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Metrics details. Reactive oxygen species ROS damage DNA, but the role of ROS in breast carcinoma may not be limited to the mutagenic activity that drives carcinoma initiation and progression. Carcinoma cells in vitro and in vivo are frequently under persistent oxidative stress. In the present review, we outline potential causes of oxygen radical generation within carcinoma cells and explore the possible impact of oxidative stress on the clinical outcome of breast carcinoma. Oxygen radicals are continuously generated within mammalian cells, this being a consequence of the use of oxygen in aerobic respiration.

Reactive Oxygen Species in Cancer Biology and Anticancer Therapy

Hot Keywords non-alcoholic fatty liver disease epidemiology microenvironment nonalcoholic steatohepatitis transplantation cholangiocarcinoma direct-acting antiviral immunotherapy hepatitis B hepatitis C liver resection imaging cancer stem cell diagnosis gene cirrhosis biomarker recurrence. Correspondence Address: Dr. E-mail: ying. E-mail: flc6 georgetown.

Hepatocellular carcinoma HCC is the second leading cause of cancer-related deaths worldwide. There are two major challenges for HCC, the first being that early detection is generally not applicable, and secondly, it is usually fatal within several months after diagnosis. HCC is an inflammation-induced cancer. In this review, the evidence between oxidative stress and liver carcinogenesis is summarized. We focused on the potential of using DNA adducts as oxidative stress biomarkers for liver carcinogenesis.

Keywords Oxidative stress, DNA adduct, hepatocellular carcinoma, prevention, hepatocarcinogenesis Introduction Hepatocellular carcinoma HCC is the second leading cause of cancer-related deaths worldwide, because of late diagnosis and poor therapeutic outcome [ 1 - 4 ]. HCC accounts for 5. The incidence of HCC strongly correlates with liver inflammation from exposure to one or several risk factors including hepatitis B virus HBV , hepatitis C virus HCV , inherited metabolic diseases, heavy alcohol exposure, obesity, type 2 diabetes and aflatoxins [ 7 - 13 ].

In this review, we will mainly discuss the role of oxidative stress in hepatocarcinogenesis. The search for reliable biomarkers for liver cancer has been executed in different areas: DNA methylation, genomics, proteomics, microRNA and liquid biopsy [ 14 - 20 ].

We want to highlight that promutagenic DNA adducts is a new field which need further investigations in the search of biomarkers for HCC. Oxidative stress has been demonstrated as an important factor to carcinogenesis since the first experiment on ROS-induced transformation of mouse fibroblast cells in the s [ 31 ].

It has emerged as an important player in the development and progression of liver carcinogenesis for different etiologies e. HCC incidences in the USA are largely associated with HCV-related cirrhosis, but changes observed by epidemiological studies have attributed obesity and diabetes as risk factors as well [ 33 ].

The increased oxidative stress in obesity and diabetes may play a crucial role in hepatatocarcinogenesis [ 34 , 35 ]. Because oxidative stress drives genomic damage and genetic instability to cause mutations, and mutations play a crucial role in carcinogeneisis. This notion is supported by the chemopreventive effect demonstrated in a large number of epidemiology studies on the relationship of high fruit and, vegetable consumption with low cancer incidences, among which, antioxidants effects and maintenance of normal DNA repair capacity are indicated to be two crucial mechanisms of actions [ 36 , 37 ].

The same concept was illustrated when knocking out antioxidant defenses significantly increased the rate of liver cancer, e. Another mouse model showed that knocking out nuclear respiratory factor-1 Nrf1 , an essential transcription for mediating oxidative stress, induces steatosis, fibrosis and liver cancer, eventually [ 39 ].

The notion that oxidative stress induces HCC is also supported by studies on hemochromatosis. In the iron-nitrilotriacetic acid rat model of hemochromatosis, elevated genotoxic products from oxidative stress, 4-hydroxyl nonenal HNE and malondialdehyde MDA , are found [ 42 ].

A more important link was discovered in patients with hemochromatosis who suffered iron overload and p53 mutations following HCC development [ 41 , 44 - 46 ] ; it suggests that oxidative stress is an underlying mechanism of HCC carcinogenesis [ 44 ]. The role of oxidative stress in liver carcinogenesis is also supported by the result of a multicenter study: using tissue microarray screening, cytochrome P 1A2 CYP1A2 oxidase in non-cancerous tissue is found and validated as the only predictive factor for HCC recurrence [ 47 ].

Oxidative stress is a crucial factor in the initiation and progression of HCC under various pathological conditions [ 48 ]. Oxidative stress can be induced by ROS produced in the mitochondria in non-alcoholic fatty liver disease, which damages hepatocytes, promotes pathologic polyploidization, triggers inflammation, and contributes to insulin resistance [ 49 - 53 ]. Additionally, oxidative stress is also involved in migration, invasion, and metastasis of HCC [ 54 - 56 ].

Quantitative methods for the evaluation of oxidative stress can be divided into three categories: 1 determination of compounds modified by oxidative stress; 2 determination of the activity of antioxidant enzymes; and 3 determination of oxidative stress indicators containing transcription factors. Serum quantification of derivatives of reactive oxygen metabolites d-ROM level, a simple method for measuring hydrogen peroxide, is found to predict the risk of HCC recurrence after surgical resection or radiofrequency ablation RFA [ 57 ].

Since cancer is a genetic disease, we think that mutagenic DNA adducts that arise from oxidative stress have the potential to serve as more direct and precise biomarkers to predict HCC risk and recurrence. It is also known that the propano DNA adducts [e. We reason that DNA adducts possibly play a role of causing mutations by HBV, but further testing should be done to prove this hypothesis.

Understanding the role of DNA adducts of lipid peroxidation and the repair pathways involved may shed light onto mutagenesis during HCC development, and this knowledge will help us to find a way to its prevention [ 73 ]. Thanks to recent advances in imaging modalities and the prevalence of a surveillance method for HCC, an increasing proportion of patients now receive local ablation therapy or curable resection. Neoadjuvant and adjuvant therapy for resectable HCC is still a difficult challenge.

There are two major postoperative recurrence mechanisms: de novo carcinogenesis usually late recurrence and metastatic recurrence usually occurs within one year and is related to intrahepatic metastasis [ 75 ]. Precise prevention strategies are needed to target these mechanisms [ 76 ]. Three major strategies have been developed to address this issue [ 77 ].

The first one is a virus eradication method using interferon. But this method is not going to rescue the hepatocytes which have been damaged by hepatitis virus [ 78 ]. The second strategy is the use of anticancer drugs. Difficulties have been reported in the STROM trial sorafenib as adjuvant treatment in the prevention of recurrence of hepatocellular carcinoma and with the use of UFT Tegafur-uracil [ 79 ]. The last strategy is to induce differentiation of liver cancer cells.

For example, using Pertinoin, an acyclic retinoid which can induce apoptosis and differentiation of cancer cells. This method has shown promising survival beneficial effects in a clinical phase II trial. Other than these strategies, branched chain amino-acid supplementation, vitamin K2 and acyclic retinoid have also been examined [ 80 ].

There is still a lot of effort to be made to win this war against HCC recurrence. Future design may require focus on combination therapy. For instance, vitamin K2 and angiotensin-converting enzyme inhibitor have shown suppression effect on cumulative recurrence of HCC after curative therapy partially through reducing VEGF-mediated neovascularization [ 81 ].

Clinical trials using oxidative stress biomarkers for HCC and predicting HCC recurrence after curable surgery have been conducted [Figure 1]. Multi-center trials should be carried out to prove this application. The link between oxidative stress, DNA adducts, mutations, and cancer needs to be systematically studied; it is an area of study that can be accelerated by emerging technologies e.

New technologies are needed to demonstrate in real-time link between exact DNA lesion sites from normal tissue and mutations from tumor tissue. The idea of using antioxidants to prevent HCC recurrence has yet to be fully tested [ 83 - 85 ]. Use of oxidative stress markers to guide these trials warrants future investigation. Figure 1. Oxidative stress and liver recurrence after surgery. HCC: hepatocellular carcinoma.

We thank Dr. Aiwu Ruth He for discussions when preparing this review. J Hepatol ; BMC Cancer ; The global burden of liver disease: the major impact of China. Hepatology ; Projecting cancer incidence and deaths to the unexpected burden of thyroid, liver, and pancreas cancers in the United States. Cancer Res ; Annual Report to the Nation on the Status of Cancer, , featuring the increasing incidence of liver cancer. Cancer ; Direct antiviral agents and risk for HCC early recurrence: much ado about nothing.

Cancer Cell ; Management of hepatocellular carcinoma: prevention, surveillance, diagnosis, and staging. Exp Clin Transplant ; Molecular biology of liver cancer stem cells. Liver Cancer ; Nature ; Distinct functions of senescence-associated immune responses in liver tumor surveillance and tumor progression.

Transarterial chemo-lipiodolization can reactivate hepatitis B virus replication in patients with hepatocellular carcinoma. The human cervical cancer oncogene protein is a biomarker for human hepatocellular carcinoma. Serum proteomics and biomarkers in hepatocellular carcinoma and chronic liver disease. Clin Cancer Res ; MicroRNA expression, survival, and response to interferon in liver cancer.

N Engl J Med ; Gene expression profiling reveals potential biomarkers of human hepatocellular carcinoma. Hepatocellular carcinoma: a global view. Nat Rev Gastroenterol Hepatol ; Nonalcoholic fatty liver disease and hepatocellular carcinoma: a weighty connection.

Sci Rep ; Fatty acid-induced T cell loss greases liver carcinogenesis. Cell Metab ; Liver inflammation and cancer: the role of tissue microenvironment in generating the tumor-promoting niche TPN in the development of hepatocellular carcinoma.

Cell Res ; Role of chronic inflammation in cancers of the gastrointestinal system and the liver: where we are now.

Cancer Lett ; Molecular pathways: the complex roles of inflammation pathways in the development and treatment of liver cancer. Chronic inflammation and oxidative stress in the genesis and perpetuation of cancer: role of lipid peroxidation, DNA damage, and repair. Langenbecks Arch Surg ;

Oxidative stress and hepatocarcinogenesis

January 24, , by Lewis Cantley and Jihye Yun. Lewis Cantley received his Ph. Jihye Yun received her Ph. The discovery and isolation of vitamin C was one of the most important advances in improving human nutrition. Scurvy, a severe vitamin C deficiency disease characterized by weakness, lethargy, easy bruising and bleeding, was particularly problematic for sailors on long voyages during the 16th century, where access to fresh fruits and vegetables was limited. In fact, scurvy was the leading cause of naval deaths between the 16th and 18th centuries, killing more sailors than all battles, storms and other diseases combined.

Role of Redox Homeostasis in Cancer Biology and Anticancer Therapy

Oncotarget a primarily oncology-focused, peer-reviewed, open access, biweekly journal aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Its scope is unique. The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. The term was introduced in the inaugural Editorial , Introducing OncoTarget. Sponsored Conferences.

During the last 30 years it has become clearly evident that oxidative stress and free radical biology play key roles in carcinogenesis, cancer progression, cancer therapy, and normal tissue damage that limits treatment efficacy during cancer therapy. These mechanistic observations have led to the realization that free radical biology and cancer biology are two integrally related fields of investigation that can greatly benefit from cross fertilization of theoretical constructs. Skip to main content Skip to table of contents.

Ankita Bansal, M. Celeste Simon; Glutathione metabolism in cancer progression and treatment resistance. J Cell Biol 2 July ; 7 : — Glutathione GSH is the most abundant antioxidant found in living organisms and has multiple functions, most of which maintain cellular redox homeostasis.

Hot Keywords non-alcoholic fatty liver disease epidemiology microenvironment nonalcoholic steatohepatitis transplantation cholangiocarcinoma direct-acting antiviral immunotherapy hepatitis B hepatitis C liver resection imaging cancer stem cell diagnosis gene cirrhosis biomarker recurrence. Correspondence Address: Dr. E-mail: ying.

Oxidative Medicine and Cellular Longevity

Alexandr V. Bazhin, Pavel P. Our understanding of reactive oxygen species ROS —a group of highly reactive chemicals containing oxygen—has changed in the last few years from ROS as just harmful substances to crucial intra- and extracellular messengers as well as important regulators controlling a wide spectrum of signaling pathways. Nevertheless, there are still many uninvestigated points and open questions regarding ROS, especially in pathophysiology. Delicately controlled ROS homeostasis is critical for maintaining normal cell functions and any disruption in the oxidation-antioxidation balance leads to oxidative stress associated with a wide spectrum of human disorders such as chronic inflammation, age-related diseases, and cancers.

Для того и предназначен этот переключатель, верно. Мидж покачала головой. - Только если файл не заражен вирусом. Бринкерхофф даже подпрыгнул. - Вирус. Кто тебе сказал про вирус. - Это единственное разумное объяснение, - сказала .

Oxidative Stress in Cancer Biology and Therapy

Однако в списке было еще одно сообщение, которого он пока не видел и которое никогда не смог бы объяснить.

К счастью, ножки стола были снабжены роликами. Упираясь ногами в толстый ковер, Сьюзан начала изо всех сил толкать стол в направлении стеклянной двери. Ролики хорошо крутились, и стол набирал скорость. Уже на середине комнаты она основательно разогналась. За полтора метра до стеклянной двери Сьюзан отпрянула в сторону и зажмурилась.

Где-то в самом низу шахты воспламенились процессоры. ГЛАВА 105 Огненный шар, рвущийся наверх сквозь миллионы силиконовых чипов, производил ни на что не похожий звук. Треск лесного пожара, вой торнадо, шипение горячего гейзера… все они слились в гуле дрожащего корпуса машины. Это было дыхание дьявола, ищущее выхода и вырывающееся из закрытой пещеры.

Glutathione metabolism in cancer progression and treatment resistance

 Я не убивал его! - Крик Хейла перекрыл вой сирены.

 Предпочитаю вид спорта, в котором я могу выиграть. - Победа любой ценой? - улыбнулась Сьюзан. Защитник Джорджтауна перехватил опасную передачу, и по трибунам пронесся одобрительный гул. Сьюзан наклонилась к Дэвиду и шепнула ему на ухо: - Доктор.

Мидж развернулась и направилась к двери. Откуда ни возьмись появился Бринкерхофф и преградил ей дорогу. - Куда держишь путь. - Домой! - солгала Мидж. Бринкерхофф не уходил с дороги.

Intravenous High-Dose Vitamin C in Cancer Therapy


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