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This document discusses a cancer theory involving four main laws or causes: mutations that disrupt group identity, inadequate energy, chronic inflammation, and suppression of normal DNA. The theory proposes these factors contribute to carcinogenesis or the development and progression of cancer.
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Presentation25
This document discusses a cancer theory involving mutations, inadequate energy, chronic inflammation, and normal DNA suppression as key factors. It references laws, groups, and identity as playing a role. The theory examines the "voiced of laws" in cancer formation and development.
Efruzhu cancer laws specific 25.
Mutations, inadequate energy, and chronic inflammation are proposed as laws that contribute to cancer formation by disrupting normal DNA suppression and group identity according to the "EFRUZHU CANCER (CARCİNOGENESİS) THEORY". A video file is referenced but no other details about the theory are provided in the document.
Efruzhu cancer carcinogenesis theory 1
Mutations, inadequate energy, chronic inflammation, and suppression of normal DNA are proposed as four laws of carcinogenesis theory for esophageal cancer. Mutations alter cell group identity while inadequate energy and chronic inflammation damage DNA. Normal DNA suppression allows damaged cells to avoid apoptosis and proliferate abnormally.
Efruzhu cancer carcinogenesis theory laws 14
This document discusses four theories of carcinogenesis or cancer development: 1) Mutations disrupt a cell's group identity, 2) Inadequate energy production leads to uncontrolled growth, 3) Chronic inflammation damages DNA, and 4) The suppression of normal DNA functions allows uncontrolled growth.
Efruzhu cancer carci̇nogenesi̇s theory 37
The document discusses a theory of cancer carcinogenesis called "EFRUZHU CANCER CARCINOGENESIS THEORY". The theory proposes that mutations use normal DNA dynamics as a vehicle, similarly to how a bad driver might operate a vehicle in a dangerous manner. Mutations are able to hijack normal DNA processes to promote abnormal cell growth and proliferation that leads to cancer development.
Efruzhu cancer carci̇nogenesi̇s theory 28
Cancer carcinogenesis theory suggests that suppression of normal DNA sequences leads to cancer due to dependence on inadequate energy. When normal DNA is suppressed, cells become dependent on insufficient energy for growth and proliferation, resulting in uncontrolled division and tumor formation. This dependence on inadequate energy allows mutations to accumulate due to DNA replication errors from an energy shortage.
Sunu 25.1.1
The document discusses a theory of cancer called the "EFRUZHU CANCER (CARCİNOGENESİS) THEORY". It states that for a normal cell to become a cancer cell, it is not enough for mutations alone and that this condition needs energy inefficiency as the main dominant mechanism in addition to mutations. It also references "MUTATİONS GROUP İDENTİTY" and "DETAİLED LAWS COMMENTS 1."
Efruzhu cancer carci̇nogenesi̇s theory laws 15
The document outlines 4 key theories behind cancer carcinogenesis: 1) Mutations disrupt a cell's group identity, 2) Inadequate energy production leads to uncontrolled growth, 3) Chronic inflammation can enable cancerous changes, 4) Suppression of normal DNA functioning allows for abnormal cell growth.
Recommended
Presentation25
This document discusses a cancer theory involving mutations, inadequate energy, chronic inflammation, and normal DNA suppression as key factors. It references laws, groups, and identity as playing a role. The theory examines the "voiced of laws" in cancer formation and development.
Efruzhu cancer laws specific 25.
Mutations, inadequate energy, and chronic inflammation are proposed as laws that contribute to cancer formation by disrupting normal DNA suppression and group identity according to the "EFRUZHU CANCER (CARCİNOGENESİS) THEORY". A video file is referenced but no other details about the theory are provided in the document.
Efruzhu cancer carcinogenesis theory 1
Mutations, inadequate energy, chronic inflammation, and suppression of normal DNA are proposed as four laws of carcinogenesis theory for esophageal cancer. Mutations alter cell group identity while inadequate energy and chronic inflammation damage DNA. Normal DNA suppression allows damaged cells to avoid apoptosis and proliferate abnormally.
Efruzhu cancer carcinogenesis theory laws 14
This document discusses four theories of carcinogenesis or cancer development: 1) Mutations disrupt a cell's group identity, 2) Inadequate energy production leads to uncontrolled growth, 3) Chronic inflammation damages DNA, and 4) The suppression of normal DNA functions allows uncontrolled growth.
Efruzhu cancer carci̇nogenesi̇s theory 37
The document discusses a theory of cancer carcinogenesis called "EFRUZHU CANCER CARCINOGENESIS THEORY". The theory proposes that mutations use normal DNA dynamics as a vehicle, similarly to how a bad driver might operate a vehicle in a dangerous manner. Mutations are able to hijack normal DNA processes to promote abnormal cell growth and proliferation that leads to cancer development.
Efruzhu cancer carci̇nogenesi̇s theory 28
Cancer carcinogenesis theory suggests that suppression of normal DNA sequences leads to cancer due to dependence on inadequate energy. When normal DNA is suppressed, cells become dependent on insufficient energy for growth and proliferation, resulting in uncontrolled division and tumor formation. This dependence on inadequate energy allows mutations to accumulate due to DNA replication errors from an energy shortage.
Sunu 25.1.1
The document discusses a theory of cancer called the "EFRUZHU CANCER (CARCİNOGENESİS) THEORY". It states that for a normal cell to become a cancer cell, it is not enough for mutations alone and that this condition needs energy inefficiency as the main dominant mechanism in addition to mutations. It also references "MUTATİONS GROUP İDENTİTY" and "DETAİLED LAWS COMMENTS 1."
Efruzhu cancer carci̇nogenesi̇s theory laws 15
The document outlines 4 key theories behind cancer carcinogenesis: 1) Mutations disrupt a cell's group identity, 2) Inadequate energy production leads to uncontrolled growth, 3) Chronic inflammation can enable cancerous changes, 4) Suppression of normal DNA functioning allows for abnormal cell growth.
Efruzhu cancer carcinogenesis theory update 2
Mutations identified by macrophages, inadequate energy, and chronic inflammation can lead to cancer formation by overriding normal DNA suppression mechanisms according to an updated carcinogenesis theory for pancreatic cancer.
Efruzhu cance theory opposi̇ti̇ons of cancer cell 4
The document outlines 4 key factors in Efruz Asiloglu's theory of cancer carcinogenesis: 1) mutations that alter group identity, 2) inadequate energy, 3) chronic inflammation, and 4) suppression of normal DNA. The theory proposes these 4 factors lead to the development of cancer cells from stem cells. The document is dated November 15, 2012 and authored by Efruz Asiloglu.
S4 efruzhu cance theory opposi̇ti̇ons of cancer cell 4
The document outlines 4 key factors in Efruz Asiloglu's theory of cancer carcinogenesis: 1) mutations that alter group identity, 2) inadequate energy, 3) chronic inflammation, and 4) suppression of normal DNA. The theory proposes these 4 factors lead to the development of cancer cells from stem cells. The document is dated November 15, 2012 and authored by Efruz Asiloglu.
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.
Efruzhu cancer carci̇nogenesi̇s theory11
Cancer cells have a binary identity with mutations that allow them to take on characteristics of both their original cell group identity and the mutated cell identity, similar to genetic recombination during reproduction where multiple crossovers can combine parts of different DNA identities into a new identity.
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.
8 oncologic research
1. Oncology is the branch of science that deals with tumors and cancers.
2. An oncologist coordinates cancer treatment which may involve surgeons, radiation oncologists, and radiotherapists.
3. New methods of early cancer detection include gamma ray detectors, analyzing blood samples to detect tumors up to 5 years before detection by other methods, and fluorescent sprays that can highlight cancer cells during surgery.
Efruzhu cancer carcinogenesis theory 3
Mutations that lead to cancer formation come from both outside and inside the body, as macrophages can introduce more than one mutation.
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This editorial discusses guidelines for managing adnexal masses and determining when to observe, intervene, or refer to a specialist. It summarizes a study finding that complex or solid adnexal masses with a CA-125 over 35 units/mL have a high risk of ovarian cancer. For postmenopausal women over 50 with these characteristics, referral to a gynecologic oncologist is recommended. However, in younger women, functional cysts are more common and the cancer risk is lower, so observation may be preferable. Simple cysts under 10 cm can usually be monitored regardless of age if CA-125 is normal. Overall, careful assessment of adnexal masses is important to guide management and surgical planning.
Unusual Nonepithelial cancers of H&N
This document discusses several types of rare head and neck tumors, including extramedullary plasmacytomas, nasopharyngeal angiofibroma, non-lentiginous melanoma, and extracranial meningiomas. It provides details on the epidemiology, clinical presentation, diagnosis, treatment options including radiation therapy techniques, and outcomes for each of these tumor types.
Metastasis of unknown origin ppt final ppt
The document discusses lymph node metastasis in head and neck squamous cell carcinoma (HNSCC). It covers topics such as:
1) The most common sites of lymph node metastasis in HNSCC are levels II and III, with less frequent involvement of levels I and IV-VI.
2) Factors that influence lymph node metastasis include primary tumor characteristics, lymphangiogenesis induced by VEGF-C/D signaling, and the genetic makeup of the tumor which regulates genes involved in invasion and migration.
3) Once tumor cells reach lymph nodes, they can proliferate, remain dormant, or enter circulation to spread hematogenously to distant sites. The presence of lymph node metastases is associated with worse
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Efruzhu cancer carcinogenesis theory update 2
Mutations identified by macrophages, inadequate energy, and chronic inflammation can lead to cancer formation by overriding normal DNA suppression mechanisms according to an updated carcinogenesis theory for pancreatic cancer.
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The document outlines 4 key factors in Efruz Asiloglu's theory of cancer carcinogenesis: 1) mutations that alter group identity, 2) inadequate energy, 3) chronic inflammation, and 4) suppression of normal DNA. The theory proposes these 4 factors lead to the development of cancer cells from stem cells. The document is dated November 15, 2012 and authored by Efruz Asiloglu.
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The document outlines 4 key factors in Efruz Asiloglu's theory of cancer carcinogenesis: 1) mutations that alter group identity, 2) inadequate energy, 3) chronic inflammation, and 4) suppression of normal DNA. The theory proposes these 4 factors lead to the development of cancer cells from stem cells. The document is dated November 15, 2012 and authored by Efruz Asiloglu.
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.
Efruzhu cancer carci̇nogenesi̇s theory11
Cancer cells have a binary identity with mutations that allow them to take on characteristics of both their original cell group identity and the mutated cell identity, similar to genetic recombination during reproduction where multiple crossovers can combine parts of different DNA identities into a new identity.
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.
8 oncologic research
1. Oncology is the branch of science that deals with tumors and cancers.
2. An oncologist coordinates cancer treatment which may involve surgeons, radiation oncologists, and radiotherapists.
3. New methods of early cancer detection include gamma ray detectors, analyzing blood samples to detect tumors up to 5 years before detection by other methods, and fluorescent sprays that can highlight cancer cells during surgery.
Efruzhu cancer carcinogenesis theory 3
Mutations that lead to cancer formation come from both outside and inside the body, as macrophages can introduce more than one mutation.
Adnexal masses _when_to_observe,_when_to.2
This editorial discusses guidelines for managing adnexal masses and determining when to observe, intervene, or refer to a specialist. It summarizes a study finding that complex or solid adnexal masses with a CA-125 over 35 units/mL have a high risk of ovarian cancer. For postmenopausal women over 50 with these characteristics, referral to a gynecologic oncologist is recommended. However, in younger women, functional cysts are more common and the cancer risk is lower, so observation may be preferable. Simple cysts under 10 cm can usually be monitored regardless of age if CA-125 is normal. Overall, careful assessment of adnexal masses is important to guide management and surgical planning.
Unusual Nonepithelial cancers of H&N
This document discusses several types of rare head and neck tumors, including extramedullary plasmacytomas, nasopharyngeal angiofibroma, non-lentiginous melanoma, and extracranial meningiomas. It provides details on the epidemiology, clinical presentation, diagnosis, treatment options including radiation therapy techniques, and outcomes for each of these tumor types.
Metastasis of unknown origin ppt final ppt
The document discusses lymph node metastasis in head and neck squamous cell carcinoma (HNSCC). It covers topics such as:
1) The most common sites of lymph node metastasis in HNSCC are levels II and III, with less frequent involvement of levels I and IV-VI.
2) Factors that influence lymph node metastasis include primary tumor characteristics, lymphangiogenesis induced by VEGF-C/D signaling, and the genetic makeup of the tumor which regulates genes involved in invasion and migration.
3) Once tumor cells reach lymph nodes, they can proliferate, remain dormant, or enter circulation to spread hematogenously to distant sites. The presence of lymph node metastases is associated with worse
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S25 presentation25
- 1. “EFRUZHU CANCER (CARCİNOGENESİS) THEORY” L A W S MUTATİONS GROUP İDENTİTY. İNADEQUATE ENERGY. CHRONİC İNFLAMMATİON. NORMAL DNA SUPPRESSİON. VOİCED OF LAWS