Ming C Liau* and Linda Liau Baker*
CDA Therapeutics, USA
*Corresponding author: Ming C Liau, CDA Therapeutics, USA
Submission: February 04, 2021;Published: March 15, 2021
ISSN: 2637-7802 Volume 6 Issue 3
Wound healing and the evolution of cancer are closely related to involve PSCs as the critical elements. Wound healing is a process to involve the breakdown of membrane bound phospholipid to release arachidonic acid (AA) for the synthesis of prostaglandins (PGs), which are differentiation inducers (DIs) critical for the perfect healing of wound [1-3]. Wound happening to a healthy person does not pose a threat of cancer development, because healthy person has an intact chemo-surveillance capability to ensure the perfect wound healing, and to deny unnecessary buildup of PSCs to evolve into cancer stems cells (CSCs), and then to progress to much faster growing cancer. PSCs and CSCs are very much alike on cell features and biological missions. Their methylation enzymes (MEs) are abnormal due to association with telomerase [4-6]. They are protected by ATP binding cassette drug pumps to resist toxic chemicals [7-9]. Their biological missions are to meet the needs of the organ including the repair of the damages. Thus, they are very responsive to differentiation inducing factors. It is very likely that CSCs are originated from PSCs, which requires only a single hit to silence TET-1 enzyme, a process well within the reach of PSCs equipped with very active abnormal MEs. TET-1 enzyme is frequently found silenced in cancer cells [10-12]. Thus, PSCs are still able to carry out differentiation programs, relying on TET-1 enzyme to accomplish DNA hypomethylation, whereas the differentiation of CSCs and their progenies is completely blocked. The breakdown of membrane bound phospholipid is a necessary evil to facilitate membrane hyperpermeability for the release of DIs and DHIs from inside of PSCs, which function as a brake to prevent the proliferation of PSCs, to allow the buildup of PSCs to heal the wound. PGs produced in response to wound are very effective DIs to promote TD of PSCs for the completion of wound healing [2,3]. Obviously, destabilization of abnormal MEs is a critical process for wound healing, which comes naturally. Natural metabolites involved in wound healing are very valuable for the eradication of PSCs and CSCs essential to the success of wound healing and cancer therapy [13,14]. TD induced by DIs alone is often incomplete due to damages caused by DIs to interrupt differentiation process [2,3]. In the presence of differentiation helper inducers (DHIs), which are inhibitors of the ternary MEs, damages caused by DIs alone can be avoid reach a perfect completion of TD. Healthy people maintain a steady level of DIs and DHIs as chemo-surveillance agents to prevent the proliferation of cells with abnormal MEs . With enough DIs and DHIs and newly synthesized PGs, perfection of wound healing can always be anticipated to take place to healthy people. But if wound happens to a person whose chemo-surveillance capability has been compromised due to immunological disorders or long-term exposure to toxic chemicals or carcinogens, then wound may not be healed properly. Immunological disorders or long-term exposure to toxic chemicals trigger immunological responses in addition to the biological responses above mentioned to result in cachexia symptom. A manifestation of cachexia symptom is the excessive excretion of low molecular weight metabolites resulting in the collapse of chemo-surveillance. Without the participation of chemo-surveillance, wound may not be healed properly. The proliferation of PSCs keeps on beyond what is needed for healing the wound, and to evolve into CSCs and then to cancer. This is exactly the process that leads to myelodysplastic syndrome (MDS) and acute myeloid leukemia.
Cancer arises because of wound not healing properly due to the
collapse of chemo-surveillance. Supplements of chemicals to perfect
wound healing are naturally the most appropriate strategy to put
cancer away. AA and PGs are the metabolites most critical for wound
healing. These metabolites are DIs to target on abnormal MEs. AA,
pregnenolone and phenylacetylglutamine are the three metabolites
most critical for chemo-surveillance. AA is a DI and pregnenolone
is a DHI to target on abnormal MEs, and phenylacetylglutamine is
an anti-cachexia chemical. These are metabolites come naturally to
deal with wound healing and to prevent cancer evolution. Abnormal
MEs stand out as the most critical issue of wound and cancer.
Wound healing comes naturally. The medications used in the wound
healing are primarily antibiotics to prevent infection. We rely on the
nature to heal the wound. We should also rely on the nature to take
care of cancer. Indeed, cancer therapies achieved by destabilization
of abnormal MEs through DIs and DHIs are in general excellent
[16,17]. All-trans retinoic acid, a DI, is the standard of care for acute
promyelocytic leukemia. Imatinib mesylate, a DHI, is the standard of
care for chronic myeloid leukemia and gist. Phenylbutyrate, another
DHI of our discovery, is very effective on untreatable malignant
brain tumors, and CDA-2, a perfect cancer drug with DIs, DHIs,
and anti-cachexia chemicals is the best drug for MDS [18,19]. The
therapeutic endpoint of destabilization of abnormal MEs is TD of
cancer cells to turn cancer cells to become non-replicating cells and
functional cells. The tumor mass may persist. We may have to come
up a different endpoint for the evaluation of therapeutic efficacy of
therapy based on destabilization of abnormal methylation enzymes.
Disappearance of circulation cancer cells, or more specifically CSCs,
is definitely a more appropriate endpoint for the assessment of
the therapeutic efficacy of destabilization of abnormal MEs. Such
endpoint is the same endpoint for the assessment of therapeutic
efficacy of hematological cancers.
The use of cytotoxic drugs and radiation for the therapy of cancer is inappropriate, which creates more wound to aggravate the already bad situation of cancer arising from wound not healing properly. Their inability to put out CSCs and the contribution to destroy chemo-surveillance lay the ground for inevitable recurrence and fatality. That is why cancer mortalities remain at old time high worldwide despite the input of all resources in the past to combat cancer. Cell differentiation agent (CDA) formulations can remedy the insufficiencies of destruction strategies. Afterall, destruction strategies have the merit as most effective to kill cancer cells and to eliminate tumor mass. The combination therapy utilizing destruction approach to eliminate most sensitive cancer cells and the CDA formulations to target on CSCs and to restore chemosurveillance may be the winning combination to put cancer away and to win the war on cancer.
Cancer is caused by multiple factors. Factors such as membrane hyperpermeability, cachexia, chemo-surveillance, blockade of differentiation, activation of oncogenes, and inactivation of suppressor genes are all contribute significantly to the evolution of cancer. A perfect solution for cancer must be the one that can resolve all issues involved in the evolution of cancer. CDA formulations are the perfect drugs for cancer prevention and therapy . The active components of CDA formulations are DIs and DHIs to target on abnormal MEs, which are the creator’s favored prescriptions for wound healing and chemo-surveillance against cancer. By pushing replicating PSCs and cancer cells out of cell cycle to undergo TD, CDA formulations can also put to rest the issues of oncogenes and suppressor genes. Afterall, oncogenes and suppressor genes are cell cycle regulatory genes, they have important roles to play when cells are in cell cycle replicating. But they have no roles to play if cells are no longer replicating. Induction of differentiation is an easy solution to otherwise very difficult problem of gene abnormalities. CDA formulations are perfect to prevent recurrence attributable to CSCs and to restore chemo-surveillance capability, the most feared adverse effects of destruction therapy.
© 2021 Ming C Liau. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and build upon your work non-commercially.