Preparing Professionals in Cancer Therapy

2012 ◽  
pp. 200-208
Author(s):  
Shiv Shanker Pandey ◽  
Vivek Ambastha ◽  
Budhi Sagar Tiwari
Keyword(s):  
Cancer Research ◽  
Cell Death ◽  
Cancer Therapy ◽  
Programmed Cell Death ◽  
Cancer Cells ◽  
Western World ◽  
Medical Oncologists ◽  
Broad Interest ◽  
Major Target

Cancer is currently the second biggest cause of death in the Western world. Cancer cells escape the normal process of programmed cell death i.e., fail to die on schedule. The ability of cancer cells to avoid programmed cell death and continue to proliferate is one of the fundamental hallmarks of cancer and is a major target of cancer therapy development. Universities and research institutes are playing a major role in progress of cancer research. The aim of this study is to attract graduates of different disciplines towards cancer research and bring together researchers from different disciplines with an interest in the role of programmed cell death in cancer therapy and exploitation of programmed cell death research for therapeutic targeting of cancer. In spite of this, it is of broad interest to make a bridge or to start collaborations in between basic researchers and medical oncologists as well as for pharmaceutical companies i.e., aim of this study is to bridging the gap between knowledge and its action or application.

scholarly journals Unraveling the Potential Role of Glutathione in Multiple Forms of Cell Death in Cancer Therapy

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Huanhuan Lv ◽  
Chenxiao Zhen ◽  
Junyu Liu ◽  
Pengfei Yang ◽  
Lijiang Hu ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Cancer Cells ◽  
Cancer Therapeutics ◽  
Antioxidant Defense System ◽  
Glutathione Depletion ◽  
Multiple Forms ◽  
Glutathione Synthesis ◽  
Glutathione Homeostasis

Glutathione is the principal intracellular antioxidant buffer against oxidative stress and mainly exists in the forms of reduced glutathione (GSH) and oxidized glutathione (GSSG). The processes of glutathione synthesis, transport, utilization, and metabolism are tightly controlled to maintain intracellular glutathione homeostasis and redox balance. As for cancer cells, they exhibit a greater ROS level than normal cells in order to meet the enhanced metabolism and vicious proliferation; meanwhile, they also have to develop an increased antioxidant defense system to cope with the higher oxidant state. Growing numbers of studies have implicated that altering the glutathione antioxidant system is associated with multiple forms of programmed cell death in cancer cells. In this review, we firstly focus on glutathione homeostasis from the perspectives of glutathione synthesis, distribution, transportation, and metabolism. Then, we discuss the function of glutathione in the antioxidant process. Afterwards, we also summarize the recent advance in the understanding of the mechanism by which glutathione plays a key role in multiple forms of programmed cell death, including apoptosis, necroptosis, ferroptosis, and autophagy. Finally, we highlight the glutathione-targeting therapeutic approaches toward cancers. A comprehensive review on the glutathione homeostasis and the role of glutathione depletion in programmed cell death provide insight into the redox-based research concerning cancer therapeutics.

scholarly journals Target Misfolded Protein Clearance Pathway for Cancer Therapy

Proceedings ◽  
2020 ◽  
Vol 40 (1) ◽  
pp. 45
Author(s):  
Apar Pataer
Keyword(s):  
Cell Death ◽  
Cancer Therapy ◽  
Cancer Cells ◽  
Prion Proteins ◽  
Misfolded Protein ◽  
Breast Cancer Patients ◽  
Protein Kinase R ◽  
Protein Clearance ◽  
Dependent Protein

The role of RNA-dependent protein kinase R (PKR) and its association with misfolded protein expression in cancer cells are unclear. Herein we report that PKR regulates misfolded protein clearance by preventing it release through exosomes and promoting lysosomal degradation of misfolded prion proteins in cancer cells. We demonstrated that PKR contributes to the lysosome function and regulates misfolded prion protein clearance. We hypothesized that PKR-associated lysosome function is critical for cancer but not normal cell survival, representing an effective approach for highly targeted cancer therapy. In screening a compound library, we identified two PKR-associated compound 1 did not affect normal cells but selectively induced cell death in cancer cells depending on their PKR expression status. Pac 1 significantly inhibited the growth of human lung and breast xenograft tumors in mice with no toxicity. Pac 1 binds to PI4K2A and disrupts the PKR/PI4K2A associated lysosome complex, contributing to destabilization of cancer cell lysosomes and triggering cell death. We observed that PKR and PI4K2A play significant prognostic roles in breast cancer patients. These results demonstrate that targeting of a PI4K2A/PKR lysosome complex may be an effective approach for cancer therapy.

scholarly journals Therapeutic targeting of the PI4K2A/PKR lysosome network is critical for misfolded protein clearance and survival in cancer cells

Oncogene ◽  
2019 ◽  
Vol 39 (4) ◽  
pp. 801-813 ◽  
Author(s):  
Apar Pataer ◽  
Bulent Ozpolat ◽  
RuPing Shao ◽  
Neil R. Cashman ◽  
Steven S. Plotkin ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Therapy ◽  
Cancer Cells ◽  
Prion Proteins ◽  
Misfolded Protein ◽  
Breast Cancer Patients ◽  
Protein Kinase R ◽  
Protein Clearance ◽  
Dependent Protein

Abstract The role of RNA-dependent protein kinase R (PKR) and its association with misfolded protein expression in cancer cells are unclear. Herein we report that PKR regulates misfolded protein clearance by preventing it release through exosomes and promoting lysosomal degradation of misfolded prion proteins in cancer cells. We demonstrated that PKR contributes to the lysosome function and regulates misfolded prion protein clearance. We hypothesized that PKR-associated lysosome function is critical for cancer but not normal cell survival, representing an effective approach for highly targeted cancer therapy. In screening a compound library, we identified two PKR-associated compounds 1 and 2 (Pac 1 and 2) did not affect normal cells but selectively induced cell death in cancer cells depending on their PKR expression status. Pac 1 significantly inhibited the growth of human lung and breast xenograft tumors in mice with no toxicity. Pac 1 binds to PI4K2A and disrupts the PKR/PI4K2A-associated lysosome complex, contributing to destabilization of cancer cell lysosomes and triggering cell death. We observed that PKR and PI4K2A play significant prognostic roles in breast cancer patients. These results demonstrate that targeting of a PI4K2A/PKR lysosome complex may be an effective approach for cancer therapy.

scholarly journals The MUDENG Augmentation: A Genesis in Anti-Cancer Therapy?

2020 ◽  
Vol 21 (15) ◽  
pp. 5583
Author(s):  
Manikandan Muthu ◽  
Sechul Chun ◽  
Judy Gopal ◽  
Gyun-Seok Park ◽  
Arti Nile ◽  
...  
Keyword(s):  
Cancer Research ◽  
Cell Death ◽  
Cancer Therapy ◽  
Cancer Cells ◽  
Tumor Necrosis ◽  
Cancer Therapeutics ◽  
Future Perspective ◽  
Normal Cells ◽  
Anti Cancer ◽  
Necrosis Factor

Despite multitudes of reports on cancer remedies available, we are far from being able to declare that we have arrived at that defining anti-cancer therapy. In recent decades, researchers have been looking into the possibility of enhancing cell death-related signaling pathways in cancer cells using pro-apoptotic proteins. Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and Mu-2/AP1M2 domain containing, death-inducing (MUDENG, MuD) have been established for their ability to bring about cell death specifically in cancer cells. Targeted cell death is a very attractive term when it comes to cancer, since most therapies also affect normal cells. In this direction TRAIL has made noteworthy progress. This review briefly sums up what has been done using TRAIL in cancer therapeutics. The importance of MuD and what has been achieved thus far through MuD and the need to widen and concentrate on applicational aspects of MuD has been highlighted. This has been suggested as the future perspective of MuD towards prospective progress in cancer research.

The role of programmed cell death ligand-1/ programmed cell death-1 (PD-L1/PD-1) in HPV-induced cervical cancer and potential for their use in blockade therapy

2020 ◽  
Vol 27 ◽  
Author(s):  
Lifang Zhang ◽  
Yu Zhao ◽  
Quanmei Tu ◽  
Xiangyang Xue ◽  
Xueqiong Zhu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Immune Escape ◽  
Hypoxia Inducible Factor ◽  
Hpv Infection ◽  
Advanced Cervical Cancer ◽  
Cervical Carcinogenesis ◽  
Programmed Cell Death 1

Background: Cervical cancer induced by infection with human papillomavirus (HPV) remains a leading cause of mortality for women worldwide although preventive vaccines and early diagnosis have reduced morbidity and mortality. Advanced cervical cancer can only be treated with either chemotherapy or radiotherapy but outcomes are poor. The median survival for advanced cervical cancer patients is only 16.8 months. Methods: We undertook a structural search of peer-reviewed published studies based on 1). Characteristics of programmed cell death ligand-1/programmed cell death-1(PD-L1/PD-1) expression in cervical cancer and upstream regulatory signals of PD-L1/PD-1 expression, 2). The role of the PD-L1/PD-1 axis in cervical carcinogenesis induced by HPV infection and 3). Whether the PD-L1/PD-1 axis has emerged as a potential target for cervical cancer therapies. Results: One hundred and twenty-six published papers were included in the review, demonstrating that expression of PD-L1/PD-1 is associated with HPV-caused cancer, especially with HPV 16 and 18 which account for approximately 70% of cervical cancer cases. HPV E5/E6/E7 oncogenes activate multiple signaling pathways including PI3K/AKT, MAPK, hypoxia-inducible factor 1α, STAT3/NF-kB and MicroRNAs, which regulate PD-L1/PD-1 axis to promote HPV-induced cervical carcinogenesis. The PD-L1/PD-1 axis plays a crucial role in immune escape of cervical cancer through inhibition of host immune response. creating an "immune-privileged" site for initial viral infection and subsequent adaptive immune resistance, which provides a rationale for therapeutic blockade of this axis in HPV-positive cancers. Currently, Phase I/II clinical trials evaluating the effects of PD-L1/PD-1 targeted therapies are in progress for cervical carcinoma, which provide an important opportunity for the application of anti-PD-L1/anti-PD-1 antibodies in cervical cancer treatment. Conclusion: Recent research developments have led to an entirely new class of drugs using antibodies against the PD-L1/PD-1 thus promoting the body’s immune system to fight the cancer. The expression and roles of the PD-L1/ PD-1 axis in the progression of cervical cancer provide great potential for using PD-L1/PD-1 antibodies as a targeted cancer therapy.

scholarly journals Ozone-Induced Cell Death in Tobacco Cultivar Bel W3 Plants. The Role of Programmed Cell Death in Lesion Formation

2003 ◽  
Vol 133 (3) ◽  
pp. 1122-1134 ◽  
Author(s):  
Stefania Pasqualini ◽  
Claudia Piccioni ◽  
Lara Reale ◽  
Luisa Ederli ◽  
Guido Della Torre ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Lesion Formation ◽  
Tobacco Cultivar

Relevance of mitochondrial dysfunction during Sorafenib-induced cell death in liver cancer cells. Role of oxidative and nitrogen reactive species

2021 ◽  
Vol 165 ◽  
pp. 54
Author(s):  
Patricia de la Cruz-Ojeda ◽  
M. Ángeles Rodríguez-Hernández ◽  
Elena Navarro-Villarán ◽  
Paloma Gallego ◽  
Pavla Staňková ◽  
...  
Keyword(s):  
Cell Death ◽  
Liver Cancer ◽  
Mitochondrial Dysfunction ◽  
Cancer Cells ◽  
Reactive Species ◽  
Liver Cancer Cells ◽  
Nitrogen Reactive Species
Sign in / Sign up

Export Citation Format

Share Document