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Guillermou's avatar
Guillermou
Feb 21

Origin and Development of Colon Cancer

1) Classical Pathway: Adenoma → Carcinoma (most frequent)

Approximately 60–70% of cases follow this sequence:

Adenomatous polyp (adenoma) → dysplasia → invasive cancer

These are the polyps:

• Tubular adenoma

• Tubulovillous adenoma

• Villous adenoma

This is called the adenoma-carcinoma sequence.

2) Serrated Pathway (increasingly recognized)

20–30% of cancers originate in serrated lesions, not in classic adenomas.

This includes:

• Sessile serrated polyp

• Traditional serrated adenoma

These are usually located in the right colon and may progress more rapidly.

3) De novo Cancer (without a previous visible polyp)

A small percentage appear to arise directly from apparently normal mucosa, without a previous identifiable polyp. This can occur due to:

• Microsatellite instability

• Rapid mutations

• Flat lesions that are difficult to detect

Associated with chronic inflammation in people with:

• Ulcerative colitis

• Crohn's disease

In summary

Origin Approximate frequency

Classic adenoma 60–70%

Serrated lesion 20–30%

De novo / inflammatory <10%

Classic pathway: adenoma → carcinoma

Accelerating factors:

• Villous adenoma

• Size >1 cm

• High-grade dysplasia

• Accumulated mutations (APC, KRAS, p53)

Serrated pathway (more unpredictable)

Lesions such as:

• Sessile serrated polyp

• Traditional serrated adenoma

5–10 years, sometimes even less.

It can progress faster because:

• It often involves genetic methylation (CIMP)

• It may be associated with microsatellite instability

It is more silent and sometimes more difficult to detect during colonoscopy.

De novo cancer

It arises without a previous visible polyp.

Estimated time:

Probably faster (3–5 years), although this is not entirely clear.

They are usually flat lesions that go unnoticed.

Associated with chronic inflammation

In diseases such as:

• Ulcerative colitis

• Crohn's disease

The risk begins to increase after:

8–10 years of continuous inflammation

Here there is no classic polyp; chronic damage generates diffuse dysplasia.

Comparative summary

Pathway Approximate time

Classic adenoma 7–15 years

Serrated lesion 5–10 years

De novo 3–5 years

Inflammatory >8–10 years of disease

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Guillermou's avatar
Guillermou
Feb 21

Among the serious health risks of ultra-processed foods, we must consider the serious problems of glycation and lipoxidation. Industrial processes, such as heating, irradiation, and ionization, all in combination with overnutrition, contribute significantly to the production, exposure, and accumulation of AGEs and ALEs in the body.

The increase in chronic diseases appears to have begun during the Industrial Revolution, primarily in the early and mid-19th century.

Chronic diseases are the leading cause of death in developed countries. The increased prevalence of chronic diseases is associated with changes in lifestyle, including increased consumption of processed foods. Advanced glycation end products (AGEs) and ALEs develop in these foods as a consequence of the reactivity of carbohydrates, proteins, lipids, and other components.

Advanced glycation end products (AGEs) are non-enzymatic interactions between reducing sugars and amino groups in proteins, lipids, and nucleic acids. In numerous diseases, such as diabetes, neuropathy, atherosclerosis, aging, nephropathy, retinopathy, and chronic kidney disease, the accumulation of AGEs (Advanced Glycation End Products) has been proposed as a pathogenic mechanism of inflammation, oxidative stress, and structural tissue damage that leads to chronic vascular problems. Current studies on AGE inhibition have focused primarily on food processing. Degenerative diseases are affected in one way or another by glycation reactions. These reactions produce significant damage in the body, including atherosclerosis, cataract formation, neurological damage, diabetes, and wrinkled and sagging skin.

Free fructose, in particular, is highly pro-inflammatory, promoting AGEs and accelerating the aging process. It also promotes the dangerous type of fat cell growth around vital organs that is a hallmark of diabetes and heart disease.

The Maillard reaction is a non-enzymatic browning process that typically involves amino acids (e.g., lysine and arginine) and reducing sugars. It progresses through a series of chemical rearrangements that result in the formation of toxic products.

At temperatures above 100/120 °C, and even more so at 140 °C, accelerated generation of these products is observed in various foods. This occurs when grilling, baking, griddling, or frying, and is facilitated by alkaline pH, copper, and iron.

Of the 20 amino acids naturally found in food proteins, lysine, due to its ε-amino acids, and arginine, due to its guanidine side group, are the most susceptible amino acids. However, histidine and tryptophan can also be involved in the Maillard reaction, as can the α-amino group or N-terminal amino group of any amino acid or peptide, respectively.

AGEs activate specific receptors and pro-inflammatory cytokines such as interleukin-1 and -6, tumor necrosis factor, and C-reactive protein (CRP). This alters the permeability and viability of cell membranes. The AGE-RAGE interaction appears to mediate most of the biological effects, including the generation of free radicals, thus creating a vicious cycle.

Free radicals also stimulate platelet activation, promoting thrombosis. They contribute to vasoconstriction through decreased nitric oxide synthesis and increased plasminogen inhibition.

The pro-inflammatory action and the promotion of thrombosis and atherosclerosis cause organ damage, primarily to the liver, kidneys, brain, lens, and connective tissue, especially the skin, cartilage, and tendons. There are compelling epidemiological and immunological mechanisms that associate AGEs with an increased risk of allergies, as well as all types of chronic and degenerative diseases, including cancer.

There are two main sources of glycation that expose us to AGEs:

-----The one that occurs naturally in our bodies when sugars bind to proteins (endogenous source). Glycation is triggered with each high blood sugar spike (i.e., with each meal). Walking or exercising for 15 minutes after eating reduces postprandial blood glucose and therefore glycation.

-----But there is also a second source of glycation that is exogenous (i.e., external to our bodies). This is simply our diet, which provides us with an excessively high dose of AGEs daily.

The more a food is cooked at high temperatures or for a longer time, the more glycation it undergoes (the cooking method matters a lot). When food is browned or charred from cooking, has a pleasant "grilled" flavor, is caramelized... This is a sign that it is loaded with harmful AGEs. Foods rich in carbohydrates, such as vegetables, fruits, and whole grains, contain relatively few AGEs, even after cooking. The formation of new AGEs during cooking was significantly reduced by moist-heat cooking, shorter cooking times, lower temperatures, and the use of acidic ingredients such as lemon juice or vinegar. A single grilled chicken thigh contains more than 16,000 kU of AGEs.

Certain foods should be avoided because they contain many glycation end products: ultra-processed foods, fried foods, grilled foods, foods cooked at high temperatures, and foods rich in protein from meat sources, sugars, and saturated fats.

Studies have shown that certain cooking methods minimize AGE production: low-temperature cooking (below 150 degrees Celsius), steaming, and the use of homemade marinades (the acidity of lemon reduces the glycation process).

Glycation in conjunction with a pro-oxidant and pro-inflammatory action may contribute to the development of cardiovascular, neurological, metabolic, joint and inflammatory disorders, among others, although its increase is usually multifactorial.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10401445/ (2023).--

https://www.frontiersin.org/articles/10.3389/falgy.2023.1148181/full (2023).--

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10401444/ (2023).—

https://pubs.rsc.org/en/content/articlehtml/2024/fo/d3fo03945e (2024).--

https://aging.utah.edu/grants/pilot/index.php

https://pubmed.ncbi.nlm.nih.gov/18332897/ (2015).—

https://pubmed.ncbi.nlm.nih.gov/20497781/ (2010).--

https://pmc.ncbi.nlm.nih.gov/articles/PMC3704564/ (2010).—

https://www.mdpi.com/2072-6643/14/12/2421 (2022).--

https://www.mdpi.com/2072-6643/14/24/5255 (2022).--

https://www.mdpi.com/2076-3921/12/8/1532 (2023)---

https://pmc.ncbi.nlm.nih.gov/articles/PMC11206686/ (2024).—

https://www.mdpi.com/2072-6643/17/7/1188 (2025).-

https://journals.lww.com/cjasn/abstract/9900/dietary_advanced_glycation_end_products_and.682.aspx (2025).--

https://www.biorxiv.org/content/10.64898/2026.01.07.698065v1.abstract (2016).-

https://journals.lww.com/co-lipidology/abstract/2026/02000/ultra_processed_foods_and_ckd__a_review_of.3.aspx (2026).--

https://www.mdpi.com/2072-6643/18/1/168 (2026).--

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