The objective of this study is to develop good cancer drugs to save cancer patients. Good cancer drugs are the drugs capable of inactivating abnormal methylation enzymes (MEs) to take out both cancer stem cells (CSCs) and cancer cells (CCs) by inducing these cells to undergo terminal differentiation, and to restore chemo-surveillance to save cancer patients. Bad cancer drugs are cytotoxic agents that can kill CCs but cannot affect CSCs, which can also destroy chemo-surveillance to contribute to the fatality of advanced cancer patients. Cell differentiation agent-2 (CDA-2) is a persuasive good cancer drug approved by the Chinese FDA. CDA-2 is a preparation of wound healing metabolites purified from urine, which can serve as a model for the development of CDA formulations as good cancer drugs. Wound healing metabolites active as differentiation inducers (DIs) and differentiation helper inducers (DHIs) are the active players of chemo-surveillance created by the nature as allosteric regulators of abnormal methylation enzymes (MEs). The elimination of abnormal MEs is very critical to the success of cancer therapy. Wound healing is a simple matter that comes naturally, because the nature creates chemo-surveillance to ensure perfection of wound healing. Cancer is the consequence of wound unhealing due to the collapse of chemo-surveillance. Cancer therapy can also be a simple matter, if the therapy follows wound healing process. PSCs and CSCs are cells with abnormal MEs, which are protected by drug resistance and anti-apoptosis mechanisms. PSCs are the cells involved in wound healing. Efficient induction of terminal differentiation of PSCs is very critical to the success of wound healing. Natural DIs and DHIs are the partners of PSCs and CSCs in wound healing, which can easily access to PSCs and CSCs. If wound is not healed, PSCs are forced to evolve into CSCs and then to progress to faster growing CCs. CCs display a high level of degradative enzymes to generate substrates for the syntheses of macro-molecules to support their faster growth. Natural DIs and DHIs may be rapidly degraded in CCs. A different set of unnatural DIs and DHIs may be necessary to achieve the induction of terminal differentiation of CCs. Thus, two sets of CDA formulations, one CDA-CSC with natural DIs and DHIs, and another CDA-CC with non-natural DIs and DHIs to accomplish induction of terminal differentiation of both CSCs and CCs to achieve effective therapy of cancer.
| Published in | International Journal of Clinical Oncology and Cancer Research (Volume 9, Issue 1) |
| DOI | 10.11648/ijcocr.20240901.13 |
| Page(s) | 15-24 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2024. Published by Science Publishing Group |
Cancer Drugs, CDA, CSCs, DIs, DHIs, Differentiation Therapy
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APA Style
Liau, M. C., Craig, C. L., Baker, L. L. (2024). CDA Formulations as Persuasive Good Cancer Drugs to Save Cancer Patients. International Journal of Clinical Oncology and Cancer Research, 9(1), 15-24. https://doi.org/10.11648/ijcocr.20240901.13
ACS Style
Liau, M. C.; Craig, C. L.; Baker, L. L. CDA Formulations as Persuasive Good Cancer Drugs to Save Cancer Patients. Int. J. Clin. Oncol. Cancer Res. 2024, 9(1), 15-24. doi: 10.11648/ijcocr.20240901.13
AMA Style
Liau MC, Craig CL, Baker LL. CDA Formulations as Persuasive Good Cancer Drugs to Save Cancer Patients. Int J Clin Oncol Cancer Res. 2024;9(1):15-24. doi: 10.11648/ijcocr.20240901.13
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Download@article{10.11648/ijcocr.20240901.13,
author = {Ming Cheng Liau and Christine Liau Craig and Linda Liau Baker},
title = {CDA Formulations as Persuasive Good Cancer Drugs to Save Cancer Patients},
journal = {International Journal of Clinical Oncology and Cancer Research},
volume = {9},
number = {1},
pages = {15-24},
doi = {10.11648/ijcocr.20240901.13},
url = {https://doi.org/10.11648/ijcocr.20240901.13},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.ijcocr.20240901.13},
abstract = {The objective of this study is to develop good cancer drugs to save cancer patients. Good cancer drugs are the drugs capable of inactivating abnormal methylation enzymes (MEs) to take out both cancer stem cells (CSCs) and cancer cells (CCs) by inducing these cells to undergo terminal differentiation, and to restore chemo-surveillance to save cancer patients. Bad cancer drugs are cytotoxic agents that can kill CCs but cannot affect CSCs, which can also destroy chemo-surveillance to contribute to the fatality of advanced cancer patients. Cell differentiation agent-2 (CDA-2) is a persuasive good cancer drug approved by the Chinese FDA. CDA-2 is a preparation of wound healing metabolites purified from urine, which can serve as a model for the development of CDA formulations as good cancer drugs. Wound healing metabolites active as differentiation inducers (DIs) and differentiation helper inducers (DHIs) are the active players of chemo-surveillance created by the nature as allosteric regulators of abnormal methylation enzymes (MEs). The elimination of abnormal MEs is very critical to the success of cancer therapy. Wound healing is a simple matter that comes naturally, because the nature creates chemo-surveillance to ensure perfection of wound healing. Cancer is the consequence of wound unhealing due to the collapse of chemo-surveillance. Cancer therapy can also be a simple matter, if the therapy follows wound healing process. PSCs and CSCs are cells with abnormal MEs, which are protected by drug resistance and anti-apoptosis mechanisms. PSCs are the cells involved in wound healing. Efficient induction of terminal differentiation of PSCs is very critical to the success of wound healing. Natural DIs and DHIs are the partners of PSCs and CSCs in wound healing, which can easily access to PSCs and CSCs. If wound is not healed, PSCs are forced to evolve into CSCs and then to progress to faster growing CCs. CCs display a high level of degradative enzymes to generate substrates for the syntheses of macro-molecules to support their faster growth. Natural DIs and DHIs may be rapidly degraded in CCs. A different set of unnatural DIs and DHIs may be necessary to achieve the induction of terminal differentiation of CCs. Thus, two sets of CDA formulations, one CDA-CSC with natural DIs and DHIs, and another CDA-CC with non-natural DIs and DHIs to accomplish induction of terminal differentiation of both CSCs and CCs to achieve effective therapy of cancer.
},
year = {2024}
}
TY - JOUR T1 - CDA Formulations as Persuasive Good Cancer Drugs to Save Cancer Patients AU - Ming Cheng Liau AU - Christine Liau Craig AU - Linda Liau Baker Y1 - 2024/02/05 PY - 2024 N1 - https://doi.org/10.11648/ijcocr.20240901.13 DO - 10.11648/ijcocr.20240901.13 T2 - International Journal of Clinical Oncology and Cancer Research JF - International Journal of Clinical Oncology and Cancer Research JO - International Journal of Clinical Oncology and Cancer Research SP - 15 EP - 24 PB - Science Publishing Group SN - 2578-9511 UR - https://doi.org/10.11648/ijcocr.20240901.13 AB - The objective of this study is to develop good cancer drugs to save cancer patients. Good cancer drugs are the drugs capable of inactivating abnormal methylation enzymes (MEs) to take out both cancer stem cells (CSCs) and cancer cells (CCs) by inducing these cells to undergo terminal differentiation, and to restore chemo-surveillance to save cancer patients. Bad cancer drugs are cytotoxic agents that can kill CCs but cannot affect CSCs, which can also destroy chemo-surveillance to contribute to the fatality of advanced cancer patients. Cell differentiation agent-2 (CDA-2) is a persuasive good cancer drug approved by the Chinese FDA. CDA-2 is a preparation of wound healing metabolites purified from urine, which can serve as a model for the development of CDA formulations as good cancer drugs. Wound healing metabolites active as differentiation inducers (DIs) and differentiation helper inducers (DHIs) are the active players of chemo-surveillance created by the nature as allosteric regulators of abnormal methylation enzymes (MEs). The elimination of abnormal MEs is very critical to the success of cancer therapy. Wound healing is a simple matter that comes naturally, because the nature creates chemo-surveillance to ensure perfection of wound healing. Cancer is the consequence of wound unhealing due to the collapse of chemo-surveillance. Cancer therapy can also be a simple matter, if the therapy follows wound healing process. PSCs and CSCs are cells with abnormal MEs, which are protected by drug resistance and anti-apoptosis mechanisms. PSCs are the cells involved in wound healing. Efficient induction of terminal differentiation of PSCs is very critical to the success of wound healing. Natural DIs and DHIs are the partners of PSCs and CSCs in wound healing, which can easily access to PSCs and CSCs. If wound is not healed, PSCs are forced to evolve into CSCs and then to progress to faster growing CCs. CCs display a high level of degradative enzymes to generate substrates for the syntheses of macro-molecules to support their faster growth. Natural DIs and DHIs may be rapidly degraded in CCs. A different set of unnatural DIs and DHIs may be necessary to achieve the induction of terminal differentiation of CCs. Thus, two sets of CDA formulations, one CDA-CSC with natural DIs and DHIs, and another CDA-CC with non-natural DIs and DHIs to accomplish induction of terminal differentiation of both CSCs and CCs to achieve effective therapy of cancer. VL - 9 IS - 1 ER -
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