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Oncogenesis and Metastasis
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Oncogenesis (or carcinogenesis):A dynamic process whereby normal cells transform into cancerous cells.Multiple rounds of genetic and epigenetic alterations occur.Results in microscopic (morphological or structural) and molecular abnormalities.Normal cells → precursor lesions → invasion and cancer.
The Evolution of Anticancer Therapies
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Although significant advances in understanding the transformation of a healthy cell into a tumor cell have been made during the past few decades, understanding of the precise biochemical mechanisms involved is still limited and is a major barrier to discovering more efficacious but less toxic therapeutic agents. In a few cases such as chronic myelogenous leukemia (i.e., Imatinib, GleevecTM), melanoma (i.e., Vemurafenib, ZelborafTM), and lung cancer (i.e., Crizotinib, XalkoriTM), our understanding of oncogenesis has been sufficient to support the development of effective treatments. Major genome sequencing projects have been undertaken to identify the genes mutated in various tumors. However, because the tumors are usually sequenced at a late stage in their development, it is often unclear which of the numerous mutations found represent the best therapeutic targets. Also, after many generations of cell replications during tumor development, late-stage mutations may only be present in a subset of tumor cells. Targeting the protein products of these mutated genes may lead to transient antitumor effects followed by overgrowth of tumor clones that do not contain these particular target mutations. Therefore, the ideal drug targets are initial key oncogenic mutations present in all tumor cells, including tumor stem cells. Targeting these mutations should lead to more substantial therapeutic effects.
Senescence
Published in Nate F. Cardarelli, The Thymus in Health and Senescence, 2019
It is unclear as to whether aging leads to cancer, whether they both share a common cause, or perhaps oncogenesis is just a slow process.51 Doll, in 1962, offered four explanations which have been elaborated upon ever since:47Aging somehow increases the susceptibility of certain tissues to cancer.Aging somehow facilitates the appearance of cancer.Carcinogens build up to a critical level, and then oncogenesis is triggered.Carcinogenesis is a long duration process in most, not all, tissues.
Time-restricted feeding alters the efficiency of mammary tumor growth
Published in Chronobiology International, 2022
William H. Walker, Alexis L. Kaper, O. Hecmarie Meléndez-Fernández, Jacob R. Bumgarner, Jennifer A. Liu, James C. Walton, A. Courtney DeVries, Randy J. Nelson
Future studies should expand on these data to further elucidate the role of improperly timed eating on mammary tumor growth. Specifically, future studies should take care to try to equalize caloric intake between groups. This could be accomplished by restricting food intake to oral gavage in all groups or including active and ad libitum fed groups under 20% caloric restriction, which would allow for comparison of groups with similar caloric intake. Additionally, to better model western high-fat diets and the ability of high-fat diets to increase mammary tumor progression (Cordain et al. 2005; Rose et al. 1991), subsequent studies should examine the dual effects of high-fat diet and time-restricted feeding on mammary tumor growth. Future studies should also expand into spontaneous models of oncogenesis, as these models allow for significantly longer tumor development. This would allow determination of the effects of improperly timed feeding on spontaneous tumor development as well as long-term effects of time-restricted feeding on tumor growth. Finally, future studies should examine these reported effects in constant darkness, as light exposure may have masked the effects of timed feeding. However, due to the continuous development of a mammary tumor without daily oversight, this would likely be difficult to receive regulatory approval.
High-grade glioma therapy: adding flexibility in trial design to improve patient outcomes
Published in Expert Review of Anticancer Therapy, 2022
Xiaobu Ye, Karisa C. Schreck, Byram H. Ozer, Stuart A. Grossman
Widespread use of next generation sequencing (NGS) and recognition of the role distinct alterations play in oncogenesis has led to an increasing number of diagnostic categories defined by molecular alterations [29]. Clinical trials in rare brain tumor subtypes, particularly targeted therapies, face unique challenges given the limited number of patients with these tumors. Identification of molecular biomarkers through assay development, verification of adequate target inhibition, and selection of appropriate endpoints and controls are key aspects of molecularly-driven trials. Further complicating matters are the issue of intratumoral heterogeneity, with differential expression of putative targets over time and space, even within the same patient [30]. These considerations have necessitated flexibility in trial design and recruitment in order to maximize enrollment of specific patient subsets and conduct trials efficiently, while maintaining trial integrity and minimizing bias in treatment effect estimation.
Possible Protective Potency of Argun Nut (Medemia argun – An Ancient Egyptian Palm) against Hepatocellular Carcinoma in Rats
Published in Nutrition and Cancer, 2022
Nabil Mohie Abdel-Hamid, Sara Gamal Abd Allah, Mohamed K. Hassan, Amal A.M. Ahmed, Nahla H. Anber, Ibrahim Adel Faried
Cell proliferation is regarded as one of the most important biological mechanisms in oncogenesis. Uncontrolled tumor cell proliferation is the hallmark of almost all types of cancer. One common approach to study the proliferative status of transformed cells is detection of proliferating cell nuclear antigen (PCNA) by immunohistochemistry. PCNA is a key factor in DNA replication and cell-cycle regulation (47). The crucial involvement of PCNA in cellular proliferation and its tight association with cancer transformation resulted in the frequent use of PCNA as a diagnostic and prognostic cell-cycle marker (48). Cancer group showed increased level of PCNA which is an indication of hyperproliferative activity. Whereas, MA treatment significantly decreased the proliferative index as revealed by down regulated protein level expression of PCNA. Moreover, caspases are crucial mediators of apoptosis; among them, caspase‐3 is a principal enzyme in the apoptotic cascade and is often used to detect apoptotic activity (49). The present study estimated a significant accumulation of caspase-3 monoclonal antibody in liver tissue of the HCC group.