S19 presentation19
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Cancer cells behave like parasites by changing their identity and stealing nutrients from healthy cells. Cancer cells mutate and form a group identity that is constantly signaling from outside the cell via abnormal receptor pathways. This stimulates proliferation but the cancer cells cannot produce enough energy to sustain their fast growth. As a result, cancer cells must act parasitically by taking more materials than they can produce, losing the balance between biosynthesis and destruction.
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Efruzhu cancer 19.
This document discusses a theory of cancer cell carcinogenesis. It proposes that cancer cells have a dual identity and behave parasitically. Cancer cells mutate and take on a group identity that is constantly signaling from outside via aberrant receptors and signaling pathways. This stimulates proliferative behavior, forcing cancer cells to carry more raw materials and products than they can produce energy for. As a result, cancer cells are obligated to behave parasitically rather than maintain a balanced biosynthetic and catabolic state like mature cells.
Efruzhu cancer 19. (2)
This document discusses a theory of cancer cell carcinogenesis. It proposes that cancer cells have a dual identity and behave parasitically. Cancer cells mutate and take on a group identity that is constantly signaling from outside via aberrant receptors and signaling pathways. This stimulates proliferative behavior, forcing cancer cells to carry large amounts of raw materials for biosynthesis. However, they do not have enough energy for this. As a result, cancer cells lose balance and work destructively like parasites through their parasitic behavior.
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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.
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This document provides an introduction to materials science chapter on dislocations and strengthening mechanisms in metals. It addresses why dislocations are primarily observed in metals, how strength and dislocation motion are related, and how strength can be increased. It discusses dislocation motion, slip systems, factors affecting slip, and strategies to strengthen metals including reducing grain size, solid solution strengthening, and cold working. Cold working increases yield strength and hardness but decreases ductility due to increased dislocation density and entanglement. Heating allows recovery which reduces dislocation density and reverses effects of cold working.
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El documento presenta la misión, visión y valores de un estudiante. Su misión es ser un profesional exitoso para ayudar a su familia y amigos aplicando valores como la responsabilidad, honestidad, puntualidad, respeto, lealtad y perseverancia. Su visión es ser una persona capaz de lograr sus objetivos aprendiendo de la vida diariamente y compartiendo con los demás.
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Efruzhu cancer 19.
This document discusses a theory of cancer cell carcinogenesis. It proposes that cancer cells have a dual identity and behave parasitically. Cancer cells mutate and take on a group identity that is constantly signaling from outside via aberrant receptors and signaling pathways. This stimulates proliferative behavior, forcing cancer cells to carry more raw materials and products than they can produce energy for. As a result, cancer cells are obligated to behave parasitically rather than maintain a balanced biosynthetic and catabolic state like mature cells.
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This document discusses a theory of cancer cell carcinogenesis. It proposes that cancer cells have a dual identity and behave parasitically. Cancer cells mutate and take on a group identity that is constantly signaling from outside via aberrant receptors and signaling pathways. This stimulates proliferative behavior, forcing cancer cells to carry large amounts of raw materials for biosynthesis. However, they do not have enough energy for this. As a result, cancer cells lose balance and work destructively like parasites through their parasitic behavior.
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.
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This document provides an introduction to materials science chapter on dislocations and strengthening mechanisms in metals. It addresses why dislocations are primarily observed in metals, how strength and dislocation motion are related, and how strength can be increased. It discusses dislocation motion, slip systems, factors affecting slip, and strategies to strengthen metals including reducing grain size, solid solution strengthening, and cold working. Cold working increases yield strength and hardness but decreases ductility due to increased dislocation density and entanglement. Heating allows recovery which reduces dislocation density and reverses effects of cold working.
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The document discusses the poor living conditions of cancer cells. It states that the life of a cancer cell is complex, with metabolic stress both inside and outside the cell. Cancer cells have abnormal DNA transcription and hypermethylated genes. Their energy production and biosynthesis abilities are impaired. They also have imbalanced ions and issues with nuclear and cytoplasmic membranes. Cancer cells live parasitically and are immortal and continuously proliferative, with multi-antigenic characteristics. All of these problems contribute to the complicated and problematic nature of cancer cell proliferation.
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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.
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 13.
The document discusses the role of cytokines, growth factors, and nitric oxide in cancer cell proliferation and differentiation. It states that high amounts of these substances cause cancer cells to constantly proliferate in an immature, cloned state as they are stimulated to divide. This creates metabolic stress for the cancer cells as they do not have enough time, energy, or biosynthesis capabilities to properly store lipids, nitrogen, and proteins. The low or normal amounts of these substances, on the other hand, have a differentiative effect and allow normal functions to occur step-by-step in a repairable manner.
Academia edu cancer short comments 1.
The document profiles an individual named Efruz Asiloglu. It includes their research interests in molecular cancer biochemistry, molecular cancer endocrinology, molecular cancer biology, and molecular cancer genetics. It also lists their status updates which discuss their "Efruzhu Cancer (Carcinogenesis) Theory" and suggest ways to potentially treat cancer at the molecular level.
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This document outlines the Efruzhu Cancer Theory which proposes that carcinogenesis can occur through two opposing dynamics. The first is through cancer stem cells that fail to fully mature due to chronic inflammation, inadequate energy or mutations. The second is through dedifferentiation of mature cells back to an immature state due to immune cells, allowing cancer cells to renew and continue living. Carcinogenesis results from a balance between the primordial and mature forms of cells being disrupted.
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This document outlines the Efruzhu Cancer Theory which proposes two pathways to carcinogenesis. The first involves cancer stem cells that fail to fully mature due to chronic inflammation, inadequate energy or mutations. The second involves the dedifferentiation of mature cells back to an immature state due to immune cells, allowing cancer cells to renew and continue living. Carcinogenesis can thus occur through either the persistence of immature cancer stem cells or the dematuration of mature cells.
Presentation14
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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.
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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.
Efruzhu cancer laws com. 25.2.
This document discusses the "Inadequate Energy Cancer (Carcinogenesis) Theory". It proposes that cancer may be triggered by mutations, but the main driver is inadequate or inefficient energy production within the cell. A variety of internal and external factors can disrupt energy production, especially oxidative processes, leading to inhibited or low-level energy generation over time. This stimulates an immune response and stresses the cell to find ways to survive, which can later lead to malignancy depending on the energy balance and accumulation of further mutations over time. Cancer cells mainly rely on anaerobic glycolysis for energy due to repression of normal aerobic pathways.
Academia edu cancer short comments 2.
Efruz Asiloglu is an independent researcher whose primary research interest is molecular cancer biochemistry. Their profile page provides information on their publications, books, talks and teaching documents related to their "Efruzhu Cancer (Carcinogenesis) Theory". They have been actively posting status updates discussing various aspects of cancer cell metabolism, signaling pathways, DNA mutations and potential treatment approaches.
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.
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 13.
The document discusses the role of cytokines, growth factors, and nitric oxide in cancer cell proliferation and differentiation. It states that high amounts of these substances cause cancer cells to constantly proliferate in an immature, cloned state as they are stimulated to divide. This creates metabolic stress for the cancer cells as they do not have enough time, energy, or biosynthesis capabilities to properly store lipids, nitrogen, and proteins. The low or normal amounts of these substances, on the other hand, have a differentiative effect and allow normal functions to occur step-by-step in a repairable manner.
Academia edu cancer short comments 1.
The document profiles an individual named Efruz Asiloglu. It includes their research interests in molecular cancer biochemistry, molecular cancer endocrinology, molecular cancer biology, and molecular cancer genetics. It also lists their status updates which discuss their "Efruzhu Cancer (Carcinogenesis) Theory" and suggest ways to potentially treat cancer at the molecular level.
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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Cancer remains one of the leading causes of death worldwide, prompting the need for innovative treatment methods. Nanotechnology offers promising new approaches, including the use of gold nanoparticles (nanogold) for targeted cancer therapy. Nanogold particles possess unique physical and chemical properties that make them suitable for drug delivery, imaging, and photothermal therapy.
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- Video recording of this lecture in English language: https://youtu.be/RvdYsTzgQq8
- Video recording of this lecture in Arabic language: https://youtu.be/ECILGWtgZko
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
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This guideline is directed principally toward new Molecular Entities that are
likely to have significant use in the elderly, either because the disease intended
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Receptor Discordance in Breast Carcinoma During the Course of Life
Definition:
Receptor discordance refers to changes in the status of hormone receptors (estrogen receptor ERα, progesterone receptor PgR, and HER2) in breast cancer tumors over time or between primary and metastatic sites.
Causes:
Tumor Evolution:
Genetic and epigenetic changes during tumor progression can lead to alterations in receptor status.
Treatment Effects:
Therapies, especially endocrine and targeted therapies, can selectively pressure tumor cells, causing shifts in receptor expression.
Heterogeneity:
Inherent heterogeneity within the tumor can result in subpopulations of cells with different receptor statuses.
Impact on Treatment:
Therapeutic Resistance:
Loss of ERα or PgR can lead to resistance to endocrine therapies.
HER2 discordance affects the efficacy of HER2-targeted treatments.
Treatment Adjustment:
Regular reassessment of receptor status may be necessary to adjust treatment strategies appropriately.
Clinical Implications:
Prognosis:
Receptor discordance is often associated with a poorer prognosis.
Biopsies:
Obtaining biopsies from metastatic sites is crucial for accurate receptor status assessment and effective treatment planning.
Monitoring:
Continuous monitoring of receptor status throughout the disease course can guide personalized therapy adjustments.
Understanding and managing receptor discordance is essential for optimizing treatment outcomes and improving the prognosis for breast cancer patients.
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