身体治愈伤口的能力是其根深蒂固的智能的一部分，是与周围环境一起进化了数千年的。 但现代世界已经阻碍了这些治愈机制，将它们变成了造成更大损害的机制。 这一点在炎症性疾病（癌症）中表现得更为明显，炎症性疾病的病因正在变得越来越清晰，并且其发病率在全球范围内不断上升。
当免疫系统发挥最佳状态时，它可以在新生癌细胞成为问题之前检测并消除它们。 这个过程称为免疫监视，对于防御癌症是不可或缺的。 免疫细胞会检查组织中是否存在细胞 DNA 损伤的迹象，当它们发现细胞 DNA 损伤的迹象时，它们可以通过迫使细胞衰老或激活细胞凋亡（细胞的程序性死亡功能）来阻止细胞的复制。 但正如我们所知，当细胞被迫衰老时，一些细胞会继续发展与衰老相关的分泌表型，从而引发炎症细胞因子的产生。 这些反过来又会导致肿瘤生长组织中的炎症微环境。 在慢性炎症组织中，癌细胞可以逃避这种免疫监视并继续生长而不被发现。 此时，癌症在临床上变得明显，从一些异常细胞发展成可以通过 CT 扫描感觉到或检测到的肿块。
随着肿瘤的生长，它们会开发出更多的技术来逃避免疫系统的检测。 它们还产生促炎细胞因子，招募和劫持多种免疫细胞以进行自我保护。 其中一种是巨噬细胞，在癌细胞的影响下，它会表达一种细胞因子，抑制 T 细胞的抗肿瘤反应，本质上是训练免疫系统耐受癌症。 这些巨噬细胞分泌促进血管生成的化合物，形成新血管。 现在，肿瘤已融入人体的营养供应以及血管和淋巴管的液体网络中，恶性细胞可以将其用作高速公路。 这就是癌症扩散或转移的方式。
许多恶性肿瘤始于感染或慢性炎症部位，这就是为什么与慢性炎症相关的疾病会增加患癌症的风险：结直肠癌导致炎症性肠病，食道癌导致胃酸反流，前列腺炎导致前列腺炎。 继吸烟之后，感染是可预防癌症的主要原因，全世界超过 15% 的恶性肿瘤都是由感染引起的。 持续感染可诱发慢性炎症。 人乳头瘤病毒可导致宫颈慢性炎症，而某些病毒株是造成全球 80-90% 宫颈癌病例的原因。 乙型肝炎病毒会引起肝炎（肝脏炎症），如果这种感染变成慢性，您患肝癌的可能性会增加 14 倍。 幽门螺杆菌会引起胃炎（胃部炎症）和消化性溃疡，从而导致胃癌。
为了解决持续感染，白细胞会产生活性氧和活性氮，这是它们对引发炎症反应的生物体正常反应的一部分。 但这些自由基也会导致我们自身组织的细胞和 DNA 损伤。 这种细胞损伤和修复的循环涉及细胞增殖的增加，产生了明显遗传不稳定的环境。 当细胞通过复制来修复受损的 DNA 时，我们的基因可能会在复制时引入错误。 这些错误如果不及时纠正，就会导致基因突变。 其中一些突变允许细胞在不受调节的情况下生长。
感染病毒还可以简单地将致癌基因插入宿主的 DNA 中。 同样，免疫抑制病毒，例如艾滋病毒，可以破坏免疫监视，使癌症逃避检测。 癌症还会破坏细胞凋亡，尽管肿瘤含有受损的 DNA，但仍能保持肿瘤的生长。 随着疾病的进展，肿瘤常常会生长超过其血液供应，导致进一步的组织损伤。 这会引发更多炎症。
如果 DNA 损伤是引发癌症的火花，那么炎症就是引发癌症的燃料。 癌症本身就是一种炎症状态。 即使在与炎症没有已知直接因果关系的肿瘤中，例如乳腺癌，也存在炎症。 使用阿司匹林等非甾体抗炎药物治疗结肠癌和某些其他癌症，可以持续降低癌症发病率和死亡率。 由于癌症在这种环境中繁殖，免疫疗法现在不仅针对肿瘤本身，还针对炎症微环境。
A WOUND THAT NEVER HEALS = CANCER
The body’s capacity to heal wounds is part of its ingrained intelligence, evolved over millennia in tandem with its surroundings. But the modern world has thwarted these mechanisms of healing, turning them into ones that do more damage. This is no more evident than in the inflammatory disease whose etiology is becoming clearer and whose rates are growing worldwide-cancer.
When the immune system functions in its optimal state, it can detect and eliminate nascent cancer cells before they become a problem. This process is called immunosurveillance and is indispensable in the defense against cancer. Immune cells survey tissues for signs of cellular DNA damage, and when they find it, they can arrest the cell’s replication by forcing it into senescence, or activating apoptosis- the cell’s programmed death function. But as we know, when cells are forced into senescence, some will go on to develop the senescence-associated secretory phenotype, prompting ore inflammatory cytokines. These in turn contribute to the microenvironment of inflammation in the tissue where a tumor grows. In chronically inflamed tissues, cancer cells can escape this immunosurveillance and continue to grow undetected. This is when cancer becomes clinically evident, growing from a few aberrant cells to a mass you can feel or detect on a CT scan.
As tumors grow, they develop more techniques to evade the immune system’s detection. They also produce pro-inflammatory cytokines, recruiting and hijacking a diverse population of immune cells for heir own self-preservation. One type is the macrophage, which , under the influence of cancer cells, expresses a cytokine that curbs the antitumor response of T cells, in essence training the immune system to tolerate the cancer. These macrophages secrete compounds that promote angiogenesis, making new blood vessels. Now the tumor is tapped into the body’s nutrient supply and into its liquid network of blood vessels and lymphatics, which malignant cells can use as a superhighway. This is how cancer spreads, or metastasizes.
Many malignancies start at a site of infection or chronic inflammation, which is why conditions associated with chronic inflammation come with an increased risk of cancer: colorectal for inflammatory bowel disease, esophageal for acid reflux, prostate for prostatitis. After tobacco smoking, infections are the leading cause of preventable cancer, responsible for over 15% of malignancies worldwide. Persistent infections can induce chronic inflammation. The human papillomavirus can lead to chronic inflammation of the cervix, and certain strains are responsible for 80-90% of all cases of cervical cancer worldwide. The hepatitis B virus brings about hepatitis (inflammation of the liver), and if that infection becomes chronic, you’re 14 times more likely to develop liver cancer. The Helicobacter pylori generates gastritis (stomach inflammation) and peptic ulcers, which can lead to gastric cancer.
To resolve a persistent infection, white blood cells produce reactive oxygen and reactive nitrogen species, part of their normal response to an organism that sets off the inflammatory response. But these free radicals cause cellular and DNA damage in our own tissues too. This cycle of cellular insult and then repair, which involves increased cellular proliferation, generates an environment of marked genetic instability. As cells replicate to repair damaged DNA, our genes can get copied with errors introduced. These mistakes slip by uncorrected, giving rise to genetic mutations. Some of these mutations allow a cell to grow without regulation.
Infecting viruses can also simply insert cancer-causing genes into the host’s DNA. Likewise, immunosuppressive viruses, such as HIV, can undermine immunosurveillance, allowing cancer to escape detection. Cancer also subverts apoptosis, keeping tumors growing in spite of their load of damaged DNA. As the disease progresses, tumors often outgrow their blood supply, resulting in further tissue damage. This sets off more inflammation.
If DNA damage is the spark that starts the fire of cancer, inflammation is fuel for that fire. And cancer itself is an inflammatory state. Even in tumors without a known direct causal link to inflammation, such as breast cancer, inflammation is present. Treatment of colon cancer and certain other cancers with nonsteroidal anti-inflammatory medications, like aspirin, consistently decreases cancer rates and deaths. Because cancer thrives in this kind of milieu, immunotherapy now targets not only the tumor itself but also the inflammatory microenvironment.
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