Journal of Lung Cancer Epidemiology

Journal of Lung Cancer Epidemiology

Journal of Lung Cancer Epidemiology

Current Issue Volume No: 1 Issue No: 1

Review Article Open Access Available online freely Peer Reviewed Citation Provisional

Challenger Treatment of Various Cancers with T Cells Engineering

Alireza Heidari 1 2 3 4,   Elena Locci 1 2 3,   Silvia Raymond 1 2 3,   Ricardo Gobato 5  

1Faculty of Chemistry, California South University, 14731 Comet St. Irvine, CA 92604, USA.

2BioSpectroscopy Core Research Laboratory, California South University, 14731 Comet St. Irvine, CA 92604, USA.

3Cancer Research Institute (CRI), California South University, 14731 Comet St. Irvine, CA 92604, USA.

4American International Standards Institute, Irvine, CA 3800, USA.

5Green Land Landscaping and Gardening, Seedling Growth Laboratory, 86130-000, Parana, Brazil

Abstract

Through T-cell engineering, researchers at the California South University (CSU) Cancer Research Institute (CRI) have shown that tumor growth can be stopped in a variety of cancers and prevented from spreading to other tissues. Findings from this study are the result of decades of research by Professor Ph.D. A. Heidari and our team of CSU, who discovered a protein called AH that can inhibit the growth and spread of cancer cells in several different ways. They become in the tissues of the body. The T cells were armed with MDA-7/AH to target cancer more widely. The engineering of T cells to produce MDA-7/AH causes cancer cells to be destroyed regardless of the expression of the target molecules. The tumor site is often very hostile to immune cells. It was found in the research that MDA-7/AH can help T cells proliferate and increase the number of cancer cells. The T cells were armed with MDA-7/ AH to target cancer more widely. The engineering of T cells to produce MDA-7/AH causes cancer cells to be destroyed regardless of the expression of the target molecules. The tumor site is often very hostile to immune cells. We discovered that MDA-7/AH can help T cells proliferate and increase the number of cancer cells.

Author Contributions
Received 22 Nov 2021; Accepted 05 Apr 2022; Published 13 Apr 2023;

Academic Editor: Ian James Martins, Edith Cowan University

Checked for plagiarism: Yes

Review by: Single-blind

Copyright © 2023 Alireza Heidari, et al.

License
Creative Commons License     This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Competing interests

The authors have declared that no competing interests exist.

Citation:

Alireza Heidari, Elena Locci, Silvia Raymond, Ricardo Gobato (2023) Challenger Treatment of Various Cancers with T Cells Engineering. Journal of Lung Cancer Epidemiology - 1(1):43-75.

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Introduction

At the subcellular level, MDA-7/AH binds to cell surface receptors and instructs them to make and release more copies of the MDA-7/AH protein. If the cell is normal, the protein is easily secreted and does not cause harm, but if the cell is cancerous, MDA-7/AH causes damage and eventual cell death not only in the primary tumor but also in the surrounding metastases; This is the cause of death in 90% of patients. As a result of this process, the immune system produces memory T cells that can be destroyed if the tumor returns to normal. Tumor levels of AH also prevent the formation of blood vessels, tumors that are very hungry and need nutrients to continue growing uncontrollably. In mice with prostate cancer, melanoma, or other cancer metastases, MDA-7 / AH-expressing T cells slowed or stopped cancer progression better than unmodified T cells. The researchers also found that arming T cells with MDA-7/AH allowed them to survive better and proliferate in the microenvironment of the tumor (the space around the cancerous mass). 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100.

Results and Discussion

The site of the tumor is often very hostile to immune cells. We discovered that MDA-7/AH can help T cells proliferate and increase the number of cancer cells. In the clinic, the procedure involves extracting the patient's own T cells from tumor samples, genetically engineering them to express MDA-7/AH, growing millions of copies of the cells in the laboratory, and finally transplanting them back into the patient. Using federal production standards, this method is generally safer and less invasive. CAR-T cells can also be engineered to express MDA-7/AH. For greater effectiveness, MDA-7/AH cells may be used in conjunction with other therapies. Clinical trials using various AH transmission methods are currently underway for several cancers. A phase 1 trial using adeno (cold-like virus) to deliver MDA-7/IL24 to a tumor has shown about 44% efficacy against various forms of cancer.

According to Liu Z. et al. (2021) taken together, arming T cells with tumoricidal and immune-potentiating MDA-7/IL24 confers new capabilities of eradicating antigen-negative cancer cell clones and improving T-cell expansion within tumors. This promising approach may be used to optimize cellular immunotherapy for treating heterogeneous solid cancers and provide a mechanism for inhibiting tumor escape.

The results of Liu Z. et al. (2021) appear to be promising, as well as the techniques employed by the research team led by Professor Ph.D. A. Heidari and our team of CSU, discovered two new ways to induce tumor cell death, activating ferroptosis, where: first, iron-dependent cell death due to oxidative stress, and second, oxidative stress. Therefore, cell death can also be induced in a different way. Both types of cell death must be caused by drugs at the same time to eliminate the majority of the tumor mass.

Conclusions

The T cells were armed with MDA-7/AH to target cancer more widely. The engineering of T cells to produce MDA-7/AH causes cancer cells to be destroyed regardless of the expression of the target molecules. The tumor site is often very hostile to immune cells. We discovered that MDA-7/AH can help T cells proliferate and increase the number of cancer cells.

A techniques employed by the research team led by biologist Dr. Raymond discovered two new ways to induce tumor cell death, activating ferroptosis, where: first, iron-dependent cell death due to oxidative stress, and second, oxidative stress. Therefore, cell death can also be induced in a different way. Both types of cell death must be caused by drugs at the same time to eliminate the majority of the tumor mass.

Acknowledgment

This study was supported by the Cancer Research Institute (CRI) Project of Scientific Instrument and Equipment Development, the National Natural Science Foundation of the United Sates, the International Joint Bio Spectroscopy Core Research Laboratory Program supported by the California South University (CSU), and the Key project supported by the American International Standards Institute (AISI), Irvine, California, USA.

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  1. 87.Gobato R, Heidari A. (2017) Calculations Using Quantum Chemistry for Inorganic Molecule Simulation BeLi2SeSi”. , Science Journal of Analytical Chemistry 5, 76-85.
  1. 88.Heidari A. (2017) Different High–Resolution Simulations of Medical, Medicinal, Clinical, Pharmaceutical and Therapeutics Oncology of Human Lung Cancer Translational Anti–Cancer Nano Drugs Delivery Treatment Process under Synchrotron and X–Ray Radiations”. , J Med Oncol 1.
  1. 89.Heidari A. (2017) A Modern Ethnomedicinal Technique for Transformation, Prevention and Treatment of Human Malignant Gliomas Tumors into Human Benign Gliomas Tumors under Synchrotron Radiation”. , Am J Ethnomed 4.
  1. 90.Heidari A. (2017) Active Targeted Nanoparticles for Anti–Cancer Nano Drugs Delivery across the Blood–Brain Barrier for Human Brain Cancer Treatment, Multiple Sclerosis (MS) and Alzheimer's Diseases Using Chemical Modifications of Anti–Cancer Nano Drugs or Drug–Nanoparticles through Zika Virus (ZIKV) Nanocarriers under Synchrotron Radiation”. , J Med Chem Toxicol 2(3).
  1. 91.Heidari A. (2017) Investigation of Medical, Medicinal, Clinical and Pharmaceutical Applications of Estradiol, Mestranol (Norlutin), Norethindrone (NET). Norethisterone Acetate (NETA), Norethisterone Enanthate (NETE) and Testosterone Nanoparticles as Biological Imaging, Cell Labeling, Anti–Microbial Agents and Anti–Cancer Nano Drugs in Nanomedicines Based Drug Delivery Systems for Anti–Cancer Targeting and Treatment”, Parana Journal of Science and Education (PJSE)–v.3, n.4 .
  1. 92.Heidari A. (2017) A Comparative Computational and Experimental Study on Different Vibrational Biospectroscopy Methods, Techniques and Applications for Human Cancer Cells in Tumor Tissues Simulation, Modeling, Research, Diagnosis and Treatment”. , Open J Anal Bioanal Chem 1(1), 014-020.
  1. 93.Heidari A. (2017) Combination of DNA/RNA Ligands and Linear/Non–Linear Visible–Synchrotron Radiation–Driven N–Doped Ordered Mesoporous Cadmium Oxide (CdO) Nanoparticles Photocatalysts Channels Resulted in an Interesting Synergistic Effect Enhancing Catalytic Anti–Cancer Activity”. , Enz Eng 6.
  1. 94.Heidari A. (2017) Modern Approaches in Designing Ferritin, Ferritin Light Chain, Transferrin, Beta–2 Transferrin and Bacterioferritin–Based Anti–Cancer Nano Drugs Encapsulating Nanosphere as DNA–Binding Proteins from Starved Cells (DPS)”, Mod Appro Drug Des. 1(1), 000504.
  1. 95.Heidari A. (2017) Potency of Human Interferon β–1a and Human Interferon β–1b in Enzymotherapy, Immunotherapy, Chemotherapy, Radiotherapy, Hormone Therapy and Targeted Therapy of Encephalomyelitis Disseminate/Multiple Sclerosis (MS). , and Hepatitis A, B, C, D, E, F and G Virus Enter and Targets Liver Cells”, J Proteomics Enzymol 6.
  1. 96.Heidari A. (2017) Transport Therapeutic Active Targeting of Human Brain Tumors Enable Anti–Cancer Nanodrugs Delivery across the Blood–Brain Barrier (BBB) to Treat Brain Diseases Using Nanoparticles and Nanocarriers under Synchrotron Radiation”. , J Pharm Pharmaceutics 4(2).
  1. 97.Heidari A, Brown C. (2017) Combinatorial Therapeutic Approaches to DNA/RNA and Benzylpenicillin (Penicillin G), Fluoxetine Hydrochloride (Prozac and Sarafem), Propofol (Diprivan), Acetylsalicylic Acid (ASA) (Aspirin), Naproxen Sodium (Aleve and Naprosyn) and Dextromethamphetamine Nanocapsules with Surface Conjugated DNA/RNA to Targeted Nano Drugs for Enhanced Anti–Cancer Efficacy and Targeted Cancer Therapy Using Nano Drugs Delivery Systems”. , Ann Adv Chem 1(2), 061-069.
  1. 98.Heidari A. (2017) High–Resolution Simulations of Human Brain Cancer Translational Nano Drugs Delivery Treatment Process under Synchrotron Radiation”. , J Transl Res 1(1).
  1. 99.Heidari A. (2017) Investigation of Anti–Cancer Nano Drugs’ Effects’ Trend on Human Pancreas Cancer Cells and Tissues Prevention. Diagnosis and Treatment Process under Synchrotron and X–Ray Radiations with the Passage of Time Using Mathematica”, Current Trends Anal Bioanal Chem 1(1), 36-41.
  1. 100.Heidari A. (2017) Pros and Cons Controversy on Molecular Imaging and Dynamics of Double–Standard DNA/RNA of Human Preserving Stem Cells–Binding Nano Molecules with Androgens/Anabolic Steroids (AAS) or Testosterone Derivatives through Tracking of Helium–4 Nucleus (Alpha Particle) Using Synchrotron Radiation”. , Arch Biotechnol Biomed 1(1), 067-0100.