He is a great explainer... Thanks MIT for sharing this... Worth watching..

Great stuff!! Keep up on sharing knowledge to the world guys!! May god repay your kindness ❤️

Excellent explanation!

Thank you sooooooooo much for those great lessons!!!!!

(On Wednesday of February 8, 2023). Cancer (Neoplasia or Proliferation Disease State) is a Pathologic Growth of Tissue (Neural, Muscle, Epithelial, or Connective Tissue): 1) Dysregulation and Degeneration of Normal Tissue Growth (Normoplasia or Euplasia); 2) Genetic Molecular Mechanism of Gene variation or Pathologic Changes within the Genome; a) Oncogene (Proto-Oncogene Transformation) is a Pathologic Growth Signaling Gene expression, usually a Transcription Factor of Growth; b) Proto-Oncogene is Beneficial and when Normal promotes Cell Survival (Growth and Proliferation); c) Loss of Regulated Proto-oncogenic Function (CDKs, E2F, Wnt, MYC Gene Variation et al) is a Possible Mechanism of Neoplasia, also known as a Gain of Function (GOF) mutation (Accelerated growth or Loss of breaks analogy); d) Tumor Suppressor Genes (TSGs) are marked by a Loss of Function Variation of a Gene (Mutation otherwise), usually a TF (p53, BRCA1,2 etcetera); e) TSGs are known also for Regulatory Function of Cell Repair (DNA Repairing) and integrity of a Cell. Caretaker or Custodians of the Genome are other epithets, f) Growth Signals (Growth Factors [GFs]) regulate Gene expression of Cyclins (G1 Cyclin Specifically to G1-S Cyclin [Commitment to Cell Cycle Signal]) and Other Cytokines (Il-6, TNFs) can be Signal of START; g) E2F (TF) where RB Protein Bind to such represses (mRNA biosynthesis of E2F) where the Phosphorylation of RB (Retinoblastoma Gene; First Cloned Gene) deactivates Such and E2F is capable to Bind the Promoter Region of DNA Molecule (Biosynthesis of mRNA or Transcription will ensue); h) RB Gene Variation (Mutation) can have Neoplastic Growth Processes leading to Neoplasm therein: 1) In Sporadic Variation, there is no History or Diathesis of Neoplasia specifically within the Retina and usually manifests unilaterally (affecting only one Eye); b) 2) Familial RB (Diathesis) is an Inherited and pathologic Variation of RB Gene (Bilaterally manifestation) and implies predisposition to this Proliferation Disease. The Inheritance pattern is Autosomal Dominant (AD) involving equally Female and Males and involves all generations therein (no Generational Latency as in Recessive Inheritance) phenotypically. However, the actual Process is Autosomal Recessive (AR) with a Predisposition (Somatic Transformation of Homozygous Significance i.e. Phenotype Post-Gametogenesis Manifestation [Retinoblastoma Neoplasm]); a) Point Mutations, b) Chromosome Loss, c) Deletion, d) Gene Repression. In Colon Cancer and Famlial Adenomatous Polyposis (FAP): 1) Dysregulate in the Wnt Signaling in the Stem Cell Niche Process; 2) Neoplasia Pathogenesis: a) Mutation of Euplastic Tissue; b) Dysplasia; c) In Situe Neoplasia (Anaplasia); And d) Francoanaplasia (Metastatic and Invasive Neoplasia); 2) Adenopolyposis Colon (APC) Gene Aberrance; a) Wnt Signaling Constituively activation; b) Further Genetic variation Inducement;......Translocation of Philadelphia Chromosome (9,22 Transformation) in CML in the Abelson Protein And Gene. (Proto-Oncogene) PhD Adam Martin, Es geht gut und nicht vergessen niemal Gesundheit werden haben warum Gesundheit geben. Heil!

It's a great class

So interesting love it!

Very good

tbh ngl, im enjoying watching these,even tho I'm still grade 11

@mdthesilver2030

2 жыл бұрын

Me too 😊😊

@tasadar1695

2 жыл бұрын

Keep watching :)

@Mystery1313m.m

Жыл бұрын

Dang....same goes for me😅...I am in 11th grade and I like watching these video lectures....idk, but its just that it gives kind of happiness and satisfaction😁.

@IvlivsCaeser

2 ай бұрын

Same here, Im in grade 7

Are there family inheritance trees out there where heterozygous individuals are marked as well (if known)?

@varaddeshmukh6095

2 жыл бұрын

Heterozygous individuals are always unmarked but can be identified by seeing if a single sex of their progenies are marked which could indicate to the disease being autosomal recessive or could be sex linked recessive in case of female progenies being affected as the X chromosome carries the recessive allele for the disease.

Chalk? What about PP slides?

Hey all, Does anyone have any lecture notes on this lecture by any chance? Thanks :)

@mitocw

2 жыл бұрын

Unfortunately, the lecture notes are not available on OCW, but the recitation notes are on the site ocw.mit.edu/7-016F18.

@vedantbhardwaj7582

2 жыл бұрын

@@mitocw Oh okay, no worries. Thanks for taking the time out to reply. And thanks to Professor for the great lecture!

What pathogen is causing the mutation…

What’s with the close up’s on the lecturer?

mere kajan ko cancers ki problam ho agi se usne bhut se doctor seelaj krwya koi frk nhi pda fer osne planet ayuveda se apna treatment krwya or oski cancers problam thik ho gai .

this is my asmr lol i fell asleep at s

😅Detailed lecture assimilated thanks

If it has defective brakes and it keeps on dividing uncontrollably it would grow to an enormous size. A fertilized egg becomes a 8ob baby in just nine months. So unregulated / uncontrolled cell growth would be at least his in a year. That is not what we see.

@rituparnaghanty6819

3 жыл бұрын

it could be due to the fact that when a fertilized egg is growing, it knows the map.. And also these cells are not abnormal mutated cells..they are not threatened by our immune system either.On the other hand, cancer cells can divide uncontrollably but with each division they try to mutate further to gain additional advantages. they are genetically unstable..and it makes cancer cells vulnerable...there is a fine line... If a cancer cell accumulate lots of mutation it may not always works in it's favor. Only few cells achive this selective advantage by random mutation.

@KenSellers

3 жыл бұрын

@@rituparnaghanty6819 I agree with your overall point, but disagree that cells "try to mutate further to gain additional advantages". The implied intelligence simply isn't there. You put it well yourself, at the end: Only a few cells achieve this selective advantage *by random mutation*.

@user-nm9fk7cb4b

3 жыл бұрын

If you’re going to hypothesise, please provide reasonable processes for these occurrences to take place

@Kyrani99

3 жыл бұрын

​@@rituparnaghanty6819 They are saying that a cell's DNA gets damaged by some "carcinogen" OR it's just plain bad luck and the DNA was miscopied in some gene. And that the cell then goes on to have more and more mutation, RANDOM changes, which may be advantageous how???? and hence selected for what???? About 97% or 98% of all cancers are solid tumors. They exhibit the characteristics of an organ. They have a basement membrane, a micro environment with a lot of other cells as found in any other organ in the body. These cells are connective tissue cells, which do all the supportive work for the specialized cells, in the case of cancer, this is the cancer cells. Anything between about 5% to as much as 85% of the cells in the tumor are connective tissue cells! Added to that the tumor forms a blood network / supply, a lymphatic supply and in many cases hey, a nerve supply, a network of nerves. AND they have stem cells, yeah cancer stem cells that have all the markers of embryonic stem cells. Yamanaka eat your heart out!. The cancer stem cells give rise to all the other cancer cells, if not all the other cells in the tumor. Come on, does this sound like evolution? If so then it is fish to man in a cool thousand years. And that is not to say they are basically trying to say DAMAGE = FUNCTION. Hello hello, I at least, smell a rat.

@Kyrani99

3 жыл бұрын

@@KenSellers what selective advantage?

I lov cancer ♋

Aneuploid.... chromosome extr??only one..?..genetic integrity caretaker genes.....

I’m not sure making science the Oscars is a good idea. I mean have you seen how scary that event has become? 😹 Thanks for another lecture about the beautiful function of our bodies.