{"id":280,"date":"2025-08-06T13:35:00","date_gmt":"2025-08-06T08:05:00","guid":{"rendered":"https:\/\/www.najao.com\/learn\/?p=280"},"modified":"2026-01-26T15:18:41","modified_gmt":"2026-01-26T09:48:41","slug":"cancer-carcinogenesis","status":"publish","type":"post","link":"https:\/\/www.najao.com\/learn\/cancer-carcinogenesis\/","title":{"rendered":"Carcinogenesis Explained: What Everyone Should Know About Cancer"},"content":{"rendered":"\n<p>Almost every family has had a brush with cancer at some point, racking up millions of lives each year across the globe. Understanding the basics of carcinogenesis\u2014the stepwise process by which normal cells turn cancerous\u2014brings hope, helps reduce stigma, and empowers us all towards prevention and better treatment.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">What Is cancer?<\/h2>\n\n\n\n<p>Cancer is, essentially, a disease that ensues when the body loses control. All the cells in our body are tightly regulated: they must know when to grow or stop, when to specialize, and ultimately, when to die off. Cancer totally disregards these rules. Its cells multiply without limit, stray further from their original form, and may invade other tissues far from their starting place, forming new tumors in distant organs (metastasis)<strong><sup>1<\/sup><\/strong>.<\/p>\n\n\n\n<p>What makes cancer particularly complicated is that it&#8217;s not just one illness, but rather a combination of many. Each cancer type has different risk factors, symptoms, and treatment choices. Still, beneath all this diversity, cancers have shared origins and behaviors.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">The global burden<\/h2>\n\n\n\n<p>The World Health Organization estimates that nearly <a href=\"https:\/\/www.who.int\/news-room\/fact-sheets\/detail\/cancer\" target=\"_blank\" rel=\"noreferrer noopener\">one in six deaths<\/a> worldwide is due to cancer, with more than 10 million people dying from it in 2020 alone. Certain cancers are more common in some regions; for instance, liver cancer burdens parts of Asia and Africa, while lung, breast, and colorectal tumors are more prevalent in Western countries<strong><sup>2,3<\/sup><\/strong>.<\/p>\n\n\n\n<p>Cancer leaves deep social and economic scars. It not only takes lives, but also causes loss of income, long-term disability, and immense psychological stress on patients and families. Prevention and early detection, therefore, are not just medical advancements, they are very much a necessity.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Cancer as a genetic disease<\/h2>\n\n\n\n<p>For centuries, the cause of cancer was a mystery. But it has now been discovered that cancer is nothing, but a disease rooted in the genes of our cells. Nearly all cancers arise because of&nbsp;acquired mutations\u2014changes in the DNA that occur during a person\u2019s lifetime, not inherited from their parents.<\/p>\n\n\n\n<p>Of course, some people do inherit genes that push them more at risk towards developing cancer, but these hereditary syndromes make up only about 5% of cases<strong><sup>4<\/sup><\/strong>. In most people, it\u2019s the slow accumulation of errors in DNA over years\u2014due to aging, environmental factors like chemicals or radiation, infections, or random chance, that eventually drives a cell to turn cancerous<strong><sup>5<\/sup><\/strong>.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">The hallmarks of cancer<\/h2>\n\n\n\n<p>Modern research has described a set of \u201challmarks\u201d, traits that cancer cells reliably acquire and which can help us distinguish them from healthy ones<strong><sup>6<\/sup><\/strong>:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>They can keep dividing, even in the absence of normal growth signals.<\/li>\n\n\n\n<li>Unlike normal cells, which self-destruct when damaged, cancer cells evade this fate.<\/li>\n\n\n\n<li>Cancer ignores signals that should halt its growth.<\/li>\n\n\n\n<li>Tumors induce new blood vessels (angiogenesis) to secure their food supply.<\/li>\n\n\n\n<li>Malignant cells break away and colonize distant tissues.<\/li>\n\n\n\n<li>Cancer adapts its metabolism and can escape the immune system\u2019s notice.<\/li>\n<\/ul>\n\n\n\n<p>Recognizing these hallmarks helps us to find targeted ways to interrupt these malignant abilities.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">The journey from healthy cells to cancer: carcinogenesis<\/h2>\n\n\n\n<h3 class=\"wp-block-heading\">How normal cells stay in line<\/h3>\n\n\n\n<p>In a healthy body, cells operate within strict rules:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>The cell cycle<\/strong>&nbsp;is tightly controlled by proteins (cyclins, CDKs) that act like green and red lights, ensuring cells only divide when appropriate<strong><sup>7<\/sup><\/strong>.<\/li>\n\n\n\n<li><strong>Apoptosis<\/strong>&nbsp;(programmed cell death) is the body&#8217;s quality control, removing damaged or excess cells<strong><sup>8<\/sup><\/strong>.<\/li>\n\n\n\n<li><strong>Differentiation and organization<\/strong>&nbsp;ensure cells take on specialized roles, forming coherent tissues and organs<strong><sup>9, 10<\/sup><\/strong>.<\/li>\n<\/ul>\n\n\n\n<p>Disruption to any of these systems sets the stage for cancer.<\/p>\n\n\n\n<h3 class=\"wp-block-heading\">Genes at the heart: oncogenes, tumor suppressors, and more<\/h3>\n\n\n\n<p>Cancer is fundamentally a disease of faulty, out-of-control genes. It is caused by both oncogenes\u2014that accelerate cell growth when they shouldn&#8217;t, and tumor suppressor genes\u2014whose job is to keep growth in check.<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Proto-oncogenes&nbsp;are normal genes that help cells grow; but when mutated, they transform into oncogenes, promoting uncontrolled cell growth and division<strong><sup>11<\/sup><\/strong>. For example, Ras, Myc and EGFR proteins lead to constitutive activation of growth and signaling pathways. &nbsp;<\/li>\n\n\n\n<li>Tumor suppressor genes&nbsp;such as TP53 or RB inhibit cell growth and division<strong><sup>12<\/sup><\/strong>. Usually, it requires loss of both of these gene copies to lead to development of cancer (Knudson&#8217;s\u201ctwo-hit hypothesis\u201d).<\/li>\n\n\n\n<li>DNA repair genes&nbsp;encode proteins essential for detecting and fixing damage<strong><sup>13<\/sup><\/strong>. Mutations in DNA repair genes lead to genomic instability, as seen in mutations of Mismatch Repair (MMR) genes such as <em>MLH1, MSH2\/6, <\/em>which account for 2-5% of all colorectal cancers<em>.<\/em><\/li>\n\n\n\n<li>Epigenetic changes, which are chemical modifications to DNA or its histone proteins\u2014also play a key role, turning critical genes on or off without altering the underlying genetic code itself<strong><sup>14<\/sup><\/strong>. These changes, involving DNA methylation, histone modification and dysregulation of non-coding RNAs lead to genomic instability.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">The path to cancer: from mutation to malignancy<\/h3>\n\n\n\n<p>The process of carcinogenesis unfolds in three broad stages<strong><sup>15<\/sup><\/strong>:<\/p>\n\n\n\n<ol start=\"1\" class=\"wp-block-list\">\n<li><strong>Initiation<\/strong>: A single cell suffers a permanent, irreversible DNA change.<\/li>\n\n\n\n<li><strong>Promotion<\/strong>: This mutated cell is induced to multiply\u2014by hormones, chronic inflammation, or repeated exposure to promoting chemicals.<\/li>\n\n\n\n<li><strong>Progression<\/strong>: As more errors accumulate, the cell\u2019s descendants become truly malignant, gaining the power to invade and spread.<\/li>\n<\/ol>\n\n\n\n<h2 class=\"wp-block-heading\">Triggers and risk factors for carcinogenesis<\/h2>\n\n\n\n<p>Cancer is caused by an interplay of triggers building up over time:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Chemical carcinogens<\/strong>&nbsp;like those in tobacco smoke, alcohol, or certain industrial byproducts can directly or indirectly damage DNA<strong><sup>16<\/sup><\/strong>.<\/li>\n\n\n\n<li><strong>Physical agents<\/strong>&nbsp;include ultraviolet light, and ionizing radiation from sources like X-rays, which significantly increase the risk of skin cancer<strong><sup>17<\/sup><\/strong>.<\/li>\n\n\n\n<li><strong>Viral infections<\/strong>&nbsp;such as human papillomavirus (HPV), hepatitis B and C, and Epstein-Barr virus introduce genes into cells or promote chronic inflammation, both raising cancer risk<strong><sup>18<\/sup><\/strong>.<\/li>\n\n\n\n<li><strong>Chronic infections<\/strong> by bacteria such as <em>Helicobacter pylori<\/em>&nbsp;that affect the stomach, or parasites including liver flukes or schistosomes that trigger persistent inflammation pose as a key risk for cancer in affected organs<strong><sup>19, 20<\/sup><\/strong>.<\/li>\n\n\n\n<li><strong>Inherited syndromes <\/strong>caused by genes such as&nbsp;BRCA1\/2 in breast and ovarian cancers, and APC in colon cancer mean that a person is already midway, or well-advanced, along the path to cancer<strong><sup>21, 22<\/sup><\/strong>.<\/li>\n\n\n\n<li><strong>Lifestyle factors<\/strong> such as smoking, alcohol abuse, obesity, poor diet, and being physically inactive\u2014all increase risk of developing cancer<strong><sup>23<\/sup><\/strong>.<\/li>\n<\/ul>\n\n\n\n<p>Some people experience more than one risk factor, which makes prevention so much more urgent.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">A look at major cancer types<\/h2>\n\n\n\n<p>Lung cancer&nbsp;continues to be the world\u2019s deadliest form of cancer, with around <a href=\"https:\/\/www.who.int\/news-room\/fact-sheets\/detail\/cancer\" target=\"_blank\" rel=\"noreferrer noopener nofollow\">one-third<\/a> of cancer-related deaths resulting from tobacco use<strong><sup>24<\/sup><\/strong>. Air pollution and genetic susceptibility also play a role. Unfortunately, it\u2019s often diagnosed late, after it has considerably spread.<\/p>\n\n\n\n<p>Breast cancer&nbsp;is infamous for affecting women worldwide, though men can also rarely be affected. It is now well-known that family genes like BRCA1\/2 is often an influencing factor<strong><sup>25, 26<\/sup><\/strong>. However, hormone exposure over a lifetime and other lifestyle factors can also play big roles.<\/p>\n\n\n\n<p>Colorectal cancer&nbsp;often starts unnoticed as a benign polyp<strong><sup>27<\/sup><\/strong>. These invasive diseases result due to gradual accumulation of genetic mutations, many of which are preventable. Screening, using techniques like colonoscopy, is often highly effective at preventing this kind of cancer<strong><sup>28<\/sup><\/strong>.<\/p>\n\n\n\n<p>Prostate cancer&nbsp;usually develops in older men<strong><sup>29<\/sup><\/strong>. It is influenced by age, testosterone, and sometimes inheritance. Some cases are slow and not life-threatening, while others are aggressive.<\/p>\n\n\n\n<p>Leukemias and lymphomas&nbsp;are blood cancers that can strike at any age<strong><sup>30, 31<\/sup><\/strong>. There are certain types closely linked to infections or inherited mutations.<\/p>\n\n\n\n<p>Liver cancer&nbsp;is common where previous cases of hepatitis B and C are common or where exposure to food contaminants such as aflatoxin is predominant<strong><sup>32<\/sup><\/strong>.<\/p>\n\n\n\n<p>Pancreatic, ovarian, and brain cancers&nbsp;are less common but often deadly<strong><sup>33\u201335<\/sup><\/strong>. This is in part because they can progress without early symptoms and are difficult to detect.<\/p>\n\n\n\n<p>Skin cancer, including melanoma, remains a leading cause of cancer<strong><sup>36<\/sup><\/strong>. These happen especially due to UV exposure, and so many are preventable with sun protection and vigilance.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Why understanding carcinogenesis matters<\/h2>\n\n\n\n<p>A deep understanding of how cancer develops has profoundly changed medicine. By unraveling the processes behind carcinogenesis, we are now able to prevent many cancers before they begin. Recognizing harmful exposures and risky behaviors has allowed for safer workplaces, healthier lifestyles, and the widespread use of vaccines against cancer-causing viruses, such as those for HPV and hepatitis B<strong><sup>37, 38<\/sup><\/strong>.<\/p>\n\n\n\n<p>This knowledge also underpins the success of early detection. Cancer screening techniques, like mammograms and colonoscopies, advanced imaging technologies, and even <a href=\"https:\/\/www.najao.com\/learn\/artificial-intelligence-applications-in-healthcare\/\" target=\"_blank\" rel=\"noreferrer noopener\">artificial intelligence<\/a> tools are increasingly being used to identify disease in its earliest, and most treatable stages, often before symptoms appear<strong><sup>39-42<\/sup><\/strong>.<\/p>\n\n\n\n<p>Perhaps most remarkably, advances in the genetic and molecular roots of cancer, driven by <a href=\"https:\/\/www.najao.com\/learn\/multi-omics\/\" target=\"_blank\" rel=\"noreferrer noopener\">multi-omics approaches<\/a> have transformed treatment through <a href=\"https:\/\/www.najao.com\/learn\/precision-medicine\/\" target=\"_blank\" rel=\"noreferrer noopener\">precision medicine<\/a><strong><sup>43, 44<\/sup><\/strong>. Doctors can now tailor therapies to target specific weaknesses in an individual\u2019s tumor, improving outcomes and minimizing side effects. This system-level understanding, often formalized through <a href=\"https:\/\/www.najao.com\/learn\/network-pharmacology\/\" target=\"_blank\" rel=\"noreferrer noopener\">network pharmacology,<\/a> helps to predict how a drug will affect the complex web of interactions within a cancer cell, guiding the development of multi-target therapies. Innovations such as <a href=\"https:\/\/www.najao.com\/learn\/immunotherapy\/\" target=\"_blank\" rel=\"noreferrer noopener\">immunotherapy<\/a>\u2014including <a href=\"https:\/\/www.najao.com\/learn\/car-t-cell-therapy\/\" target=\"_blank\" rel=\"noreferrer noopener\">CAR T-cell therapy<\/a>, <a href=\"https:\/\/www.najao.com\/learn\/immune-checkpoint-inhibitors\/\" target=\"_blank\" rel=\"noreferrer noopener\">immune checkpoint inhibitors<\/a>, therapeutic monoclonal antibodies, and <a href=\"https:\/\/www.najao.com\/learn\/oncolytic-viruses\/\" target=\"_blank\" rel=\"noreferrer noopener\">oncolytic viruses<\/a>, as well as emerging fields like <a href=\"https:\/\/www.najao.com\/learn\/theranostics\/\" target=\"_blank\" rel=\"noreferrer noopener\">theranostics<\/a> and <a href=\"https:\/\/www.najao.com\/learn\/nanomedicine\/\" target=\"_blank\" rel=\"noreferrer noopener\">nanomedicine<\/a>, all stem from this deeper understanding of carcinogenesis<strong><sup>45-51<\/sup><\/strong>. Additionally, <a href=\"https:\/\/www.najao.com\/learn\/disease-modeling\/\" target=\"_blank\" rel=\"noreferrer noopener\">disease modeling<\/a>, including the use of <a href=\"https:\/\/www.najao.com\/learn\/organoids\/\" target=\"_blank\" rel=\"noreferrer noopener\">organoids<\/a> helps researchers predict cancer behavior and optimize treatment approaches<strong><sup>52, 53<\/sup><\/strong>.<\/p>\n\n\n\n<p>In short, studying how cancer begins not only helps us prevent and detect the disease sooner but also fuels the development of more effective, less harmful treatments, changing the outlook for people worldwide.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">The path forward<\/h2>\n\n\n\n<p>The numerous small missteps in DNA that give rise to cancer, influenced by the environment and chance, makes it a challenging opponent. Yet, this same complexity opens the door to numerous opportunities for prevention, smarter treatment, early detection, and, hopefully, cures, one day.<\/p>\n\n\n\n<p>Today, with every new discovery, scientists and doctors are as close as ever to making cancer a manageable or even preventable disease. And while the fight continues, understanding the hidden logic of cancer\u2019s origins is the first, and most hopeful step.<\/p>\n\n\n\n<!--nextpage-->\n\n\n\n<h2 class=\"wp-block-heading\">FAQs<\/h2>\n\n\n\n<h4 class=\"wp-block-heading\">1. Do all cancers require aggressive treatment like chemotherapy or surgery?<\/h4>\n\n\n\n<p>Not all cancers require the same treatment. Some are managed with less aggressive therapies, surveillance, or alternative options depending on the type and stage.<\/p>\n\n\n\n<h4 class=\"wp-block-heading\">2. Can mobile phone use or exposure to Wi-Fi cause cancer?<\/h4>\n\n\n\n<p>Scientific evidence so far does not support a causative link between cell phones, Wi-Fi, and cancer. These devices emit low-frequency energy that does not damage DNA.<\/p>\n\n\n\n<h4 class=\"wp-block-heading\">3. Can herbal remedies or superfoods cure cancer?<\/h4>\n\n\n\n<p>There is no scientific evidence that herbal products or so-called &#8220;superfoods&#8221; cure cancer. Relying solely on them can prove dangerous.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Reference<\/h2>\n\n\n\n<p>1. Gerstberger, S., Jiang, Q., &amp; Ganesh, K. (2023). Metastasis.&nbsp;<em>Cell<\/em>,&nbsp;<em>186<\/em>(8), 1564-1579.<\/p>\n\n\n\n<p>2. Jiang, Z., Zeng, G., Dai, H., <em>et al<\/em>. (2025). Global, regional and National burden of liver cancer 1990\u20132021: a systematic analysis of the global burden of disease study 2021.&nbsp;<em>BMC Public Health<\/em>,&nbsp;<em>25<\/em>(1), 931.<\/p>\n\n\n\n<p>3. Palshof, F. K., M\u00f8rch, L. S., K\u00f8ster, B., <em>et al<\/em>. (2024). Non-preventable cases of breast, prostate, lung, and colorectal cancer in 2050 in an elimination scenario of modifiable risk factors.&nbsp;<em>Scientific Reports<\/em>,&nbsp;<em>14<\/em>(1), 8577.<\/p>\n\n\n\n<p>4. Rahner, N., &amp; Steinke, V. (2008). Hereditary cancer syndromes.&nbsp;<em>Deutsches \u00c4rzteblatt International<\/em>,&nbsp;<em>105<\/em>(41), 706.<\/p>\n\n\n\n<p>5. Parsa, N. (2012). Environmental factors inducing human cancers.&nbsp;<em>Iranian journal of public health<\/em>,&nbsp;<em>41<\/em>(11), 1.<\/p>\n\n\n\n<p>6. Fouad, Y. A., &amp; Aanei, C. (2017). Revisiting the hallmarks of cancer.&nbsp;<em>American journal of cancer research<\/em>,&nbsp;<em>7<\/em>(5), 1016.<\/p>\n\n\n\n<p>7. Barnum, K. J., &amp; O\u2019Connell, M. J. (2014). Cell cycle regulation by checkpoints. In&nbsp;<em>Cell cycle control: mechanisms and protocols<\/em>&nbsp;(pp. 29-40). New York, NY: Springer New York.<\/p>\n\n\n\n<p>8. Elmore, S. (2007). Apoptosis: a review of programmed cell death.&nbsp;<em>Toxicologic pathology<\/em>,&nbsp;<em>35<\/em>(4), 495-516.<\/p>\n\n\n\n<p>9. Coskun, V., &amp; Luskin, M. B. (2002). Intrinsic and extrinsic regulation of the proliferation and differentiation of cells in the rodent rostral migratory stream.&nbsp;<em>Journal of neuroscience research<\/em>,&nbsp;<em>69<\/em>(6), 795-802.<\/p>\n\n\n\n<p>10. Bich, L., Pradeu, T., &amp; Moreau, J. F. (2019). Understanding multicellularity: the functional organization of the intercellular space.&nbsp;<em>Frontiers in Physiology<\/em>,&nbsp;<em>10<\/em>, 1170.<\/p>\n\n\n\n<p>11. Kontomanolis, E. N., Koutras, A., Syllaios, A., <em>et al<\/em>. (2020). Role of oncogenes and tumor-suppressor genes in carcinogenesis: a review.&nbsp;<em>Anticancer research<\/em>,&nbsp;<em>40<\/em>(11), 6009-6015.<\/p>\n\n\n\n<p>12. Lee, E. Y., &amp; Muller, W. J. (2010). Oncogenes and tumor suppressor genes.&nbsp;<em>Cold Spring Harbor perspectives in biology<\/em>,&nbsp;<em>2<\/em>(10), a003236.<\/p>\n\n\n\n<p>13. Lahtz, C., &amp; Pfeifer, G. P. (2011). Epigenetic changes of DNA repair genes in cancer.&nbsp;<em>Journal of molecular cell biology<\/em>,&nbsp;<em>3<\/em>(1), 51-58.<\/p>\n\n\n\n<p>14. Kanwal, R., &amp; Gupta, S. (2012). Epigenetic modifications in cancer.&nbsp;<em>Clinical genetics<\/em>,&nbsp;<em>81<\/em>(4), 303-311.<\/p>\n\n\n\n<p>15. Loeb, L. A., &amp; Harris, C. C. (2008). Advances in chemical carcinogenesis: a historical review and prospective.&nbsp;<em>Cancer research<\/em>,&nbsp;<em>68<\/em>(17), 6863.<\/p>\n\n\n\n<p>16. Petrick, J. L., Campbell, P. T., Koshiol, J., <em>et al<\/em>. (2018). Tobacco, alcohol use and risk of hepatocellular carcinoma and intrahepatic cholangiocarcinoma: The Liver Cancer Pooling Project.&nbsp;<em>British journal of cancer<\/em>,&nbsp;<em>118<\/em>(7), 1005-1012.<\/p>\n\n\n\n<p>17. Rivas, M., Rojas, E., Araya, M. C., <em>et al<\/em>. (2015). Ultraviolet light exposure, skin cancer risk and vitamin D production.&nbsp;<em>Oncology letters<\/em>,&nbsp;<em>10<\/em>(4), 2259-2264.<\/p>\n\n\n\n<p>18. Moore, P. S., &amp; Chang, Y. (2010). Why do viruses cause cancer? Highlights of the first century of human tumour virology.&nbsp;<em>Nature reviews cancer<\/em>,&nbsp;<em>10<\/em>(12), 878-889.<\/p>\n\n\n\n<p>19. Polk, D. B., &amp; Peek Jr, R. M. (2010). Helicobacter pylori: gastric cancer and beyond.&nbsp;<em>Nature reviews cancer<\/em>,&nbsp;<em>10<\/em>(6), 403-414.<\/p>\n\n\n\n<p>20. Correia da Costa, J. M., Vale, N., Gouveia, M. J., <em>et al<\/em>. (2014). Schistosome and liver fluke derived catechol-estrogens and helminth associated cancers.&nbsp;<em>Frontiers in genetics<\/em>,&nbsp;<em>5<\/em>, 444.<\/p>\n\n\n\n<p>21. Hawsawi, Y. M., Al\u2010Numair, N. S., Sobahy, T. M., <em>et al<\/em>. (2019). The role of BRCA1\/2 in hereditary and familial breast and ovarian cancers.&nbsp;<em>Molecular genetics &amp; genomic medicine<\/em>,&nbsp;<em>7<\/em>(9), e879.<\/p>\n\n\n\n<p>22. Rustgi, A. K. (2007). The genetics of hereditary colon cancer.&nbsp;<em>Genes &amp; development<\/em>,&nbsp;<em>21<\/em>(20), 2525-2538.<\/p>\n\n\n\n<p>23. Sharman, R., Harris, Z., Ernst, B., <em>et al<\/em>. (2024). Lifestyle factors and cancer: a narrative review.&nbsp;<em>Mayo Clinic Proceedings: Innovations, Quality &amp; Outcomes<\/em>,&nbsp;<em>8<\/em>(2), 166-183.<\/p>\n\n\n\n<p>24. Thandra, K. C., Barsouk, A., Saginala, K., <em>et al<\/em>. (2021). Epidemiology of lung cancer.&nbsp;<em>Contemporary Oncology\/Wsp\u00f3\u0142czesna Onkologia<\/em>,&nbsp;<em>25<\/em>(1), 45-52.<\/p>\n\n\n\n<p>25. Sun, Y. S., Zhao, Z., Yang, Z. N., <em>et al<\/em>. (2017). Risk factors and preventions of breast cancer.&nbsp;<em>International journal of biological sciences<\/em>,&nbsp;<em>13<\/em>(11), 1387.<\/p>\n\n\n\n<p>26. Wang, F., Shu, X., Meszoely, I., <em>et al<\/em>. (2019). Overall mortality after diagnosis of breast cancer in men vs women.&nbsp;<em>JAMA oncology<\/em>,&nbsp;<em>5<\/em>(11), 1589-1596.<\/p>\n\n\n\n<p>27. Sullivan, B. A., Noujaim, M., &amp; Roper, J. (2022). Cause, epidemiology, and histology of polyps and pathways to colorectal cancer.&nbsp;<em>Gastrointestinal Endoscopy Clinics<\/em>,&nbsp;<em>32<\/em>(2), 177-194.<\/p>\n\n\n\n<p>28. Bretthauer, M., L\u00f8berg, M., Wieszczy, P., <em>et al<\/em>. (2022). Effect of colonoscopy screening on risks of colorectal cancer and related death.&nbsp;<em>New England Journal of Medicine<\/em>,&nbsp;<em>387<\/em>(17), 1547-1556.<\/p>\n\n\n\n<p>29. Stangelberger, A., Waldert, M., &amp; Djavan, B. (2008). Prostate cancer in elderly men.&nbsp;<em>Reviews in urology<\/em>,&nbsp;<em>10<\/em>(2), 111.<\/p>\n\n\n\n<p>30. Chennamadhavuni, A., Lyengar, V., Mukkamalla, S. K. R., <em>et. al<\/em>. (2023). In StatPearls [Internet]. StatPearls&nbsp;Publishing.<\/p>\n\n\n\n<p>31. Jamil, A., &amp; Mukkamalla, S. K. R. (2023). Lymphoma. In&nbsp;<em>StatPearls [Internet]<\/em>. StatPearls Publishing.<\/p>\n\n\n\n<p>32. Sia, D., Villanueva, A., Friedman, S. L., <em>et al<\/em>. (2017). Liver cancer cell of origin, molecular class, and effects on patient prognosis.&nbsp;<em>Gastroenterology<\/em>,&nbsp;<em>152<\/em>(4), 745-761.<\/p>\n\n\n\n<p>33. Vincent, A., Herman, J., Schulick, R., <em>et al<\/em>. (2011). Pancreatic cancer.&nbsp;<em>The lancet<\/em>,&nbsp;<em>378<\/em>(9791), 607-620.<\/p>\n\n\n\n<p>34. Matulonis, U. A., Sood, A. K., Fallowfield, L., <em>et al<\/em>. (2016). Ovarian cancer.&nbsp;<em>Nature reviews Disease primers<\/em>,&nbsp;<em>2<\/em>(1), 1-22.<\/p>\n\n\n\n<p>35. Quail, D. F., &amp; Joyce, J. A. (2017). The microenvironmental landscape of brain tumors.&nbsp;<em>Cancer cell<\/em>,&nbsp;<em>31<\/em>(3), 326-341.<\/p>\n\n\n\n<p>36. Apalla, Z., Nashan, D., Weller, R. B., <em>et al<\/em>. (2017). Skin cancer: epidemiology, disease burden, pathophysiology, diagnosis, and therapeutic approaches.&nbsp;<em>Dermatology and therapy<\/em>,&nbsp;<em>7<\/em>(Suppl 1), 5-19.<\/p>\n\n\n\n<p>37. Harper, D. M., &amp; DeMars, L. R. (2017). HPV vaccines\u2013a review of the first decade.&nbsp;<em>Gynecologic oncology<\/em>,&nbsp;<em>146<\/em>(1), 196-204.<\/p>\n\n\n\n<p>38. Pattyn, J., Hendrickx, G., Vorsters, A., <em>et al<\/em>. (2021). Hepatitis B vaccines.&nbsp;<em>The Journal of infectious diseases<\/em>,&nbsp;<em>224<\/em>(Supplement_4), S343-S351.<\/p>\n\n\n\n<p>39. Ribli, D., Horv\u00e1th, A., Unger, Z., <em>et al<\/em>. (2018). 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A., &amp; Price, N. D. (2010). In silico models of cancer.&nbsp;<em>Wiley Interdisciplinary Reviews: Systems Biology and Medicine<\/em>,&nbsp;<em>2<\/em>(4), 438-459.<\/p>\n\n\n\n<p>53. Tuveson, D., &amp; Clevers, H. (2019). Cancer modeling meets human organoid technology.&nbsp;<em>Science<\/em>,&nbsp;<em>364<\/em>(6444), 952-955.<\/p>\n","protected":false},"excerpt":{"rendered":"<p>We all have had our fair share of association with the disease that cancer is. Cancer develops as genetic and cellular controls fail, allowing unchecked cell growth. 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