Efruzhu cancer theory oppositions of cancer cell3
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This document presents Efruz Asiloglu's theory of cancer carcinogenesis. It suggests that cancer starts with mutations in nuclear DNA and mitochondrial DNA that suppress apoptosis and promote anti-apoptotic activity. These mutations allow cancer cells to avoid identification and removal by macrophages through aberrant signaling pathways, enabling uncontrolled growth.
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S3 efruzhu cancer theory opposi̇ti̇ons of cancer cell3
Mutations in mitochondrial DNA can lead to cancer through several mechanisms. Mutations may dominate over normal DNA and suppress apoptosis, the programmed cell death of damaged or abnormal cells. This allows mutated cells to proliferate unchecked. Additionally, mutations can cause aberrant signaling in macrophages, immune cells that typically identify and destroy mutated cells. As a result of these pathways being disrupted, mutated cells are not identified and removed by the immune system, further enabling cancer progression.
Efruzhu cancer theory opposi̇ti̇ons of cancer cell3
Mutations in mitochondrial DNA can lead to cancer through three mechanisms. Mutations are not suppressed by normal DNA and can dominate. This results in aberrant signaling pathways that promote antiapoptotic activity instead of apoptosis. Mitochondria have dual actions of both promoting and inhibiting apoptosis through mutations in their DNA. When mutations are dominant, apoptosis is unsuccessful and cancer can develop.
Single Nucleotide Polymorphism
Single nucleotide polymorphisms (SNPs) are genetic variations that occur when a single nucleotide differs between members of a species. SNPs are very common, occurring around every 300 bases, and are useful for studying genetic contributions to diseases and drug responses. Researchers can identify SNPs by comparing genome sequences from many individuals and generating SNP maps and profiles that show common genetic variations.
Topoisomerase inhibitor
1) The study identifies topoisomerase inhibitors like irinotecan and topotecan as potential therapeutics for Angelman syndrome by unsilencing the paternally inherited UBE3A allele.
2) In vitro experiments show that irinotecan and topotecan upregulate UBE3A protein levels in a time- and dose-dependent manner by inhibiting antisense transcription of the paternal allele.
3) In vivo experiments demonstrate that topotecan can unsilence UBE3A expression throughout the nervous system and restore wild-type UBE3A levels after direct brain infusion or intrathecal delivery, indicating its potential as a non-invasive
Presentation12
The document discusses cancer cell immortality and apoptosis. It states that cancer cells cannot govern themselves and have derived problems. Macrophages pour nitric oxide, cytokines, growth factors, and prostaglandins onto cancer cells via mutated receptors and aberrant signaling pathways. These signals continuously direct cancer cells to proliferate. However, normal DNA wants to undergo apoptosis due to mutations but lacks sufficient energy. Both cancer cells and normal DNA have opposing actions but share the same problem of inadequate energy. The document likens foreign and normal DNA within cancer cells to having separate identities or personalities.
Efruzhu cancer laws com. 25.1.
This document presents the "Efruzher Cancer (Carcinogenesis) Theory". It proposes that for a normal cell to become cancerous, it requires more than just mutations - it needs energy inefficiency, chronic inflammation, or suppression of normal DNA. Cancer cells take on a group identity defined by many mutations, seeking to live irregularly and being transferred from outside influences like macrophages. The malignancy level depends on energy ratios - low energy means more mutations and malignancy, while high energy means fewer mutations and potential benign conditions. Cancer cells are seen as selfish, parasitic, irregular and immortal due to their transferred mutational group identity from outside influences.
Presentation4
Mutations from outside sources express a foreign identity in cancer cells. These mutation groups want to immortalize themselves by continuously signaling to bypass normal cell death mechanisms. Cancer cells have a dual identity with the mutation identity dominant over the normal DNA sequence. The normal DNA sequence is suppressed and unable to be transcribed and expressed due to inadequate energy and changes to histone proteins. The normal DNA wants to die through apoptosis but cell death is unsuccessful as there is not enough energy for apoptosis to occur. Apoptotic and anti-apoptotic molecules have dual roles that depend on the cancer cell's dual identity.
Efruzhu cancer 4.
A group of 10-100 thousand mutations collectively form a foreign identity that is transferred by immune cells from outside the body, unlike a cell's normal DNA sequence. This mutated identity wants to immortalize itself by continuously signaling from outside through things like nitric oxide and growth factors. The cancer cell has a dual identity with the mutated identity dominant and normal DNA suppressed, resulting in varying degrees of malignancy due to inadequate energy levels that prevent normal DNA transcription and expression. The normal DNA is affected by mutations and wants to die physiologically through apoptosis, but apoptosis is unsuccessful because of insufficient energy. Apoptotic and anti-apoptotic molecules have dual roles and actions depending on the cell's binary identity.
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S3 efruzhu cancer theory opposi̇ti̇ons of cancer cell3
Mutations in mitochondrial DNA can lead to cancer through several mechanisms. Mutations may dominate over normal DNA and suppress apoptosis, the programmed cell death of damaged or abnormal cells. This allows mutated cells to proliferate unchecked. Additionally, mutations can cause aberrant signaling in macrophages, immune cells that typically identify and destroy mutated cells. As a result of these pathways being disrupted, mutated cells are not identified and removed by the immune system, further enabling cancer progression.
Efruzhu cancer theory opposi̇ti̇ons of cancer cell3
Mutations in mitochondrial DNA can lead to cancer through three mechanisms. Mutations are not suppressed by normal DNA and can dominate. This results in aberrant signaling pathways that promote antiapoptotic activity instead of apoptosis. Mitochondria have dual actions of both promoting and inhibiting apoptosis through mutations in their DNA. When mutations are dominant, apoptosis is unsuccessful and cancer can develop.
Single Nucleotide Polymorphism
Single nucleotide polymorphisms (SNPs) are genetic variations that occur when a single nucleotide differs between members of a species. SNPs are very common, occurring around every 300 bases, and are useful for studying genetic contributions to diseases and drug responses. Researchers can identify SNPs by comparing genome sequences from many individuals and generating SNP maps and profiles that show common genetic variations.
Topoisomerase inhibitor
1) The study identifies topoisomerase inhibitors like irinotecan and topotecan as potential therapeutics for Angelman syndrome by unsilencing the paternally inherited UBE3A allele.
2) In vitro experiments show that irinotecan and topotecan upregulate UBE3A protein levels in a time- and dose-dependent manner by inhibiting antisense transcription of the paternal allele.
3) In vivo experiments demonstrate that topotecan can unsilence UBE3A expression throughout the nervous system and restore wild-type UBE3A levels after direct brain infusion or intrathecal delivery, indicating its potential as a non-invasive
Presentation12
The document discusses cancer cell immortality and apoptosis. It states that cancer cells cannot govern themselves and have derived problems. Macrophages pour nitric oxide, cytokines, growth factors, and prostaglandins onto cancer cells via mutated receptors and aberrant signaling pathways. These signals continuously direct cancer cells to proliferate. However, normal DNA wants to undergo apoptosis due to mutations but lacks sufficient energy. Both cancer cells and normal DNA have opposing actions but share the same problem of inadequate energy. The document likens foreign and normal DNA within cancer cells to having separate identities or personalities.
Efruzhu cancer laws com. 25.1.
This document presents the "Efruzher Cancer (Carcinogenesis) Theory". It proposes that for a normal cell to become cancerous, it requires more than just mutations - it needs energy inefficiency, chronic inflammation, or suppression of normal DNA. Cancer cells take on a group identity defined by many mutations, seeking to live irregularly and being transferred from outside influences like macrophages. The malignancy level depends on energy ratios - low energy means more mutations and malignancy, while high energy means fewer mutations and potential benign conditions. Cancer cells are seen as selfish, parasitic, irregular and immortal due to their transferred mutational group identity from outside influences.
Presentation4
Mutations from outside sources express a foreign identity in cancer cells. These mutation groups want to immortalize themselves by continuously signaling to bypass normal cell death mechanisms. Cancer cells have a dual identity with the mutation identity dominant over the normal DNA sequence. The normal DNA sequence is suppressed and unable to be transcribed and expressed due to inadequate energy and changes to histone proteins. The normal DNA wants to die through apoptosis but cell death is unsuccessful as there is not enough energy for apoptosis to occur. Apoptotic and anti-apoptotic molecules have dual roles that depend on the cancer cell's dual identity.
Efruzhu cancer 4.
A group of 10-100 thousand mutations collectively form a foreign identity that is transferred by immune cells from outside the body, unlike a cell's normal DNA sequence. This mutated identity wants to immortalize itself by continuously signaling from outside through things like nitric oxide and growth factors. The cancer cell has a dual identity with the mutated identity dominant and normal DNA suppressed, resulting in varying degrees of malignancy due to inadequate energy levels that prevent normal DNA transcription and expression. The normal DNA is affected by mutations and wants to die physiologically through apoptosis, but apoptosis is unsuccessful because of insufficient energy. Apoptotic and anti-apoptotic molecules have dual roles and actions depending on the cell's binary identity.
S4 presentation4
Mutations from outside sources accumulate in cells over time and express a foreign identity. This group of mutations wants to immortalize the cell by continuously signaling it to bypass normal apoptosis. The mutations situate themselves into the normal DNA sequence, making the cancer cell have a dual identity with the mutation identity dominant over the normal DNA. The normal DNA is suppressed and unable to be transcribed or expressed properly due to inadequate energy. Apoptosis is unsuccessful because the cell does not have enough energy to die physiologically as the normal DNA wants to, despite being affected by the mutations.
Efruzhu cancer carcinogenesis theory quora documents
The document discusses the "Efruzhu Cancer-Carcinogenesis Theory", which proposes that cancer cells can be understood through analogies to human behaviors and identities. The theory asserts that cancer cells have a dual identity of mutations and normal DNA, and that various behaviors and conditions of cancer cells can be equated to behaviors of civilized, emigrant, or oppressed people. The document provides numerous examples of these proposed equivalencies between cancer cells and human conditions.
Socrate
The document outlines a strategy to improve translational research and clinical trials through more tailored and personalized approaches. It proposes combining basic research on topics like DNA repair mechanisms with biology-driven therapies and immunotherapies guided by a patient's specific biomarkers. The goal is to move beyond one-size-fits-all approaches to cancer treatment and instead target therapies based on a patient's individual cancer biology and vulnerabilities to achieve better outcomes.
Folding
This document discusses recent research on RNA repair technology for diseases caused by defective RNA. Scientists have designed molecules that can bind to toxic RNA sequences and inhibit their negative effects, showing promise for treating myotonic dystrophy. Molecular biology is increasingly used for clinical diagnosis and understanding genetic causes of disease at the RNA level. Further research aims to develop more targeted RNA-based treatments.
Presentación3
This document discusses the central dogma of genetics, how DNA is replicated and transcribed into RNA which is then translated into protein. It also discusses how mutations in genes can cause cancer and be inherited. Scientists found that inherited susceptibility to bowel cancer was common among patients with a family history of the disease. Retroviruses can incorporate their RNA genome into host cell DNA using reverse transcriptase. Endogenous retroviruses make up around 5% of human DNA and may play a role in brain cell development and function. Understanding genetic mutations could help develop new cancer therapies like gene editing. Retroviruses may also be used in the future for gene therapy and cancer prevention.
SCIENTISTS CREATE NOVEL RNA REPAIR TECHNOLOGY and SCIENTISTS CREATE POTENT MO...
1. Scientists have discovered a small molecule that binds to defective RNA and inhibits its toxicity, providing a potential new therapeutic approach for diseases caused by RNA abnormalities.
2. Myotonic dystrophy type 1 is an example of a disease caused by a defective RNA "triplet repeat", and scientists have designed molecules that act against the RNA defect and improved biological defects in models of the disease.
3. Molecular biology research is increasingly being used for clinical diagnosis and understanding the genetic causes of diseases, opening possibilities for prevention and future solutions.
Sunu 25.1.2
Cancer cells have a binary identity - one originating from outside immune cells like macrophages, making them non-self. Cancer cells have accumulated so many mutations that their group identity wants to live exceptionally and irregularly, transferred from outside. The main point is that cancer cells depend on inadequate energy, which increases mutations. Malignancy occurs with increasing mutations due to low energy. Benign conditions are possible with high energy and low mutations. Cancer cells are selfish, parasitic, irregular, immortal and immature due to their transferred mutated group identity from outside. Normal DNA sequences cannot be transcribed or expressed due to inadequate energy.
Sunu 25.1.2
Cancer cells have a binary identity - one originating from outside immune cells like macrophages, making them non-self. Cancer cell personalities become defined by many mutations that allow them to live exceptionally and irregularly. Malignancy occurs when energy levels are inadequate, increasing mutations, while benign conditions are possible when energy levels increase and mutations decrease. Cancer cells are selfish, parasitic, irregular, immortal, and immature due to their dependence on transferred group identities and mutations from outside influences, causing normal DNA sequences to not be transcribed or expressed due to inadequate energy levels.
07 joão lauro viana
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Mutagênicas - Experiências Internacionais e Nacional
Lecture 1. DNA Organisation 13 Aug 21.ppt
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Efruzhu cancer 24.
The document discusses the lifestyle of cancer cells, describing it as complicated and stressful. Cancer cells experience metabolic stress, have hypermethylated DNA that should not be transcribed, and have impaired energy production and biosynthesis. They also display characteristics like immortality and continuous proliferation. The document suggests that cancer cell renewal is transformed from normal to neoplastic by chronic inflammation from immune cells like macrophages, representing a stress response and cultural adaptation.
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Mutations from outside sources accumulate in cells over time and express a foreign identity. This group of mutations wants to immortalize the cell by continuously signaling it to bypass normal apoptosis. The mutations situate themselves into the normal DNA sequence, making the cancer cell have a dual identity with the mutation identity dominant over the normal DNA. The normal DNA is suppressed and unable to be transcribed or expressed properly due to inadequate energy. Apoptosis is unsuccessful because the cell does not have enough energy to die physiologically as the normal DNA wants to, despite being affected by the mutations.
Efruzhu cancer carcinogenesis theory quora documents
The document discusses the "Efruzhu Cancer-Carcinogenesis Theory", which proposes that cancer cells can be understood through analogies to human behaviors and identities. The theory asserts that cancer cells have a dual identity of mutations and normal DNA, and that various behaviors and conditions of cancer cells can be equated to behaviors of civilized, emigrant, or oppressed people. The document provides numerous examples of these proposed equivalencies between cancer cells and human conditions.
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This document discusses the central dogma of genetics, how DNA is replicated and transcribed into RNA which is then translated into protein. It also discusses how mutations in genes can cause cancer and be inherited. Scientists found that inherited susceptibility to bowel cancer was common among patients with a family history of the disease. Retroviruses can incorporate their RNA genome into host cell DNA using reverse transcriptase. Endogenous retroviruses make up around 5% of human DNA and may play a role in brain cell development and function. Understanding genetic mutations could help develop new cancer therapies like gene editing. Retroviruses may also be used in the future for gene therapy and cancer prevention.
SCIENTISTS CREATE NOVEL RNA REPAIR TECHNOLOGY and SCIENTISTS CREATE POTENT MO...
1. Scientists have discovered a small molecule that binds to defective RNA and inhibits its toxicity, providing a potential new therapeutic approach for diseases caused by RNA abnormalities.
2. Myotonic dystrophy type 1 is an example of a disease caused by a defective RNA "triplet repeat", and scientists have designed molecules that act against the RNA defect and improved biological defects in models of the disease.
3. Molecular biology research is increasingly being used for clinical diagnosis and understanding the genetic causes of diseases, opening possibilities for prevention and future solutions.
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Cancer cells have a binary identity - one originating from outside immune cells like macrophages, making them non-self. Cancer cells have accumulated so many mutations that their group identity wants to live exceptionally and irregularly, transferred from outside. The main point is that cancer cells depend on inadequate energy, which increases mutations. Malignancy occurs with increasing mutations due to low energy. Benign conditions are possible with high energy and low mutations. Cancer cells are selfish, parasitic, irregular, immortal and immature due to their transferred mutated group identity from outside. Normal DNA sequences cannot be transcribed or expressed due to inadequate energy.
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Cancer cells have a binary identity - one originating from outside immune cells like macrophages, making them non-self. Cancer cell personalities become defined by many mutations that allow them to live exceptionally and irregularly. Malignancy occurs when energy levels are inadequate, increasing mutations, while benign conditions are possible when energy levels increase and mutations decrease. Cancer cells are selfish, parasitic, irregular, immortal, and immature due to their dependence on transferred group identities and mutations from outside influences, causing normal DNA sequences to not be transcribed or expressed due to inadequate energy levels.
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This document provides an overview of DNA organization and the steps of DNA replication. It defines key terms like chromosome, chromatin, histones, and nucleosomes. It describes how DNA is packaged in the cell through winding around nucleosomes and further condensation. The document also outlines the main steps of replication in prokaryotes and eukaryotes, including initiation, elongation at the replication fork, and termination. It notes some of the key enzymes involved in replication like DNA polymerases and topoisomerases.
Efruzhu cancer 24.
The document discusses the lifestyle of cancer cells, describing it as complicated and stressful. Cancer cells experience metabolic stress, have hypermethylated DNA that should not be transcribed, and have impaired energy production and biosynthesis. They also display characteristics like immortality and continuous proliferation. The document suggests that cancer cell renewal is transformed from normal to neoplastic by chronic inflammation from immune cells like macrophages, representing a stress response and cultural adaptation.
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