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Radiation Therapy and Radiation Safety in Medicine
Published in Suzanne Amador Kane, Boris A. Gelman, Introduction to Physics in Modern Medicine, 2020
Suzanne Amador Kane, Boris A. Gelman
Cell growth and division, as well as programmed cell death, are all regulated by an elaborate system of checks and balances, the genetic regulatory system, only now being unraveled by science. Some of the players in this system serve to promote the reproduction of cells. For example, genes called oncogenes (or tumor promoters) code for proteins that promote the reproduction of cells. Conversely, cell proliferation is usually held in check by the opposing action of tumor suppressors, which limit cell division. Both tumor promoter and tumor suppressor genes are beneficial when present in the normal balance: the tumor promoters are often compared to the accelerator pedal of a car, and the tumor suppressors to the brakes. However, defects in either gene can predispose the cell to uncontrolled division: a car with a stuck accelerator or brake failure is equally out of control. A mutation can inactivate or prevent the production of tumor suppressors in any of a number of ways, whereas causing a tumor promoter to promote unchecked cell division requires a more specific alteration. Consequently, most of the genetic defects associated with cancer discovered thus far involve tumor suppressor genes.
Preclinical and Clinical Safety Assessment of Transdermal and Topical Dermatological Products
Published in Tapash K. Ghosh, Dermal Drug Delivery, 2020
Lindsey C. Yeh, Howard I. Maibach
Tumor development in initiated skin can be accomplished if a tumor promoter is present in a TTS that is locally applied. One common feature of tumor-promoting agents is that they induce skin inflammation and epidermal hyperplasia (Agarawal and Mukhtar, 1991). The TTS may be tested by repeated application over a period of several weeks to determine the potential of the TTS component to act as a tumor promoter.
Nutraceutical’s Role in Proliferation and Prevention of Colorectal Cancer
Published in Sheeba Varghese Gupta, Yashwant V. Pathak, Advances in Nutraceutical Applications in Cancer, 2019
Mayur M. Patel, Shruti U. Rawal, Jayvadan K. Patel
Consumption of whole grains, vegetables, and fruits containing high fiber content has been associated in reducing CRC risks in several research works (plants, fiber, and colon cancer). There are several proposed mechanisms that are believed to be responsible for their chemopreventive action. Dietary fibers help in increasing fecal weight while reducing gastric transit time to reduce the carcinogen-mucosal lining contact time [107]. In addition to this, they prevent polyp recurrence and tumor promoter gene expression. Soluble fibers enhance the excretion of tumor promoters like the secondary bile acids. Besides this, short chain fatty acids are formed on the digestion of dietary fibers that induce differentiation and apoptosis of colon tumor cells via decrease in fecal pH, which in turn affects bile acid conversion [107]. The prebiotics and probiotics are collectively referred as “synbiotics.” They help in the recuperation of patients with CRC [103].
Erianin Exerts Antineoplastic Effects on Esophageal Squamous Cell Carcinoma Cells by Activating the cGMP-PKG Signaling Pathway
Published in Nutrition and Cancer, 2023
Xin Deng, Qianfeng Wu, Dong Li, Youping Liu
The role of activated cGMP-PKG signaling in cancer is tumor-specific. For instance, the cGMP-PKG signaling pathway acts as a tumor suppressor in prostate, melanoma, breast, and kidney cancers (17, 18, 20, 33, 34). However, it acts as a tumor promoter in head and neck squamous cell carcinoma as well as gastric and cervical cancers (35–37). Our present data imply that activation of the cGMP-PKG signaling pathway may play a tumor-suppressive role in ESCC. To clarify the function of the cGMP-PKG signaling pathway, we added the PKG inhibitor KT5823. KT5823 is a selective cGMP-dependent protein kinase (PKG) inhibitor that has been used extensively in functional investigations of the cGMP-PKG signaling pathway (38, 39). A previous study reported that KT5823 could relieve the STEAP4 knockdown-mediated suppression of prostate cancer cell proliferation (17). Indeed, treatment with KT5823 significantly reduced the inhibition of cell proliferation, migration, and pro-apoptotic abilities by erianin, which is consistent with a previous study. These findings imply that the anti-ESCC effect of erianin is partially mediated by activation of the cGMP-PKG signaling pathway. However, further research is needed to clarify the target by which erianin activates the cGMP-PKG signaling pathway in ECSS cells and to confirm the mechanism of erianin anti-ESCC growth in vivo.
Approaches for the setting of occupational exposure limits (OELs) for carcinogens
Published in Critical Reviews in Toxicology, 2023
Positive responses in 2-year animal bioassays were partially interpreted in the light of results obtained from initiation-promotion animal research (Solano et al. 2016). Consistent with a long latency period for cancer development (Section 2.2), the initiation-promotion model emphasises two phases of cancer development. The initiation phase is associated with mutations caused by a mutagenic chemical (a tumour initiator) and leads to the appearance of “initiated cells”. Each of these cells with a presumed first mutation has the potential to constitute a single cell origin of a tumour. The promotion phase requires multiple doses of the same or a different chemical, over an extended period of time. The tumour promoter may target initiated cells to proliferate. During the promotion phase, the number of initiated cells thus multiply, and it was soon discovered that new mutations were acquired via indirect mechanisms such as stimulated cell replication. The discovery that chemicals can act as promoters gave rise to the concept of non-genotoxic carcinogens (Cohen and Ellwein 1990). Later, the terms genotoxic (direct and indirect genotoxic) and non-genotoxic carcinogens became established nomenclature to distinguish in risk assessments between non-threshold (DNA-reactive) and threshold (indirect genotoxic and non-genotoxic) carcinogens (Chapter 5).
Pharmabiotic beads with improved encapsulation and gut survival for management of colonic inflammation associated gut derangements
Published in Journal of Drug Targeting, 2020
Parneet Kaur Deol, Pragyanshu Khare, Dhirendra Pratap Singh, Mahendra Bishnoi, Kanthi Kiran Kondepudi, Indu Pal Kaur
The production of free radicals in the gut can exert cytotoxic effects on the membrane phospholipids of the intestinal epithelial cells, resulting in the formation of toxic products such as malondialdehyde (MDA). The key antioxidant enzymes which include superoxide dismutase (SOD) and catalase (CAT) form the backbone of the enzymatic antioxidant cascade and offer protection to cells and tissues against oxidative injury [33]. MDA itself, owing to its high cytotoxicity and inhibitory action on protective antioxidant enzymes, is suggested to act as a tumour promoter and a co-carcinogenic agent [34]. Encapsulated LAB (LBs) showed significant (p < .05) reduction in LPO and elevation of both SOD and catalase levels (Figure 3) while its free form (FL group) failed to produce any significant effect. This could be attributed to inability of free viable LAB to reach the colon in a sufficient number to exert significant antioxidant effect.