Cancer treatment and research最新文献

Advances in molecular genetics have revolutionized our understanding of the pathogenesis, progression, and therapeutic options for treating gastrointestinal (GI) cancers. This chapter provides a comprehensive overview of the molecular landscape of GI cancers, focusing on key genetic alterations implicated in tumorigenesis across various anatomical sites including GIST, colon and rectum, and pancreas. Emphasis is placed on critical oncogenic pathways, such as mutations in tumor suppressor genes, oncogenes, chromosomal instability, microsatellite instability, and epigenetic modifications. The role of molecular biomarkers in predicting prognosis, guiding treatment decisions, and monitoring therapeutic response is discussed, highlighting the integration of genomic profiling into clinical practice. Finally, we address the evolving landscape of precision oncology in GI cancers, considering targeted therapies and immunotherapies.

Gallbladder carcinoma (GBC) is the most common biliary epithelial malignancy, with an estimated incidence of 1.13 cases per 100,000 in the United States (Hundal and Shaffer in Clin Epidemiol 6:99-109, 2014 1; Henley et al. in Cancer Epidemiol Biomarkers Prev 24:1319-1326, 2015 2). The insidious nature and late presentation of this disease place it among the most lethal invasive neoplasms. Gallbladder cancer spreads early by lymphatic or hematogenous metastasis, as well as by direct invasion into the liver. While surgery may be curative at early stages, both surgical and nonsurgical treatments remain largely unsuccessful in patients with more advanced diseases (Rahman et al. in Cancer Med 6:874-880, 2017 3).

By the beginning of the year 2021, the estimated number of new cancer cases worldwide was about 19.3 million and there were 10.0 million cancer-related deaths. Cancer is one of the deadliest diseases worldwide that can be attributed to genetic and environmental factors, including nutrition. The good nutrition concept focuses on the dietary requirements to sustain life. There is a substantial amount of evidence suggesting that a healthy diet can modulate cancer risk, particularly the risk of colorectal and breast cancers. Many studies have evaluated the correlation between our diet and the risk of cancer development, prevention, and treatment. The effect of diet on cancer development is likely to happen through intertwining mechanisms including inflammation and immune responses. For instance, a greater intake of red and processed meat along with low consumption of fruits and vegetables has been associated with increased levels of inflammatory biomarkers that are implicated in cancer development. On the other hand, the consumption of phytosterols, vitamins, and minerals, which exert antioxidant and anti-inflammatory roles have been linked to lower cancer risk, or even its occurrence prevention. In this book, we aim to summarize the current knowledge on the role of nutrition in cancer to provide the best scientific advice in this regard.

Polyunsaturated fatty acids (PUFAs), notably omega-3 (n-3) and omega-6 (n-6), have received much attention owing to their multifaceted effects not only in the management of diverse pathological conditions but also in the maintenance of overall health of an individual. A disproportionately high n-6 to n-3 ratio contributes to the development of various disorders including cancer, which ranks as a leading cause of death worldwide with profound social and economic burden. Epidemiological studies and clinical trials combined with the animal and cell culture models have demonstrated the beneficial effects of n-3 PUFAs in reducing the risk of various cancer types including breast, prostate and colon cancer. The anti-cancer actions of n-3 PUFAs are mainly attributed to their role in the modulation of a wide array of cellular processes including membrane dynamics, apoptosis, inflammation, angiogenesis, oxidative stress, gene expression and signal transduction pathways. On the contrary, n-6 PUFAs have been shown to exert pro-tumor actions; however, the inconsistent findings and controversial data emphasize upon the need to further investigation. Nevertheless, one of the biggest challenges in future is to optimize the n-6 to n-3 ratio despite the genetic predisposition, age, gender and disease severity. Moreover, a better understanding of the potential risks and benefits as well as the cellular and molecular mechanisms of the basic actions of these PUFAs is required to explore their role as adjuvants in cancer therapy. All these aspects will be reviewed in this chapter.

Neuroendocrine neoplasms are a heterogeneous group of tumors that can occur in almost any organ and share a common neuroendocrine phenotype.

The oxidative stress defined as an event caused by an imbalance between production and accumulation of reactive oxygen species (ROS), which lead to a damage in the structure of proteins, lipids, and DNA. Therefore, the production of ROS may alter the normal physiological process by provoking damage to multiple cellular organelles and processes. Oxidative stress has been linked to heart disease, cancer, respiratory diseases, immune deficiency, stroke, Parkinson's disease, and other inflammatory or ischemic conditions. Antioxidants are substances that can prevent or slow damage to cells and tissues caused by ROS, unstable molecules that the body produces as a reaction to environmental and other pressures. The β-carotene, catechins, flavonoids, polyphenols, lycopene, lutein, selenium, vitamins A, C, D, E, and zeaxanthin are all common types of antioxidants and found in plant-based foods, especially fruits and vegetables. Each antioxidant has its own role and can interact with others to process and remove free radicals efficiently. Several studies have been conducted to investigate whether the use of dietary antioxidant supplements is associated with decreased risks of developing cancer in humans, mixed results were reported. For instance, daily use of supplement such as vitamin c, vitamin E, β-Carotene, and minerals such as selenium and zinc have shown its effectiveness by reducing the risk of developing prostate cancer among men and skin cancer among women.

Cancer morbidity and mortality incidence are rapidly increasing over the period of time. Cancer prevention, alongside innovative therapies and earlier detection, is considered a key strategy for reducing the overall cancer burden. Substantial evidence indicates a clear correlation between lifestyle factors and changes in nutrient metabolism. Approximately 5-10% of all cancer cases are attributed to genetic factors, whereas 90-95% are due to environmental and lifestyle factors, suggesting that lifestyle interventions have significant prospects for preventing various cancers. Healthy lifestyle changes, in particular healthy diets, physical activity, staying at a healthy weight, reduction or elimination of tobacco/alcohol consumption, and avoiding exposure to radiation and other carcinogens, are significant factors to be considered to tackle the challenges associated with cancer in modern society. This chapter aims to provide lifestyle intervention strategies to improve cancer prevention and risk reduction while promoting the health of cancer patients. The therapeutic role of some dietary regimens and supplements, as well as complementary and alternative health approaches, in cancer treatment is also discussed.

Diet play an important role in the development of cancer. A lot of research has been done on the role of individual nutrients or phytochemicals and cancer risk. Both harmful and beneficial associations of this nutrient have been observed with cancer. However, there is an interaction of individual dietary constituents to influence disease risk. On the other hand, examining the diet as a whole as is done in dietary patterns research may produce more accurate estimates and data that can be more easily translated into dietary recommendations. Dietary patterns and cancer research are becoming increasingly common in the epidemiology literature, and novel dietary patterns are being generated at a rapid pace. However, major issues remain over whether one general "healthy" dietary pattern can be suggested for cancer prevention or whether several diets should be advocated for different forms of cancer protection. It is challenging to study typical human diet in animal model that is appropriate for cancer prevention. Some dietary patterns, such as the ketogenic diet or macronutrient composition alteration, have been investigated more extensively in animal models than in humans in terms of cancer prevention, and bigger human observational studies are now needed to advise dietary guidelines. The question of whether to adapt nutritional guidelines to population subgroups based on susceptibility factors (for example, family history, sex, age, other lifestyle factors or comorbidities, metabolomics signatures, or microbiota-based profiles) is still open and will be crucial in moving the field forward.

Gut microbes are important and may play important role in spreading cancers specially the gastrointestinal malignancies preferably colorectal cancers. Gut microbes and diet can influence the tissues in gastrointestinal tract increasing the risk of cancer spread. Insufficient nutrient intake and imbalance diet can disturb the microbiome of gastrointestinal tract causing metabolism of xenobiotics which is beneficial as well as detrimental. Dietary imbalance may also weaken the immune system which is another reason for spreading and development of cancers. The triage of gut microbiome, host immune system, and dietary patterns may help the initiation of mechanism of carcinogenesis. In addition to its role in carcinogenesis and tumor development, there is still growing evidence as to how intestinal microflora influences the efficacy and toxicity of chemotherapy and immunotherapy by the gut microbiome. It can therefore be used as a biomarker to predict treatment response or poor response and can also be modified to improve cancer treatment.

Cancer, a non-communicable disease with diverse kinds is one of the major global problems with high incidence and no proven method to prevent or treat. Minerals including trace elements are significant micronutrients for preserving the body's typical physiological function. In contrast to extremely processed industrial food, they are rich in natural sources of food and frequently included in nutritional supplements. The daily intake, storage capacities, and homeostasis of micronutrients depend on specific dietary practices in contemporary civilization and can be disturbed by various malignancies. Varied minerals have different effects on the status of cancer depending on how they affect these pathways. The outcomes could differ depending on the mineral such as calcium's supply and the cancer's location. A mineral called zinc helps the immune system function better and aids in wound healing. On the other hand, selenium exhibits anti-oxidant functions and has a dose-response relationship with many cancer types. However, this component can make the patient's condition worse. Although the body produces free radicals when iron is deficient, anaemia affects a patient's quality of life and ability to receive therapy. This chapter compiles the knowledge of minerals connected to unusual accumulation or depletion states in various malignancies.