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Understanding the unimodal distributions of cancer occurrence rates: it takes two factors for a cancer to occur.

ABSTRACT: Data from the SEER reports reveal that the occurrence rate of a cancer type generally follows a unimodal distribution over age, peaking at an age that is cancer-type specific and ranges from 30+ through 70+. Previous studies attribute such bell-shaped distributions to the reduced proliferative potential in senior years but fail to explain why some cancers have their occurrence peak at 30+ or 40+. We present a computational model to offer a new explanation to such distributions. The model uses two factors to explain the observed age-dependent cancer occurrence rates: cancer risk of an organ and the availability level of the growth signals in circulation needed by a cancer type, with the former increasing and the latter decreasing with age. Regression analyses were conducted of known occurrence rates against such factors for triple negative breast cancer, testicular cancer and cervical cancer; and all achieved highly tight fitting results, which were also consistent with clinical, gene-expression and cancer-drug data. These reveal a fundamentally important relationship: while cancer is driven by endogenous stressors, it requires sufficient levels of exogenous growth signals to happen, hence suggesting the realistic possibility for treating cancer via cleaning out the growth signals in circulation needed by a cancer.

SUBMITTER: Qiu S

PROVIDER: S-EPMC8294564 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Schizophrenia is a chronic debilitating mental disorder characterized by perturbations in thinking, perception, and behavior, along with brain connectivity deficiencies, neurotransmitter dysfunctions, and loss of gray brain matter. To date, schizophrenia has no cure and pharmacological treatments are only partially efficacious, with about 30% of patients describing little to no improvement after treatment. As in most neurological disorders, the main descriptions of schizophrenia physiopathology have been focused on neural network deficiencies. However, to sustain proper neural activity in the brain, another, no less important network is operating: the vast, complex and fascinating vascular network. Increasing research has characterized schizophrenia as a systemic disease where vascular involvement is important. Several neuro-angiogenic pathway disturbances have been related to schizophrenia. Alterations, ranging from genetic polymorphisms, mRNA, and protein alterations to microRNA and abnormal metabolite processing, have been evaluated in plasma, post-mortem brain, animal models, and patient-derived induced pluripotent stem cell (hiPSC) models. During embryonic brain development, the coordinated formation of blood vessels parallels neuro/gliogenesis and results in the structuration of the neurovascular niche, which brings together physical and molecular signals from both systems conforming to the Blood-Brain barrier. In this review, we offer an upfront perspective on distinctive angiogenic and neurogenic signaling pathways that might be involved in the biological causality of schizophrenia. We analyze the role of pivotal angiogenic-related pathways such as Vascular Endothelial Growth Factor and HIF signaling related to hypoxia and oxidative stress events; classic developmental pathways such as the NOTCH pathway, metabolic pathways such as the mTOR/AKT cascade; emerging neuroinflammation, and neurodegenerative processes such as UPR, and also discuss non-canonic angiogenic/axonal guidance factor signaling. Considering that all of the mentioned above pathways converge at the Blood-Brain barrier, reported neurovascular alterations could have deleterious repercussions on overall brain functioning in schizophrenia.

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Understanding the unimodal distributions of cancer occurrence rates: it takes two factors for a cancer to occur.

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