Cancer immunotherapy through the prism of adaptation: Will Achilles catch the tortoise?

There is no secret that despite the rapid development of new methods of cancer therapy, we still are not able to completely destroy the tumor. Every time we attack the tumor, the tumor neutralizes our attempts. Carcinogenesis can be presented as a tree whose branches are different pro-tumor mechanisms and whose trunk is a biological phenomenon that "feeds" those branches.

Macrophages Reprogrammed In Vitro Towards the M1 Phenotype and Activated with LPS Extend Lifespan of Mice with Ehrlich Ascites Carcinoma.

BACKGROUND The majority of tumors trigger macrophage reprogramming from an anti-tumor M1 phenotype towards a pro-tumor M2 phenotype. The M2 phenotype promotes tumor growth. We hypothesized that increasing the number of M1 macrophages in a tumor would limit carcinogenesis and extend the lifespan of the tumor host.

Physiological organization of immune response based on the homeostatic mechanism of matrix reprogramming: implication in tumor and biotechnology.

It is accepted that the immune system responds to pathogens with activation of antigen-independent innate and antigen-dependent adaptive immunity. However many immune events do not fit or are even inconsistent with this notion. We developed a new homeostatic model of the immune response.

Adaptation to intermittent hypoxia restricts nitric oxide overproduction and prevents beta-amyloid toxicity in rat brain.

This study tested the hypothesis that adaptation to intermittent hypoxia (AIH) can prevent overproduction of nitric oxide (NO) in brain and neurodegeneration induced by beta-amyloid (Aβ) toxicity. Rats were injected with a Aβ protein fragment (25-35) into the nucleus basalis magnocellularis. AIH (simulated altitude of 4000 m, 14 days, 4h daily) was produced prior to the Aβ injection.

Possible use of adaptation to hypoxia in Alzheimer's disease: a hypothesis.

Disorders in memory and other cognitive functions in Alzheimer's disease (AD) may result from an exhaustion of adaptive reserves in the brain. Therefore it is a challenge to find methods to increase the adaptive reserve of the organism to combat AD. Excitotoxicity, Ca2+ homeostasis disruptions, oxidative stress, disturbed synthesis of NO, and impaired cerebral circulation are suggested as key pathogenic factors of AD.

Nitric oxide production and intensity of free radical processes in young men with high normal and hypertensive blood pressure.

Background: Young individuals with high normal blood pressure (HNBP) are at risk for hypertension. The aim of our study was to compare NO production and the intensity of free radical processes in young males with different BP levels.

Material/methods: Male subjects aged 18-45 years with normal BP, HNBP, and hypertension underwent physical and cardiological examination.