CPMV) is a plant virus that─while noninfectious toward mammals─activates mammalian PRRs. Application of CPMV as in situ vaccine (ISV) results in a potent and durable efficacy in tumor mouse models and canine patients; data indicate that CPMV outperforms small molecule PRR agonists and other nonrelated plant viruses and virus-like particles (VLPs). In this work, we set out to compare the potency of CPMV versus other plant viruses from the Secoviridae. We developed protocols to produce and isolate cowpea severe mosaic virus (CPSMV) and tobacco ring spot virus (TRSV) from plants. CPSMV, like CPMV, is a comovirus with genome and protein homology, while TRSV lacks homology and is from the genus nepovirus. When applied as ISV in a mouse model of dermal melanoma (using B16F10 cells and C57Bl6J mice), CPMV outperformed CPSMV and TRSV─again highlighting the unique potency of CPMV. Mechanistically, the increased potency is related to increased signaling through toll-like receptors (TLRs)─in particular, CPMV signals through TLR2, 4, and 7. Using knockout (KO) mouse models, we demonstrate here that all three plant viruses signal through the adaptor molecule MyD88─with CPSMV and TRSV predominantly activating TLR2 and 4. CPMV induced significantly more interferon β (IFNβ) compared to TRSV and CPSMV; therefore, IFNβ released upon signaling through TLR7 may be a differentiator for the observed potency of CPMV-ISV. Additionally, CPMV induced a different temporal pattern of intratumoral cytokine generation characterized by significantly increased inflammatory cytokines 4 days after the second of 2 weekly treatments, as if CPMV induced a “memory response”. This higher, longer-lasting induction of cytokines may be another key differentiator that explains the unique potency of CPMV-ISV."

https://pubs.acs.org/doi/10.1021/acs.molpharmaceut.2c00058

[morganism]

A Significant Question in Cancer Risk and Therapy: Are Antibiotics Positive or Negative Effectors?
Current Answers and Possible Alternatives
Received: 31 July 2020; Accepted: 31 August 2020; Published: 6 September 2020


Abstract: Cancer is predominantly considered as an environmental disease caused by genetic or
epigenetic alterations induced by exposure to extrinsic (e.g., carcinogens, pollutants, radiation) or
intrinsic (e.g., metabolic, immune or genetic deficiencies). Over-exposure to antibiotics, which is
favored by unregulated access as well as inappropriate prescriptions by physicians, is known to have
led to serious health problems such as the rise of antibiotic resistance, in particular in poorly developed
countries. In this review, the attention is focused on evaluating the effects of antibiotic exposure on
cancer risk and on the outcome of cancer therapeutic protocols, either directly acting as extrinsic
promoters, or indirectly, through interactions with the human gut microbiota. The preponderant
evidence derived from information reported over the last 10 years confirms that antibiotic exposure
tends to increase cancer risk and, unfortunately, that it reduces the efficacy of various forms of cancer
therapy (e.g., chemo-, radio-, and immunotherapy alone or in combination). Alternatives to the
current patterns of antibiotic use, such as introducing new antibiotics, bacteriophages or enzybiotics,
and implementing dysbiosis-reducing microbiota modulatory strategies in oncology, are discussed.
The information is in the end considered from the perspective of the most recent findings on the
tumor-specific and intracellular location of the tumor microbiota, and of the most recent theories
proposed to explain cancer etiology on the notion of regression of the eukaryotic cells and systems
to stages characterized for a lack of coordination among their components of prokaryotic origin,
which is promoted by injuries caused by environmental insults


snip:
3. Antibiotics and Cancer Risk
As correctly expressed by McCormack and Boffetta in the title of one of their articles (“Today’s
lifestyles, tomorrow’s cancers: trends in lifestyle risk factors for cancer in low- and middle-income
countries”) [110 ], the reality is that it is precisely in those countries where not only the unregulated
consumption of antibiotics happens more frequently, but also where, unlike what happens in developed
counties [ 111 ], accurate records of cancer incidence are not periodically updated or not even maintained
at all. Given this situation, epidemiological assessments about antibiotic exposure and cancer risk are
very valuable. In the course of the last fifteen years, studies on possible effects of antibiotic exposure
on cancer risk have focused primarily on the cancer types more frequent in humans, and generally
have been designed to include cohorts of cancer patients and randomly selected non-cancer patients
as controls.
In studies related to breast cancer, the data suggested an association between antibiotic
consumption and cancer risk. Although in some studies the association was qualified as weak [112 , 113 ],
other studies reported a clearly positive association with the number of prescriptions and the cumulative
days of antibiotic use [114 ,115 ]. While in some studies the same patterns of association were observed
with all classes of antibiotics tested [ 114 ,115 ], a better association was reported by different antibiotic
classes [112 , 116 ]. The situation was not clear with regard to lung cancer, as the data provided insufficient
evidence to support or refute a possible carcinogenic effect of antibiotics [117]. The information from
studies on colorectal cancer (CRC) seems more conclusive, most likely due to the greater number of
studies published much more frequently because of the general trend of increased scientific interest
in the gut microbiota. Most CRC-related studies report an association, even at the adenoma stage,
with both timing and duration of antibiotic exposure [ 118 – 120 ]. In addition, and more importantly,
some of these studies allowed the dissociation between the effects of antibiotic usage on the risk of
colon cancer vs. rectal cancer, as the data consistently showed a positive association between antibiotic
use and colon cancer, but there was either no association or a negative correlation with cancer of the
rectum [121–123].
In more general studies of other digestive cancers (esophagus, stomach, small intestine,
hepatobiliary, and pancreas), positive associations were found between certain antibiotic classes
and particular tumor types, which increased with dose [124 , 125]. Positive associations were found
between the use of penicillins and esophageal, gastric and pancreatic cancer, with clearer dose-response
effects in the latter type [124 ]. Nitroimidazoles and quinolones showed more modest associations
with all digestive tumor types investigated [125 ]. Studies on non-melanoma skin cancer showed
that there was an increased risk of developing skin cancer associated with the use of photosensitive
antibiotics [ 126– 130 ]. Exposure to antibiotics such as ciprofloxacin, ketoconazole, and sulfamethoxazole
increased the risk of developing basal cell carcinoma (BCC), whereas the use of doxycycline and
sulfamethoxazole increased the risk of squamous cell carcinoma (SCC) [126 , 127 ,129 ]. Although some
studies associated the use of tetracycline with BCC risk [126 ,127 ], it was also reported that the use of
tetracycline demonstrated positive interactions regarding simultaneous UV light exposure and the risk
of SCC [129 ]. An association was also observed between the use of moxifloxacin and an increased
risk of developing SCC during the first year after lung post-transplantation [ 128 ]. In addition, the use
of a mathematical model also predicted, and somehow confirmed, that the risk of developing skin
cancer is positively associated with the use of antibiotics [130 ]. Finally, two large multi-tumor type
studies [ 131 ,132 ] are worthwhile mentioning. In the first one [ 131 ], researchers followed for a period
of six years the number of cancers diagnosed in a sample of 3,112,624 individuals with no previous
history of cancer, and analyzed that information with regard to the patterns of antibiotic usage in the
study population. Data from this study showed that cancer incidence increased with the number
of prescriptions, and that the extent of the association of the relative risk with antibiotic exposure
varied with tumor type, being greatest in tumors of endocrine glands, followed in decreasing order by
cancers of the prostate, breast, lung, colon and ovary [ 131 ]. The second multi-tumor type study [ 132 ],
the largest reported to date, reported results from the systemic review of about 7.9 million individuals
Antibiotics 2020, 9, 580 8 of 19
showing that, on average, antibiotic use increased cancer risk by about 18%, although the effect varied
with tumor type: 30% increased incidence of lung, pancreatic and genitourinary cancers; smaller risk
increases (6–8%) for CRC, gastric cancer and melanoma; and no association was found with esophageal
or cervical cancer. With regard to antibiotic types, the highest risk was associated with the use of
β-lactams, cephalosporins and fluoroquinolones"

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7558931/pdf/antibiotics-09-00580.pdf


Lynn Margulis and the endosymbiont hypothesis: 50 years later

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5426843/

(tripped across this while reading some astrobio, so leaving it here)

[morganism]

CF33-hNIS-antiPDL1 for the Treatment of Metastatic Triple Negative Breast Cancer (cancer virus)

This phase I trial tests the safety, side effects, and best dose of CF33-hNIS-antiPDL1 in treating patients with triple negative breast cancer that has spread to other places in the body (metastatic). CF33-hNIS-antiPDL1 is an oncolytic virus. This is a virus that is designed to infect tumor cells and break them down. "



PRIMARY OBJECTIVE:

I. To determine the safety and tolerability of a novel chimeric oncolytic orthopoxvirus, oncolytic virus CF33-expressing hNIS/Anti-PD-L1 antibody (CF33-hNIS-antiPDL1), by the evaluation of toxicities including: type, frequency, severity, attribution, time course, reversibility and duration according to Common Terminology Criteria for Adverse Events (CTCAE) 5.0 criteria.

SECONDARY OBJECTIVES:

I. To determine the optimal biologic dose (OBD) (defined as a safe dose that induces an immune response in tumors [increase checkpoint target PD-L1 by at least 5% and/or increase T cell infiltration by at least 10%]) and the recommended phase II dose (RP2D) for future expansion trial.

II. To determine tumor response rates by Response Evaluation Criteria in Solid Tumors (RECIST) version (v)1.1 (primary) and immune-modified (i)RECIST (secondary).

III. To document possible therapeutic efficacy and evaluate progression-free survival, overall survival and response.

EXPLORATORY OBJECTIVE:

I. To determine the immune and genomic profiles of tumors before and after CF33-hNIS-antiPDL1 therapy.

OUTLINE: This is a dose-escalation study.

Patients receive CF33-hNIS-antiPDL1 intratumorally (IT) on days 1 and 15. Treatment repeats every 28 days for up to 3 cycles in the absence of disease progression or unacceptable toxicity.

After completion of study treatment, patients are followed up at 30 days, then every 3 months for 1 year

https://www.cancer.gov/about-cancer/treatment/clinical-trials/search/v?id=NCI-2021-08983

[morganism]

Tiny DNA circles are key drivers of cancer, Stanford Medicine-led international study finds. (April 12, 2023)

Tiny circles of DNA harbor cancer-associated oncogenes and immunomodulatory genes promoting cancer development. They arise during transformation from pre-cancer to cancer, say Stanford Medicine-led team.

(...)
“When we think about how a tumor evolves in a patient and in response to treatment, we think of the branching trees of life proposed by Charles Darwin,” Mischel said. “This idea is so powerful that researchers often sequence the DNA from multiple parts of a tumor and draw these trees to learn about its evolution. If a mutation is there at the trunk of the tree and in all of its branches, we assume it is a key driver event in the formation of the tumor; if it is in only some branches, we assume it happened later in tumor development and may not be a good target for drug development.”

But these assumptions hinge on the idea that all of a tumor’s DNA is neatly contained on chromosomes, which are evenly divided among daughter cells each time a cancer cell divides — ensuring that each new cell gets one, and only one, copy of each chromosome.

In contrast, the tiny ecDNA circles swirl in a dividing cell like bubbles circling a bathtub drain and are portioned willy-nilly between the new daughter cells. One may get nearly all the circles; the other, almost none. As the generations accumulate, the evolutionary tree favored by Darwin begins to look decidedly odd, with the appearance of ecDNA-bearing cells sprinkled among the branches like haphazardly hung Christmas lights.

“Some researchers have looked at the evolutionary trees and decided that, because you see it here, but not there, it must be that ecDNA formation is a late event and probably isn’t important when considering treatments,” Mischel said. “Our team thought that interpretation was wrong.”
Pinpointing a reason

To get to the bottom of the tiny circles, Mischel, Chang and their collaborators turned to a specific example of cancer development — people with a condition known as Barrett’s esophagus, which occurs when the cells lining the lower part of the esophagus are damaged by acid reflux and become more like cells lining the intestine than healthy esophageal tissue. About 1% of these people develop esophageal cancer, which is difficult to treat and has a high mortality rate. Because the outcome is so poor, people with Barrett’s esophagus are routinely monitored with endoscopies and biopsies of the abnormal tissue. Because of these frequent biopsies, the researchers had access to tissue samples collected both before and after cancers developed.

The researchers assessed the prevalence of ecDNA, and identified the genes they carried, in biopsies from nearly 300 people with Barrett’s esophagus or esophageal cancer treated at the University of Cambridge or at Seattle’s Fred Hutchison Cancer Center, where individual patients were studied as the cancer developed. They found that the prevalence of ecDNA increased from 24% to 43% in early- versus late-stage esophageal cancer, indicating the continual formation of the DNA circles during cancer progression. More tellingly, they found that 33% of people with Barrett’s esophagus who developed esophageal cancer had ecDNA in their precancerous cells. In contrast, only one out of 40 people who didn’t develop cancer had cells with ecDNA, and that individual passed away due to another cause.

“The conclusions were remarkable,” Mischel said. “We see that ecDNA can arise in these precancerous cells, and that if it is there, the patient is going to get cancer. We also saw the continuous formation of ecDNA as the cancer progresses, indicating that it is advantageous to cancer growth. Finally, we saw that the ecDNA can contain immune-modulatory genes in addition to oncogenes.”

https://med.stanford.edu/news/all-news/2023/04/ecDNA-cancer.html?sf176823295=1

[morganism]

The complete set of T cell receptors in an individual carries evidence of both past and current immune responses. These traces can act as biomarkers for diseases mediated by the immune system, such as infectious diseases, autoimmune disorders, and cancer. Recent technological advancements enable us to sequence T cell receptors from patients. Nonetheless, only a small number of sequenced T cell receptors from a patient are expected to contain traces relevant to a specific disease. In this repository, we introduce the latest source code for our method to identify these traces.
(...)
In this repository, we present several examples illustrating our method for identifying immune traces that can serve as biomarkers. Each example is self-contained, complete with the associated datasets required to re-run the model. Some results are successful, while others are not (perhps there are bugs in the code). Our examples demonstrate the ability to:

    distinguish malignant from non-malignant ovarian tissue,
    diagnose breast cancer from peripheral blood,
    predict clearance of preneoplastic cervical lesions,
    and provide an example where our code performed poorly.

Publications

    Cervical Cancer Screening
    Ovarian Cancer
    Breast and Colorectal Cancer
    Multiple Sclerosis


https://github.com/jostmey/msm