Efruzhu cancer 24.
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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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Presentation24
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.
Answer Pigmented Lesions On The Noise.
Basal cell carcinoma and melanocytic nevus are two different skin lesions. Basal cell carcinoma is characterized by the absence of a pigment network, linear and branching blood vessel growth (telangiectasia), and multiple blue-grey spots, while melanocytic nevus shows a pigment pseudo-network and typical symmetrical growth pattern with uniform structure. Surgical excision is used to treat basal cell carcinoma.
Efruzhu cancer carci̇nogenesi̇s theory 35
Cancer cells develop extra and intracellularly as well as in nuclear regions under conditions of deep oxidative metabolic stress according to the Efruzhu Cancer Carcinogenesis Theory. The theory proposes that cancer forms in cells experiencing high levels of oxidative stress at the extracellular, intracellular, cytoplasmic, and nuclear levels.
Efruzhu cancer carci̇nogenesi̇s theory 44
This document discusses the "Efruzhu Cancer Carcinogenesis Theory" and the need to design molecular drugs for cancer therapy that can bombard cancer cells to renormalize stem cell and macrophage genetics and make cells function normally again. It focuses on finding drugs that can alter DNA to treat cancer at the molecular level.
Efruzhu cancer carci̇nogenesi̇s theory22
Malignant cancer cells are governed dominantly by mutations, while normal cells are governed absolutely by their original DNA sequence. Benign cells are governed to varying degrees by both mutations and original DNA.
Review and Updates of Immunohistochemistry in Selected Salivary Gland and Hea...
This document provides an overview of immunohistochemistry markers that can help diagnose various salivary gland and head and neck tumors. It discusses the cell types that stain positively for different markers in normal salivary gland tissue and then examines the immunohistochemistry profiles of tumors like acinic cell carcinoma, mammary analogue secretory carcinoma, mucoepidermoid carcinoma, myoepithelial carcinoma, salivary duct carcinoma, adenoid cystic carcinoma, and polymorphous low-grade adenocarcinoma. Having an understanding of the typical marker expression in these tumors can aid pathologists in making accurate diagnoses.
Meghana - neoplastic lesions of lymph node - part 1
This document summarizes neoplastic lesions of lymph nodes, including Hodgkin lymphoma and non-Hodgkin lymphoma. It describes the classification, histopathology, cytology, and variants of several types of lymphoma such as Hodgkin lymphoma, follicular lymphoma, diffuse large B-cell lymphoma, and Burkitt lymphoma. References including textbooks and the WHO classification of tumors of hematopoietic and lymphoid tissue are provided.
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This document summarizes two breast biopsy cases of invasive ductal carcinoma and invasive lobular carcinoma. It provides details on histologic grading, immunohistochemical staining results, tumor characteristics like size and margins. It also describes lymph node sampling and definitions of treatment response. In both biopsy cases, the tumors were grade 2 with no lymphovascular invasion seen and further testing was recommended to determine biomarker status.
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Presentation24
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.
Answer Pigmented Lesions On The Noise.
Basal cell carcinoma and melanocytic nevus are two different skin lesions. Basal cell carcinoma is characterized by the absence of a pigment network, linear and branching blood vessel growth (telangiectasia), and multiple blue-grey spots, while melanocytic nevus shows a pigment pseudo-network and typical symmetrical growth pattern with uniform structure. Surgical excision is used to treat basal cell carcinoma.
Efruzhu cancer carci̇nogenesi̇s theory 35
Cancer cells develop extra and intracellularly as well as in nuclear regions under conditions of deep oxidative metabolic stress according to the Efruzhu Cancer Carcinogenesis Theory. The theory proposes that cancer forms in cells experiencing high levels of oxidative stress at the extracellular, intracellular, cytoplasmic, and nuclear levels.
Efruzhu cancer carci̇nogenesi̇s theory 44
This document discusses the "Efruzhu Cancer Carcinogenesis Theory" and the need to design molecular drugs for cancer therapy that can bombard cancer cells to renormalize stem cell and macrophage genetics and make cells function normally again. It focuses on finding drugs that can alter DNA to treat cancer at the molecular level.
Efruzhu cancer carci̇nogenesi̇s theory22
Malignant cancer cells are governed dominantly by mutations, while normal cells are governed absolutely by their original DNA sequence. Benign cells are governed to varying degrees by both mutations and original DNA.
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This document provides an overview of immunohistochemistry markers that can help diagnose various salivary gland and head and neck tumors. It discusses the cell types that stain positively for different markers in normal salivary gland tissue and then examines the immunohistochemistry profiles of tumors like acinic cell carcinoma, mammary analogue secretory carcinoma, mucoepidermoid carcinoma, myoepithelial carcinoma, salivary duct carcinoma, adenoid cystic carcinoma, and polymorphous low-grade adenocarcinoma. Having an understanding of the typical marker expression in these tumors can aid pathologists in making accurate diagnoses.
Meghana - neoplastic lesions of lymph node - part 1
This document summarizes neoplastic lesions of lymph nodes, including Hodgkin lymphoma and non-Hodgkin lymphoma. It describes the classification, histopathology, cytology, and variants of several types of lymphoma such as Hodgkin lymphoma, follicular lymphoma, diffuse large B-cell lymphoma, and Burkitt lymphoma. References including textbooks and the WHO classification of tumors of hematopoietic and lymphoid tissue are provided.
MDT conference case
This document summarizes two breast biopsy cases of invasive ductal carcinoma and invasive lobular carcinoma. It provides details on histologic grading, immunohistochemical staining results, tumor characteristics like size and margins. It also describes lymph node sampling and definitions of treatment response. In both biopsy cases, the tumors were grade 2 with no lymphovascular invasion seen and further testing was recommended to determine biomarker status.
Efruzhu cancer carcinogenesis theory22
Cancer carcinogenesis is governed by mutations in malignant cancer cells, whereas normal cells are governed absolutely by the original DNA sequence. Benign cells are governed to varying degrees by both mutations and the original DNA.
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1. The document discusses a MCV biopsy showing lobular hyperplasia of the epidermis resulting in cup-shaped lesions, with enlarged keratinocytes containing inclusion bodies.
2. MCV can be purified from skin biopsies and particles are around 220-450nm in size. Attempts to grow MCV in cell culture have been unsuccessful.
3. MCV only infects humans, shows tropism for epidermal tissue, and causes epidermal dedifferentiation, hyperproliferation, and benign tumor formation through immune evasion and receptor overexpression.
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Chronic inflammation is mainly caused by macrophages that remain in an area for a long time. These macrophages secrete various molecules like nitric oxides, prostaglandins, growth factors, and cytokines that can cause mutations in cells and potentially lead to the development of cancerous cells over time if multiple macrophages are involved. A single cancer cell may then develop among the macrophages.
Epidermal nevi and basal cell carcinoma
A 65-year-old woman was referred for assessment of a congenital lesion on her back that had changed over the past 2 years. Examination found she had both a basal cell carcinoma and an epidermal nevus occupying the same site on her back. Dermoscopic examination revealed features characteristic of both lesions, including telangiectasias, ovoid nests, and globules for the basal cell carcinoma and milia-like cysts, crypts, and fissures for the epidermal nevus.
Multiple facial papules
A 16-year-old male presented with multiple facial papules and nodules over 10 years. Similar lesions were seen in other family members. A biopsy showed keratinized stratified squamous epithelium overlying proliferating packets of basoloid cells with hyperchromatic nuclei, along with keratin horn cysts and a moderate chronic inflammatory cell infiltrate.
Presentation21
This document discusses a cancer cell mutation identity theory. It proposes that cancer cells have a binary identity with both mutated and normal DNA. The mutations are proposed to originate from outside the cell, with macrophages sending DNA sequences from different immune cells during chronic inflammation. This introduces thousands to millions of mutations from carcinogens, mutagens, mitochondrial breakdown and chronic inflammation. As a result, the cancer cell identity is comprised of more non-self mutated DNA than original self DNA, giving them different antigenic positions.
Basal cell carcinoma with unusual dermatoscopic aspects.
A 35-year-old woman presented with a lesion on her abdomen that had been present for 6 months. Upon examination, the lesion showed ulceration, arborizing telangiectasia, hairpin vessels, and glomerular vessels on dermatoscopy. The absence of a pigmented network and presence of these unusual vascular features indicated a diagnosis of basal cell carcinoma.
Efruzhu cancer carci̇nogenesi̇s theory18
Cancer cell identity can be changed by macrophages through a process of cultural adaptation and renewal. This cellular adaptation allows cancer cells to survive under suboptimal conditions.
Efruzhu cancer carci̇nogenesi̇s theory12
Cancer cells are immortal, immature, parasitic and continuously proliferative. They depend on mutations and inadequate energy to continue signaling in order to proliferate without control or limits, according to the Efruzhu Cancer Carcinogenesis Theory. The theory proposes that cancer cells are able to proliferate continuously due to their dependence on mutations, inadequate energy levels, and continued signaling.
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Meghana neoplastic lesions of lymph node - part 2
This document discusses various neoplastic lesions that can occur in lymph nodes, including lymphomas such as angioimmunoblastic T-cell lymphoma and anaplastic large cell lymphoma, tumors of the accessory immune system like follicular dendritic cell tumor and interdigitating dendritic cell tumor, vascular tumors like Kaposi's sarcoma, spindle cell tumors, and metastatic tumors from other organs. It provides descriptions of the histopathological features of these different types of lymph node tumors.
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.
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 8.
This document discusses the Efruzhu Cancer (Carcinogenesis) Theory which proposes that cancer develops through two opposing dynamics. The first is through cancer stem cells that need maturation but interact with chronic inflammation or mutations and become neoplastic cancer cells. The second is through dedifferentiation of mature cells into immature cells by immune cells. This theory states that cancer cells renew themselves through cultural adaptation to continue living under suboptimal conditions in a microenvironment with oxidative stress and low energy production, relying on anaerobic glycolysis and producing excess lactic acid.
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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.
Presentation8
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.
S5 presentation5
Aberrant signaling pathways in cancer work through guanylate cyclase and guanosine monophosphate molecules, as well as continuous nitric oxide and cytokine-growth factor signaling from outside cells. Chronic inflammation from immune cells like macrophages and cytokines can cause cell proliferation and differentiation dependence on ligand amounts. High ligand amounts promote proliferation while low amounts enable differentiation. Normal signaling pathways use adenylate cyclase via cyclic adenosine monophosphate dependent on ATP. Phosphorylation is important as conformational changes activate molecules. In normal cells, DNA in promoter regions is hypermethylated and histones are not sufficiently modified, suppressing transcription and expression.
Presentation5
The document discusses aberrant and normal signaling pathways in relation to cancer development. Aberrant signaling pathways involve guanylate cyclase and guanosine monophosphate molecules, as well as continuous nitric oxide and cytokines from outside cells. Chronic inflammation from immune cells and cytokines can cause cell proliferation and differentiation dependence on ligand amounts. Normal signaling pathways use adenylate cyclase and cyclic adenosine monophosphate dependent on ATP. Phosphorylation is important for conformational changes that activate molecules. Normal DNA sequences have hypermethylated CpG islands in promoter areas and decreased histone modifications, which suppress transcription and expression.
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1. The document discusses a MCV biopsy showing lobular hyperplasia of the epidermis resulting in cup-shaped lesions, with enlarged keratinocytes containing inclusion bodies.
2. MCV can be purified from skin biopsies and particles are around 220-450nm in size. Attempts to grow MCV in cell culture have been unsuccessful.
3. MCV only infects humans, shows tropism for epidermal tissue, and causes epidermal dedifferentiation, hyperproliferation, and benign tumor formation through immune evasion and receptor overexpression.
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Multiple facial papules
A 16-year-old male presented with multiple facial papules and nodules over 10 years. Similar lesions were seen in other family members. A biopsy showed keratinized stratified squamous epithelium overlying proliferating packets of basoloid cells with hyperchromatic nuclei, along with keratin horn cysts and a moderate chronic inflammatory cell infiltrate.
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This document discusses a cancer cell mutation identity theory. It proposes that cancer cells have a binary identity with both mutated and normal DNA. The mutations are proposed to originate from outside the cell, with macrophages sending DNA sequences from different immune cells during chronic inflammation. This introduces thousands to millions of mutations from carcinogens, mutagens, mitochondrial breakdown and chronic inflammation. As a result, the cancer cell identity is comprised of more non-self mutated DNA than original self DNA, giving them different antigenic positions.
Basal cell carcinoma with unusual dermatoscopic aspects.
A 35-year-old woman presented with a lesion on her abdomen that had been present for 6 months. Upon examination, the lesion showed ulceration, arborizing telangiectasia, hairpin vessels, and glomerular vessels on dermatoscopy. The absence of a pigmented network and presence of these unusual vascular features indicated a diagnosis of basal cell carcinoma.
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Cancer cell identity can be changed by macrophages through a process of cultural adaptation and renewal. This cellular adaptation allows cancer cells to survive under suboptimal conditions.
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Cancer cells are immortal, immature, parasitic and continuously proliferative. They depend on mutations and inadequate energy to continue signaling in order to proliferate without control or limits, according to the Efruzhu Cancer Carcinogenesis Theory. The theory proposes that cancer cells are able to proliferate continuously due to their dependence on mutations, inadequate energy levels, and continued signaling.
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Presentation5
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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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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.
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https://www.flickr.com/photos/efruzhucancerfinished/ …
THE BIG BANG THEORY AND THE EVOLUTIONARY THEORY THE END COMPLETELY FINISHED
New holy collision 9999999
1. APEX DEGREE MEDICAL PHILOSOPHER EFRUZHU1 PHRMP "HOLY COLLISION" THEORYEM NCY. TCY ®© INSTEAD OF BIG BANG THEORY
https://essafihucancertrea.wixsite.com/universalspaceallahu …
https://www.flickr.com/photos/efruzhucancerfinished/ …
THE BIG BANG THEORY AND THE EVOLUTIONARY THEORY THE END COMPLETELY FINISHED
New holy collision 999999
1. APEX DEGREE MEDICAL PHILOSOPHER EFRUZHU1 PHRMP "HOLY COLLISION" THEORYEM NCY. TCY ®© INSTEAD OF BIG BANG THEORY
https://essafihucancertrea.wixsite.com/universalspaceallahu …
https://www.flickr.com/photos/efruzhucancerfinished/ …
THE BIG BANG THEORY AND THE EVOLUTIONARY THEORY THE END COMPLETELY FINISHED
New holy collision 99999
1. APEX DEGREE MEDICAL PHILOSOPHER EFRUZHU1 PHRMP "HOLY COLLISION" THEORYEM NCY. TCY ®© INSTEAD OF BIG BANG THEORY
https://essafihucancertrea.wixsite.com/universalspaceallahu …
https://www.flickr.com/photos/efruzhucancerfinished/ …
THE BIG BANG THEORY AND THE EVOLUTIONARY THEORY THE END COMPLETELY FINISHED
New holy collision 9999
1. APEX DEGREE MEDICAL PHILOSOPHER EFRUZHU1 PHRMP "HOLY COLLISION" THEORYEM NCY. TCY ®© INSTEAD OF BIG BANG THEORY
https://essafihucancertrea.wixsite.com/universalspaceallahu …
https://www.flickr.com/photos/efruzhucancerfinished/ …
THE BIG BANG THEORY AND THE EVOLUTIONARY THEORY THE END COMPLETELY FINISHED
New holy collision 999
1. APEX DEGREE MEDICAL PHILOSOPHER EFRUZHU1 PHRMP "HOLY COLLISION" THEORYEM NCY. TCY ®© INSTEAD OF BIG BANG THEORY
https://essafihucancertrea.wixsite.com/universalspaceallahu …
https://www.flickr.com/photos/efruzhucancerfinished/ …
THE BIG BANG THEORY AND THE EVOLUTIONARY THEORY THE END COMPLETELY FINISHED
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