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Research Article
James Randall Kennedy
Manatee Memorial Hospital and Health System: Manatee Memorial Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0003-3310-014X
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This work is licensed under a CC BY 4.0 License. Read Full License
One constant in all malignant somatic tumors is their continuous growth and it is hypothesized that there are only two types of cell mutations that can cause this and that their microenvironments are determined by how those mutated cells eventually die and by how phosphatidylserine (PS) is exposed on their surface. When a mutation in a cell causes its rate of mitotic cell division to continuously exceed the rate necessary for its replacement after its programed cell death (PCD) a continuously growing tumor will form and all of the tumor cells will expose PS by the Xkr8 transmembrane scramblase molecule when they die causing an inflammatory and immune suppressive microenvironment. When a mutation in a cell eliminates PCD a continuous tumor growth begins because all those cells will continue dividing until they die a senescent death where PS is exposed by the TMEM16F scramblase molecule and causes an inflammatory microenvironment. Inflammation stresses somatic cells to expose checkpoint molecules (CPMs) on them and on immune cells that could potentially eliminate them. Only in tumors where PCD has been eliminated will CPM be exposed and only in them will immune checkpoint inhibitors (ICIs) be effective.
Keywords
cancer, checkpoint, Kxr8, mutation, phosphatidylserine, TMEM16F
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research Article
James Randall Kennedy
Manatee Memorial Hospital and Health System: Manatee Memorial Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0003-3310-014X
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 08 Jun, 2021
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cell Communication and Signaling
License:
This work is licensed under a CC BY 4.0 License. Read Full License
One constant in all malignant somatic tumors is their continuous growth and it is hypothesized that there are only two types of cell mutations that can cause this and that their microenvironments are determined by how those mutated cells eventually die and by how phosphatidylserine (PS) is exposed on their surface. When a mutation in a cell causes its rate of mitotic cell division to continuously exceed the rate necessary for its replacement after its programed cell death (PCD) a continuously growing tumor will form and all of the tumor cells will expose PS by the Xkr8 transmembrane scramblase molecule when they die causing an inflammatory and immune suppressive microenvironment. When a mutation in a cell eliminates PCD a continuous tumor growth begins because all those cells will continue dividing until they die a senescent death where PS is exposed by the TMEM16F scramblase molecule and causes an inflammatory microenvironment. Inflammation stresses somatic cells to expose checkpoint molecules (CPMs) on them and on immune cells that could potentially eliminate them. Only in tumors where PCD has been eliminated will CPM be exposed and only in them will immune checkpoint inhibitors (ICIs) be effective.
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