身體治愈傷口的能力是其根深蒂固的智能的一部分，是與周圍環境一起進化了數千年的。 但現代世界已經阻礙了這些治愈機製，將它們變成了造成更大損害的機製。 這一點在炎症性疾病（癌症）中表現得更為明顯，炎症性疾病的病因正在變得越來越清晰，並且其發病率在全球範圍內不斷上升。
當免疫係統發揮最佳狀態時，它可以在新生癌細胞成為問題之前檢測並消除它們。 這個過程稱為免疫監視，對於防禦癌症是不可或缺的。 免疫細胞會檢查組織中是否存在細胞 DNA 損傷的跡象，當它們發現細胞 DNA 損傷的跡象時，它們可以通過迫使細胞衰老或激活細胞凋亡（細胞的程序性死亡功能）來阻止細胞的複製。 但正如我們所知，當細胞被迫衰老時，一些細胞會繼續發展與衰老相關的分泌表型，從而引發炎症細胞因子的產生。 這些反過來又會導致腫瘤生長組織中的炎症微環境。 在慢性炎症組織中，癌細胞可以逃避這種免疫監視並繼續生長而不被發現。 此時，癌症在臨床上變得明顯，從一些異常細胞發展成可以通過 CT 掃描感覺到或檢測到的腫塊。
隨著腫瘤的生長，它們會開發出更多的技術來逃避免疫係統的檢測。 它們還產生促炎細胞因子，招募和劫持多種免疫細胞以進行自我保護。 其中一種是巨噬細胞，在癌細胞的影響下，它會表達一種細胞因子，抑製 T 細胞的抗腫瘤反應，本質上是訓練免疫係統耐受癌症。 這些巨噬細胞分泌促進血管生成的化合物，形成新血管。 現在，腫瘤已融入人體的營養供應以及血管和淋巴管的液體網絡中，惡性細胞可以將其用作高速公路。 這就是癌症擴散或轉移的方式。
許多惡性腫瘤始於感染或慢性炎症部位，這就是為什麽與慢性炎症相關的疾病會增加患癌症的風險：結直腸癌導致炎症性腸病，食道癌導致胃酸反流，前列腺炎導致前列腺炎。 繼吸煙之後，感染是可預防癌症的主要原因，全世界超過 15% 的惡性腫瘤都是由感染引起的。 持續感染可誘發慢性炎症。 人乳頭瘤病毒可導致宮頸慢性炎症，而某些病毒株是造成全球 80-90% 宮頸癌病例的原因。 乙型肝炎病毒會引起肝炎（肝髒炎症），如果這種感染變成慢性，您患肝癌的可能性會增加 14 倍。 幽門螺杆菌會引起胃炎（胃部炎症）和消化性潰瘍，從而導致胃癌。
為了解決持續感染，白細胞會產生活性氧和活性氮，這是它們對引發炎症反應的生物體正常反應的一部分。 但這些自由基也會導致我們自身組織的細胞和 DNA 損傷。 這種細胞損傷和修複的循環涉及細胞增殖的增加，產生了明顯遺傳不穩定的環境。 當細胞通過複製來修複受損的 DNA 時，我們的基因可能會在複製時引入錯誤。 這些錯誤如果不及時糾正，就會導致基因突變。 其中一些突變允許細胞在不受調節的情況下生長。
感染病毒還可以簡單地將致癌基因插入宿主的 DNA 中。 同樣，免疫抑製病毒，例如艾滋病毒，可以破壞免疫監視，使癌症逃避檢測。 癌症還會破壞細胞凋亡，盡管腫瘤含有受損的 DNA，但仍能保持腫瘤的生長。 隨著疾病的進展，腫瘤常常會生長超過其血液供應，導致進一步的組織損傷。 這會引發更多炎症。
如果 DNA 損傷是引發癌症的火花，那麽炎症就是引發癌症的燃料。 癌症本身就是一種炎症狀態。 即使在與炎症沒有已知直接因果關係的腫瘤中，例如乳腺癌，也存在炎症。 使用阿司匹林等非甾體抗炎藥物治療結腸癌和某些其他癌症，可以持續降低癌症發病率和死亡率。 由於癌症在這種環境中繁殖，免疫療法現在不僅針對腫瘤本身，還針對炎症微環境。
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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