mitotic spindle

sun-su  asked:

hi! i sent u tht ask abt my mom having cancer, n i have a (rly dumb) question. i know shes on epoch-r, and i read about that, but im just. confused about how chemo in general works? ive tried looking it up but everywhere i looked says "chemo attacks cancer cells" and doesn't explain further.

hi hi hi!!! 

that’s totally not a dumb question. i’ve always been confused too, especially since there are so many cancer treatment terms and honestly it gets really confusing sometimes (like holy cow are cancer drug names awful to pronounce?)

historically, the term “chemotherapy” used to mean just any chemical compound (aka a drug) that can be used to treat a disease, such as antibacterial chemotherapy. and then the nomenclature slowly became known as just any drug that’s used to attack and kill cancer cells. this was way before anything like “targeted therapy” or “immunotherapy” was discovered, so you can look at chemotherapy being the grandfather or umbrella term for cancer-killing agents. 

chemotherapy is also used to describe a treatment that’s given systemically–as in it goes everywhere in the body, usually through intravenous (IV) injections. therefore it’s pretty darn useful to, for example, treat cancers that have metastasized to different organs. (that’s not the exclusive use of chemo tho; patients with primary tumors that haven’t metastasized can still use chemo). this is in comparison to radiation therapy, which uses radiation to blast a very very specific area of the body where the tumor is. 

the majority of the time, chemotherapy is a group of drugs that kill cancer cells because they attack their more-or-less unique characteristic of being crazy fast cell dividers. these drugs will often go after the mitosis machinery, and cause so much chaos that the cells have no choice but to undergo apoptosis, or a type of programmed cell death. 

however, chemo can’t really tell the different between a cancer cell and a healthy normal cell; it just so happens to be more effective at killing cells that divide quickly. so that’s why chemo regimens aren’t given over a really long period of time (treatment usually only lasts days), and why patients can experience side effects such as immunosuppression and gastrointestinal issues, as the immune cells and the cells lining our intestines are also fast dividers. they’re civilian casualties, so to say :(

certain chemos tend to work better with certain cancers, which is why there are specific chemo regimens. chemos are oftentimes given as a batch rather than individually. for example, EPOCH-R is a combo of drugs that work as a team to attack different aspects of the NHL cells, and can achieve much better results than if any of them went on a solo mission. here’s a breakdown of what each drug does:

Rituximab: this is an antibody that can bind specifically to B-cells, which in NHL have gone rogue and replication-happy. B-cells have a very specific protein on their surface, CD20, and rituximab gloms on like velcro. This causes natural killer cells and macrophages to recognize the B-cells as “foreign” and attack them. It also causes the complement system to be activated by the B-cells, which also furthers destruction of the cell. The downside of rituximab is it doesn’t discriminate between cancerous B-cells and normal B-cells though. 

Etoposide: these dudes inhibit the topoisomerase, which is an enzyme that helps unwind DNA during cell replication. when DNA unwinds, the downstream strands tend to get tangled and bent (think of unwinding one of those old-school phone cords–the part of the cord you’re not straightening gets super stressed and coils in on itself). Cells don’t like that, so they tell topoisomerase to go in and form small harmless nicks in the DNA to help relax it, and then when the DNA is unwound, it seals back the nick again. That last step is pretty crucial; without that action, DNA will just be floating around in fragments and the cell can’t function and will undergo apoptosis. so by inhibiting topoisomerase, etoposide is able to kill the cell. like most chemos tho, it can’t distinguish between cancer cells and non-cancer cells, but because cancer cells replicate so much faster than normal cells, and thus rely on topoisomerase so much more frequently, etoposide should be more effective in killing the cancer cells. 

Prednisolone: i don’t think the exact mechanism of how prednisolone kills cancer cells is well known. it’s used generally in low doses to dampen the immune system during allergic reactions, but with a high dose during chemo, it specifically causes immune cells (like NHL cells) to undergo apoptosis. 

Oncovin: aka vincristine (which imo is a much prettier name). this drug binds to a protein called tubulin. tubulin is required during mitosis, or cell division, to form microtubules–think of tubulin as like the fibers of a rope. microtubules form the mitotic spindles which separates the two daughter cells during cell division, so without tubulin, the cells can’t separate, things go haywire, and the cells undergo apoptosis. again, this drug isn’t specific to cancer cells, but relies on the faster rate of cell division in cancer cells to “spare” as many normal cells as possible. 

Cyclophosphamide: this drug has a metabolite that’s formed in NHL cells that’s able to form crosslinks in the DNA, rendering it almost impossible for the cell to create RNA (and protein), or to replicate. without these functions, the cell undergoes apoptosis. 

Hydroxydaunorubicin: aka doxorubicin. this drug is able to interacalate DNA, which means it’s able to get all nice and snug inside the DNA strand, and now the cell can’t synthesize RNA or proteins, or replicate (much like the effect of crosslinking of DNA). it’s akin to getting a rock in your shoe, and the presence of the rock causes you to cease all normal function and undergo apoptosis. that’s one deadly rock. it can also prevent topoisomerase from sealing DNA nicks (much like etoposide).

I hope that was a bit helpful! i maaayyy have delved into more detail than what you were looking for, but it’s all just really fascinating stuff…and i hope it gives you something to launch off of if you’re curious to learn more (and also feel free to ask me any questions you may have!)

good luck to your mom! i’m still rooting for her <3

Metaphase and Anaphase

Upon entry into anaphase, the mitotic spindle reorganizes dramatically: kinetochore fibers attached to chromosomes shorten, bringing chromatids toward the poles. The astral microtubules, which radiate from each spindle pole, elongate until they reach the cell surface. Meanwhile, a bundle of antiparallel microtubules, called the ‘central spindle,’ remains at the midpoint between the two poles. The central spindle and astral microtubules collaborate to position the division plane during cytokinesis.

anonymous asked:

Hey there! I was just wondering, seeing you have answered a couple questions, if you could explain shortly what the different parts of the chromosome do and where they are place/their "structure". I'm studying for a DNA test but having trouble figuring out precisely what the functions of the different parts of the chromosome is- Thank you and keep running this awesome site as excellent as you do now! Greetings from Denmark.

Hi there,

Well first of all you probably need to know enough about the organisation of the chromosome. This is essentially how the chromosome is condensed to form the characteristic chromatid structure (heterochromatin) from loosely packaged DNA (euchromatin).

The image above (source) shows how proteins called histones (the balls in the image), encourage DNA to wrap around them, resulting in the packaging of DNA. This is how large amounts of DNA can be condensed into such a small space within the cell. 

It is worth noting the centromere on the condensed chromosome. This is the site of assembly for the kinetocore; a protein complex responsible for attaching to microtubles of the mitotic spindle allowing the separation of the sister chromatids. 

At the other end of the chromosome you have telomeres. Telomeres are specialized DNA sequence that form the ends of the linear DNA molecules of the eukaryotic chromosomes. A telomoere consists of up to hundreds of copies of a short repeated sequence(5′-TTAGGG-3′ in humans), which is synthesized by the enzyme telomerase in a mechanism independent of normal DNA replication.

It is important for you to know that the stage of the cell cycle the cell is in will have an effect on the condensation of the chromosome and that signalling events check the state of the DNA as the cycle progresses.

I hope this has helped give you a basic overview of chromosomes but I’ve found a really comprehensive website that you should follow this up with.



Once chromosomes are pulled to either side, the cell start reversing the steps of prophase and prometaphase: the nuclear envelop reforms around decompacting chromosomes. Near the end of telophase, a thin bridge between the daughter cells, called the midbody contains the remnants of the mitotic spindle. A ring of actin filaments (i.e., the cleavage furrow) pulls like ‘purse strings’ to pinch the cells into two.

Image: Two HeLa cervical cancer cells captured in telophase, as sister chromatids are separated into the two ends of the dumbbell-shaped cell. Green fluorescence is from Aurora B protein kinase fused to eGFP with white and red marking DNA and tubulin. The image was taken using a DeltaVision deconvolution/restoration microscope.