if anyone wants some further reading to go along with his cancer lectures, i really recommend reading the Hallmarks of Cancer: The Next Generation in the journal Cell, it's an excellent review paper
I don't know the bird just came and told me what they doing looking for a cheap solution? I told them let me leave the game then you can make any plan you want as I won't be in the game anymore I promise 😭
Please read Robert Weinberg's classic text Cancer Biology. Tyler Jacks did postdoctoral studies in his lab. It's an excellent cancer biology book with comprehensive coverage.
My great grandpa had spinal cancer. My grandpa and his sisters had different types of cancer (prostate, breast and stomach). Now my Uncle (Mom’s brother) have lung cancer. My grandma had goiter, has undergone surgery and my Mom had undergone thyroidectomy (hyperthyroidism) as well. Is there any hereditary chance of getting Cancer to any of us? (Mom has 2 son and a daughter)
Thanks for these lectures, they are really good! Anyone else notice that BCR-ABL was written on the chalkboard incorrectly both times? Might want to add a subtitle correction.
(On Thursday of January 26, 2023). Biology and the Disease of Proliferation Pathology; whereas one is The Subject, the latter is the most significant effect a science can have as far as to applications of acquired Knowledge--but not necessarily! Gene Variation (Mutated and Disease-Causing Changes) in Tumor Suppressor Genes (Recessive process) or Dominant Proto-oncogenes: 1) Missense Mutation (Blocking the Function of the Protein Gene Product); 2) Deletion (Loss-of-Function by Loss of Gene); 3) Frameshift Mutation is also inhibitor at the Translational Level of the Gene Product, namely the Protein Product; and Through Chromosomal Loss (Loss of a Bigger DNA Locus than any other Type of Mechanism); Cytological Mechanism of Neoplasia: 1) Cell Cycle is the Process by which the Body is formed and maintained at a cellular level via Mitosis Cell Division; and 2) Apoptosis (Cell Death of Normal Development or non-pathological Significance); 3) P53 Gene and Product is a Tumor Suppressor Gene of the Most Significant Investigation and Presence in Proliferation Disease; 4) Normal Checks (known as Checkpoints of Cell Cycle) and other Arresting Mechanism Therein (DNA Repairing Mechanisms and Abnormal Proliferation Arrest) are Lost in p53 Pathologic Variation; 5) Two-hit Scenario (Recessive pattern) is Applicable for TS Gene Variation Phenotype Manifestation and is a Sporadic Occurrence rather than a Predictable (Inherited Mechanism) Diathesis; Genomic Sequencing in Particular Applied to Neoplasia: 1) Hundred to Thousands of Mutations in The Gene Variation Pathology; 2) Driver Mutation(s) within a Range of 5-20 are the Primary Variation in Proliferation Dysregulation Pathology; while 3) Passenger Mutations are idle or somewhat inconsequential to phenotypic Manifestation; and 4) Silent Mutation (Passenger Significance) are one of the same present but merely latently; Neoplasia (Cancer) Therapeutics: 1) Prophylaxis of Cancer is the focus but if such arises: a) Gardasil, Component Vaccine (Purified Protein Derivative [PPD] or Recombinant Protein) for Human Papilloma Virus (HPV) in Cervical Cancer Prevention; b) E6 and E7 Viral Genes are Transfected to the Human Cells upon the Infection Process; c) Natural Viral E6 Protein is Anti-complementary to p53 (Human Protein) and thereby Inhibitory; d) Natural Viral Protein E7 is Inhibitory to Human Protein pRB (RB Gene Product); e) Hepatitis B Virus (HBV, HCV is likely being Formulated also) is an up and coming Vaccine Prophylaxis (Hepatocellular Carcinoma); 2) Therapeutics: 1) Immunotherapy (Biologics Drug Class) as a potential Therapeutics with gaining Impetus and Momentum Pharmacologically; 2) Conventional Therapy: a) Surgery (Excision of Neoplasm)can be curative if Early Detection Happens; b) Radiation (Irradiation of the Affected Tissue and/or organ area); c) Chemotherapeutic Agents: 1) Antibiotics like Adriamycin along (Usually) with Radiation forms complexes with DNA by intercalation between base pairs; 2) Cisplatin (Purine [DNA Nucleotide] Binding Metal Complex) is a metal complex cytotoxic drug (Non-Cell Cycle Specific Cytotoxicity) which covalent binding leads to Intra-strand and Inter-strand crosslinks causing subsequent strand breaks of Cancer Cell DNA Molecule; Taxanes (Stabilize GDP -bound tubulin in the Microtubule, and thereby inhibiting the process of cell division as Depolymerization is Inhibited) are all Cell Cycle Specific (M-Phase Cytotoxicity) Targeting Pharmaceuticals 1) Side Effects (Antimetabolites and Analogs) are Very non Specific and Highly Detrimental to all Cells of the Body while some Normal Cells are actually oversensitive and are to affected by the Cytotoxicity Mechanism; 2) Resistance of Cancer Cells to Chemical Agents (due to P53 Absence) making such ineffective; 3) New Therapeutic Pharmaceuticals: 1) HER2 Gene Positive (Tumor markers or Biomarkers of Neoplasia) is Specific to 30% of Breast Cell Cancers (Ductal in Situ Carcinoma) and the 2) Gene Amplification Mechanism or (upregulation of HER2 Product) and thereby Growth Factor Signaling Upregulation; 3) Monoclonal Antibodies Biologics (Herceptin) Driven Immunotherapy specific to HER2 Receptor (Inhibiting the overexpressed HER2 Receptor By Binding Such); known for High Rate of Curative Treatment in Early Stage Breast Cancer and Five Year Expectancy in later Staged Cancers; 4) Philadelphia Chromosome (ABL-BCR Translocation-Fusion of Chronic Myelogenous Leukemia [CML] in Chromosome 22 [BCR Gene] and 9 [ABL Gene Site]) leads to proliferation by increases in Kinase Expression; 5) Imatinib or GLEEVEC binds Kinase by Binding the Activating Site and Highly Effective (As Seen in the High Remission or Curative Rates; or Low Relapsing Rates) in the Blast Crisis Stage; However, Relapse is Highly likely anyway with this Type of Leukemia. PhD Tyler Jacks is an extraordinary Pharmacologist or Pharmaceuticalist (Biologics and Monoclonal Antibodies are magical). Es ist gut. Heil!
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if anyone wants some further reading to go along with his cancer lectures, i really recommend reading the Hallmarks of Cancer: The Next Generation in the journal Cell, it's an excellent review paper
I don't know the bird just came and told me what they doing looking for a cheap solution? I told them let me leave the game then you can make any plan you want as I won't be in the game anymore
I promise 😭
Amazing lectures and this teacher is superb at conveying his message.
Nah as the curls where deployed by the comedians to come outside the hijab as a cover and then we found the HH curls in the tunnel 😭
Daughter medicine anybody! 😭
Please read Robert Weinberg's classic text Cancer Biology. Tyler Jacks did postdoctoral studies in his lab. It's an excellent cancer biology book with comprehensive coverage.
long live MIT and its lecturers, tyler is another great teacher....thanks a lot.
Great lecture. Thank you for the series.
My great grandpa had spinal cancer. My grandpa and his sisters had different types of cancer (prostate, breast and stomach). Now my Uncle (Mom’s brother) have lung cancer. My grandma had goiter, has undergone surgery and my Mom had undergone thyroidectomy (hyperthyroidism) as well. Is there any hereditary chance of getting Cancer to any of us? (Mom has 2 son and a daughter)
We hanging around again? As the short grave from the heart lungs when washed away with a dumb sock 😭
very good lecture ....and very informative
Thanks for these lectures, they are really good!
Anyone else notice that BCR-ABL was written on the chalkboard incorrectly both times? Might want to add a subtitle correction.
On 45:22 It's written as "BRC-ABL", isn't it meant to be "BCR-ABL"?
Thanks 🤍❤️
I finished lecture 3. Are there more lectures, if so what is the hyperlink? Thanks.😃
ocw.mit.edu/courses/7-013-introductory-biology-spring-2013/pages/video-lectures/
Best wishes on your studies!
This is helpful ❤️🤍
(On Thursday of January 26, 2023). Biology and the Disease of Proliferation Pathology; whereas one is The Subject, the latter is the most significant effect a science can have as far as to applications of acquired Knowledge--but not necessarily! Gene Variation (Mutated and Disease-Causing Changes) in Tumor Suppressor Genes (Recessive process) or Dominant Proto-oncogenes: 1) Missense Mutation (Blocking the Function of the Protein Gene Product); 2) Deletion (Loss-of-Function by Loss of Gene); 3) Frameshift Mutation is also inhibitor at the Translational Level of the Gene Product, namely the Protein Product; and Through Chromosomal Loss (Loss of a Bigger DNA Locus than any other Type of Mechanism); Cytological Mechanism of Neoplasia: 1) Cell Cycle is the Process by which the Body is formed and maintained at a cellular level via Mitosis Cell Division; and 2) Apoptosis (Cell Death of Normal Development or non-pathological Significance); 3) P53 Gene and Product is a Tumor Suppressor Gene of the Most Significant Investigation and Presence in Proliferation Disease; 4) Normal Checks (known as Checkpoints of Cell Cycle) and other Arresting Mechanism Therein (DNA Repairing Mechanisms and Abnormal Proliferation Arrest) are Lost in p53 Pathologic Variation; 5) Two-hit Scenario (Recessive pattern) is Applicable for TS Gene Variation Phenotype Manifestation and is a Sporadic Occurrence rather than a Predictable (Inherited Mechanism) Diathesis; Genomic Sequencing in Particular Applied to Neoplasia: 1) Hundred to Thousands of Mutations in The Gene Variation Pathology; 2) Driver Mutation(s) within a Range of 5-20 are the Primary Variation in Proliferation Dysregulation Pathology; while 3) Passenger Mutations are idle or somewhat inconsequential to phenotypic Manifestation; and 4) Silent Mutation (Passenger Significance) are one of the same present but merely latently; Neoplasia (Cancer) Therapeutics: 1) Prophylaxis of Cancer is the focus but if such arises: a) Gardasil, Component Vaccine (Purified Protein Derivative [PPD] or Recombinant Protein) for Human Papilloma Virus (HPV) in Cervical Cancer Prevention; b) E6 and E7 Viral Genes are Transfected to the Human Cells upon the Infection Process; c) Natural Viral E6 Protein is Anti-complementary to p53 (Human Protein) and thereby Inhibitory; d) Natural Viral Protein E7 is Inhibitory to Human Protein pRB (RB Gene Product); e) Hepatitis B Virus (HBV, HCV is likely being Formulated also) is an up and coming Vaccine Prophylaxis (Hepatocellular Carcinoma); 2) Therapeutics: 1) Immunotherapy (Biologics Drug Class) as a potential Therapeutics with gaining Impetus and Momentum Pharmacologically; 2) Conventional Therapy: a) Surgery (Excision of Neoplasm)can be curative if Early Detection Happens; b) Radiation (Irradiation of the Affected Tissue and/or organ area); c) Chemotherapeutic Agents: 1) Antibiotics like Adriamycin along (Usually) with Radiation forms complexes with DNA by intercalation between base pairs; 2) Cisplatin (Purine [DNA Nucleotide] Binding Metal Complex) is a metal complex cytotoxic drug (Non-Cell Cycle Specific Cytotoxicity) which covalent binding leads to Intra-strand and Inter-strand crosslinks causing subsequent strand breaks of Cancer Cell DNA Molecule; Taxanes (Stabilize GDP -bound tubulin in the Microtubule, and thereby inhibiting the process of cell division as Depolymerization is Inhibited) are all Cell Cycle Specific (M-Phase Cytotoxicity) Targeting Pharmaceuticals 1) Side Effects (Antimetabolites and Analogs) are Very non Specific and Highly Detrimental to all Cells of the Body while some Normal Cells are actually oversensitive and are to affected by the Cytotoxicity Mechanism; 2) Resistance of Cancer Cells to Chemical Agents (due to P53 Absence) making such ineffective; 3) New Therapeutic Pharmaceuticals: 1) HER2 Gene Positive (Tumor markers or Biomarkers of Neoplasia) is Specific to 30% of Breast Cell Cancers (Ductal in Situ Carcinoma) and the 2) Gene Amplification Mechanism or (upregulation of HER2 Product) and thereby Growth Factor Signaling Upregulation; 3) Monoclonal Antibodies Biologics (Herceptin) Driven Immunotherapy specific to HER2 Receptor (Inhibiting the overexpressed HER2 Receptor By Binding Such); known for High Rate of Curative Treatment in Early Stage Breast Cancer and Five Year Expectancy in later Staged Cancers; 4) Philadelphia Chromosome (ABL-BCR Translocation-Fusion of Chronic Myelogenous Leukemia [CML] in Chromosome 22 [BCR Gene] and 9 [ABL Gene Site]) leads to proliferation by increases in Kinase Expression; 5) Imatinib or GLEEVEC binds Kinase by Binding the Activating Site and Highly Effective (As Seen in the High Remission or Curative Rates; or Low Relapsing Rates) in the Blast Crisis Stage; However, Relapse is Highly likely anyway with this Type of Leukemia. PhD Tyler Jacks is an extraordinary Pharmacologist or Pharmaceuticalist (Biologics and Monoclonal Antibodies are magical). Es ist gut. Heil!
Kid with tumors in his eyes.. I imagine the atheism rate is high in pediatric providers