#tumor suppressor gene

[womanguy]

drinking while doing hw always seems like a good idea and I don’t know how

[medicomunicare]

Retinoblastoma gets "viewed" from within: and the nuclear receptor hopes for drug agonist sightin'

Retinoblastoma gets “viewed” from within: and the nuclear receptor hopes for drug agonist sightin’

Retinoblastoma is a rare cancer affecting the retina – the tissue in the back of the eye that receives light and converts it into signals to the brain. It is most often diagnosed in children under 2 and has been associated with mutations in the RB1 gene. However, there are currently no specific, targeted therapies; doctors rely on broad-acting chemotherapy drugs that carry numerous side effects…

[pooksgetspooked]

Teacher’s Pet

Summary: Leon was never good with people. Not since Raccoon City, not after the DSO, and certainly not after he’s involuntarily signed up to be a temporary professor at a University. He simply didn’t have the same charm that others envied, so thank the heavens he didn’t have to be when you were there to charm him instead.

Pairing(s): Professor!Leon s. Kennedy x Student!Fem!Reader

Word Count: 3.6k

Content Warnings: MDNI! Age gap, Both of them are a bit of a creep, But they’re cute so it’s okay, Obsessive & Stalker undertones

“So, does anyone have an answer for this first question? Yeast deletion library can be used to validate tumor suppressor genes identified in tumors from humans. From such studies, we can infer that these genes function mainly as…? Anyone?” A lengthy silence followed, cut short by a sigh. “Mainly as cell cycle regulators.” The air of confidence ebbed away, leaving a soft murmur meant for his ears only as he slumped into his chair in behind the front desk.“Come on Leon, this is stupid. Awful. Am I even doing this right?” 

A calloused hand carded through blonde locks, tousling them as the man took a deep breath while sifting through his slides once more. “Is there anyone who knows what cell cycle regulators do? No, that’s too textbook, they’ll understand better in a real life application question,” he grumbled once more to himself within the vacant classroom, “real life application… I better start bringing lab samples if I’m gonna start talking about real life application,” he snorted dryly. Odd, maybe that’s an inside joke between him and himself. You couldn’t help but giggle softly to yourself; actually to yourself, unlike Prof Kennedy. Poor sod. Sat outside the classroom with your ears pressed against the door, you were jotting down notes to yourself with some scribbles for entertainment purposes. 

Your attention was rapt however, when you heard him murmur your name. Breath hitched, you froze while scrambling to pack your things and get away before he could open the door. “Yes, you. Do you have an answer to this question? It’s alright if you get the answer wrong, but i’d like you to try.” You let out a sigh of relief, shoulders sagging as you realized he was just practicing, but that didn’t stop the warm flush of your cheeks while your hand came up to cover your lips. Was he practicing with the thought of you in mind?

Professor Leon Kennedy, or Prof Kennedy as some of your classmates preferred to address him by, was the new professor teaching the principles of genetics module. You had heard whispers about him being younger than most of the geriatric professors, something something government involvement and a temporary break.

You were more concerned about this guy’s ability to teach, because you were damn sure if you had someone with the teaching capacity of a TA as your prof, you might personally see to that he clocks in his early retirement. 

But turns out, he was a pretty alright professor. You’ve definitely had better, he wasn’t exemplary. No, Prof Redfield took the cake for that. Eye candy, and brutal at Chemistry. You didn’t hate O chem any less than when you first started, but he was convincing enough to keep you from skipping. 

While Prof Redfield was masterful at his subject and teaching, Prof Kennedy was diligent but at the same time, kind of a grouch. It was kind of sweet to see how hard he was actually trying to make lectures more bearable, but you had every reason to believe that he himself could hardly stand being there when he never had anything beyond an impassive expression. You were pretty sure you’ve seen cadavers with more life in their face than he did 95 percent of the time. The other 5 percent was when class ends and he’s got the same urgency to match the pace he’s packing, because somehow he’s always the last guy in and first guy out of the lecture theatre.

“Alright class! Can anyone tell me about- no that’s not right, what am I saying?” Leon was near his wits end. Couldn’t recall why on earth he agreed to teach at some university as a break. Actually no, he did recall. 

He recalled how Chris and Claire had both coaxed him into the idea during one of their nights out drinking, and he recalled not recalling signing anything, but apparently he was already signed up for it within the same week of his disgruntled verbal agreement. He wished the government would work just a fraction as fast as whatever organization body that was desperate enough to take him in as a professor. Oh, but I think you’d be a good match Leon, what with all your lab background, you’ve got the knowledge they’re looking to teach. Plus, it’s an easy paid holiday from work! Leon rolled his eyes as he recalled the muddled voice of Claire, or was it Chris? Doesn’t matter. They considered a whole lot of his technical abilities, and a lot less of his social skills neck to neck with a nut. Tipping his head back as he stared up at the fluorescent lights, he thought back to his first lecture. Fucking terrifying, mind you. Facing BOWs with the ability to detach his spine from his head wasn’t anywhere near the same kind of nerve-wrecking when he had to stand in front of a whole auditorium of students. The second lecture was better, but only but the smallest sliver.

Lesser students this time, but still too many eyes for comfort. The only saving grace was that this time, he practiced. Spent an embarrassing amount of time going through the lecture materials with himself before stepping up on stage. 

Asides from that however, he had a little more brain capacity to actually observe the students during his second attempt. Most of which, jotting down notes on their ipads, using their phones; he couldn’t blame them, genetics can be pretty dry, and he would’ve chosen to teach something else as well if he was given the choice. However a little something stood out from the crowd. You were nearer to the front, rather dolled up. You were cute. And not only that, lo and behold, you were a nodder. Lecturers must love you, because Leon sure as hell did when he finally caught notice of you, and how you seemed to reciprocate his lectures with an encouraging nod and a smile whenever your gaze met. He found it a little easier to go up on stage after that. His gaze deviated more towards you, and at some point he just pretended like he was just teaching you. Drowned out the rest of the auditorium, and acted like it was just the two of you. 

That’s how he first came to know of you. Not actually though; professors don’t actually interact with the students. He didn’t get paid enough for that, and he didn’t want to come off as a creep, so he left you alone for the most part. 

Just did his own private digging to find out your name, and oh, would you look at that? You should really learn to safeguard your particulars better because it took him less than 5 to find your address, birthday, education history and wow, your grades were nothing to scoff at. Pretty, and smart? A girl after his heart, except that was a violation of so many school conducts that the idea was quickly carted off. He noticed starting from the fourth week that you were starting to find a voice in the class, and his attention all but zeroed in on you. The immense relief Leon felt when for the first time ever, a student actually tried to answer his question and not leave him to bask in awkward silence. It was only near the end of the lesson that he realized that his question was meant to be a rhetoric. It was an opening to the next chapter. You weren’t supposed to know what he was talking about, so how’d you know the answer? Do dean-listers just study ahead of class? “I just do some extra studying outside of class,” you had smiled sweetly up at him the one time he mustered the courage to approach you after the lecture ended, “you did a good job with this week’s lecture, by the way. The math was a little dry and confusing, but you made it a lot more bearable than it would’ve been.” The man was a real slump, but you could appreciate his effort, even if the exact opposite was reflected on his face every lesson. 

“Thank you,” caught off guard by the compliment, Leon sheepishly scratched at his chin, cheeks tinged warm, “if you ever need help, i’m usually free outside of lectures.” Both you and Leon blinked at each other. Whoa. Did the grumpiest professor you’ve ever interacted with just offer their time outside of class? Willingly? You were going to buy a lottery ticket later for your course code.

“Oh, I appreciate the offer,” your lips parted and closed as you tried to think of how to carry the conversation. You almost turned him down out of reflex, and frankly you never thought you’d make it to this stage. Sure, you were creeping just a little bit with the one sided after school supplementary class, but were you really about to push it? “how’s this friday?” The answer was yes. Yes, you were. Who knows? It might even be fun. This friday? Leon was going back home this friday to sleep away the school air and hopefully into a coma. Maybe he could sneak some drinks in, in his couch alone at home. That’s what he was doing this Friday. “This friday? I can do friday. I’ll email you later, and we can work out a time?” Or maybe not. “Sure! Thanks Prof,” he remembered how you beamed so warmly up at him, almost blinding, before strutting off with your bag hauled over one shoulder. With only the linger scent of your perfume tickling his nose, he was left to stand there by his lonesome.

It took a grand total of one and a half occasions for him to cave. The first was Friday. 

Friday came quick. Too quick, really. Maybe all that alcohol from a couple years back was finally coming back to fragment his memory, but it was like time was lost on him. Whatever time between that week’s lecture and Friday was lost on him while he was too busy imagining what the tutoring session would look like. Maybe he should smile a little more, come off more amicable and nice. Or should he just stick with the grumpy vibe? He knows that’s been hitting it off with some of the girls in school, he’s heard some of the passing comments. No, but you seem like a nice girl who would like a sweet guy. “Hey Prof, you okay?” Oh, why would you look at that? It seems his sense of time was failing him again. 

“Hm? I’m okay, just a little tired is all,” he blinked back to life, rubbing his face as he gave you a nonchalant wave of his hand, “don���t worry about me.” You frowned softly, eyes scanning him with an intensity that made Leon feel the same tingly warmth from last lecture. Before he could convince you any further, you leaned in close, and that might’ve been the closest Leon has ever been to a woman who didn’t have the ability nor intention to kill him in 3 seconds flat in a very long time.

He swallowed nervously, adam’s apple bobbing, but he otherwise made no move to push you away. Blue eyes flitted from your eyes; soft and glittery, down to your lips; Plump, pillowy and shiny. He noticed you usually had a tube of lip gloss on your desk during lectures. He went to google it, said it was strawberry flavoured. Suddenly, he was having cravings for strawberries. 

His lids fluttered, half lidded as he stared down at you, mind empty yet reeling all the same. What were you doing, little minx? “Your eyebags are pretty bad, a little too pale, your cheeks are kind of sunken as well. You should take care of your health a little more,” you suddenly said, before pulling away and returning back to your seat, back straightened as though nothing had happened. As though you didn’t lean in close enough for him to smell the strawberries off your lips. Didn’t threaten Leon’s self restraint to close the gap between the both of you. “ I can take care of myself. Thanks for the concern, but don’t worry about me kid,” he coughed, voice a low rumble as he glanced away. Right. He remembered reading about you being a medical student. He was getting ahead of himself. A doll like you with damaged goods like him? The notion was laughable, but Leon would never admit to the tinge of warmth that bloomed at the thought of it.

“Everyone could use a little help regardless of what stage of life you’re in,” you shrugged all to nonchalantly, like you were stating a fact. Which you were, before glancing towards him as you fished out this week’s study materials from your bag. “And you think you can help me?” “I’m sure I could be of some help, one way or another,” You flipped open your notebook, ipad on the side with your questions all prepared. What Leon wouldn’t give to have coworkers as efficient and enthused as you. Maybe he could put in a good word for you in his lab, pull you in for your internships. A relationship between co-workers would be alot less inappropriate than a relationship between professor and student. He knew he was still going to get shit from it from his office though, but that was a problem for later. Maybe then you could help him out. Out of his ditch of misery, out of his wandering mind, help him out of his pants. Whoa. Where did that come from?

He cleared his throat, swallowing his spit before picking up your notes. “We can talk about that another time. For now, what’re you having trouble with?” Half an hour in, and Leon was struggling. Fighting for his life, actually, because he’d been sporting a boner beneath the table 10 minutes in after your legs accidentally brushed against each other. He couldn’t tell if he was suffering from acute testosterone poisoning, and the horniness was deluding him into thinking that you were dropping him hints, or if you were genuinely showing some sort of interest in him. Your lashes fluttered when you stared up at him, lips coated in a sheen of gloss puffed into a soft pout everytime he explained something through tripped words and stutters. Everytime he found it in himself to knock the thoughts out of his head, you always found some innocuous way to enthrall him and his dick back into your whimsy, imaginary grasp. He wondered if your hands grab onto dicks as hard as you grabbed his attention. Just as Leon felt like he was finally going to see which would pop first; his dick or his blood pressure, the lesson was cut short. He wasn’t sure if he found the hour long session too short or too agonizingly long. Your eyes finally flickered away from him to your ringing cell, your lips rounded in surprise. “Sorry, this’ll be quick,” you gave him a sheepish little chuckle, manicured nails plucking the cell as you stood upright. To match, Leon’s cock sprung upright too. As you waltzed off, humming a small hello through the phone, all he could really see or hear was your bare thighs and waist, easily small enough for him to grab. And your ass? By god. He could see it from your physique. You were soft. Far softer than any of the ladies he had worked with for the last miserable 10 something years, all of which could easily deck and curbstomp him for having the thoughts he had towards you. 

You had a habit of leaning on one leg, Leon had noticed by the third class. You’d rest on one leg, your hips jutting out in that direction while the plush of your thigh squeezed beneath the hem of your pants to give a small pudge. Denim shorts day was a particular treat for him. Shame that today wasn’t one of those days, but it was still shorts day, so it was half a win for him. 

“Fine,” Leon blinked hard, gaze snapping right back up at the sound of your reluctant little sigh, “I’ll go, sure, but I’m not going for next week’s, I have some papers coming up. I’ll see about the week after,” you huffed into the phone, swapping the cell to the other hand so you could lean on your other leg. “Yeah?” He could hear your giggle, sweet and lithe. What other way more fitting words were there to describe you? “Alright, I’ll see you tonight. See you! Mhm, bye bye!” “Sorry about that, I thought I had my phone on silent, but I must’ve forgotten,” you slipped yourself back into your seat, your gaze rising from the screen of your phone back up to find leon’s, who was watching you ever so intently. “Some friends invited me to a party,” you supplemented, mistaking his stare for one of curiosity. 

Well, he wasn’t that curious before, but he certainly was now. He had heard all sorts of things about university parties, but never got the chance to actually experience one for obvious reasons. He had just about accepted his life ended at the tender age of 21 back in Raccoon City, before it was handed over and detained by the DSO for the unforeseeable remainder of his hopefully clipped life. 

So the idea of something as normal as a party charmed him, and through the shine of his eyes, you could tell. Your head tilted, an amusing little quirk of yours whenever your attention was hooked on something and the cogs in your head was turning. 

“You go to parties a lot?” he cleared his throat awkwardly, his turn to be fidgety under your scrutiny. He knew you were thinking. He knew you were thinking something of him, specifically. But he didn’t know what you were thinking. 

“I wouldn’t say a lot, I get invited a bunch but I don’t always go,” you word trailed off into a soft drone, mind pacing with considerations before you cracked a smile, “but would you like to come to this one?” “Uh, join you to a party?” the nervous chuckle slipped past his lips before he could even think to hold it back. You didn’t seem the slightest bit dejected from his apprehension however, instead choosing to press on. “You don’t have to of course, but if you’d like, you’re welcome to come to this one, it’s an open party, so other people will be there too!” 

 Oh god, what was happening. “I’ll uh, I’ll think about it?” He did. Sort of? He slept on it, more than anything. The rest of the session was a blur, you were a fast learner who pretty much solved the remainder of your own questions once you picked up on the first couple of questions. That, and he was pretty sure all the blood meant for his head was relocated to his dick, so forgive him if he was tripping over himself in a rush to get home and jerk himself off until his dick went raw.

By the next afternoon when he had stumbled out of bed with his crotch still sticky and bedside tissues stiff, imagine his surprise when we saw that you went ahead and did him the liberty of actually emailing him the party address; he had thought you were just saying it to be nice, honestly. 

‘Hey Professor Kennedy! Here’s the address for the party, again no pressure if you don’t feel like coming, but there’ll be free drinks if you do!

Take care!’ 

He spent way more time than he cared to admit considering your offer. Somehow, you’ve reduced him from a grouch wagering bets as to whether tomorrow would be the day he bites the bullet, into still too old of a man feeling like a perverted youth with a libido to match.

He thought long and hard through the myriad of fantasies that played out while he went to shower. As his hands absentmindedly lathered his soapy, blonde locks, his gaze fixed on the water stained glass. He could picture the droplets sliding down your back and past the curves of your ass. The size of the shower would force you to press flush against his chest, his stiff mast resting on your lower back, balls against the perk of your butt. 

Would you pant as he lays his weight on you, your breast pressed up against the glass and the shaft of his dick shower in the slippery dip of your pussy? Maybe you’d mewl as he toys with your nipples, rough pads pinching and twisting at the nipples while grubby hands knead and paw at the plush of your chest. He bet he could make your breath hitch and your eyes well with tears as he feeds just the tip of his dick to your gummy walls, never pushing himself all the way in. Just the tip, until you’re begging like he was your lifeline and that you’d be his good girl. 

His jaw clenched, chest tight and knees buckled as milky fluids splattered against the glass, catching the drops of water that rolled down. Leon’s lips parted as he blinked himself back to the present, the fluorescent light making it difficult for his sight to return, his ears ringing while his chest heaved desperately for air. 

For that second that your imaginary presence coaxed his undoing, he forgot how to breathe.For as much as he wants to be your lifeline, you were quickly becoming his.

[shiut]

Homunculus Research (the kinda scientific edition)

Time for me to do the thing that I do where I think way too much about barely explained fictional science and try my best to apply actual science to it. For fun.

So, here is my biological summary for the homunculi of Rain Code, which will be mostly non-canon speculation.

What is a homunculus? A homunculus is an artificially created, cloned individual using the genetic information of a human for the purpose of developing immortality and regeneration applicable to military use.

What is a homunculus made of and how? A homunculus is created from gram-negative bacteria and human cells through complete recombinant DNA cloning. This technique is achieved through taking the genes of the human donor and incorporating the information into a bacterial chromosomal DNA and plasmid(the secondary circular DNA molecule of bacteria used for gene replication and transfer). Additionally, the incorporation of the enzyme telomerase and protein p53 is applied.

What contributes to a homunculus's regenerative properties and immortality? Homunculi exhibit accelerated initial growth and healing thanks to the bacterial hybridization of their cells. Bacteria have one of the fastest replication rates, and can replicate at a rate of about every 10 minutes compared to the average human cell's replication rate of every 24 hours. Gram-negative bacteria also have a complex layering of membrane that allow them to be more resistant to antibiotics and a more sturdy structure. Bacteria have the ability to go through inactivation, where they go into a state of metabolic dormancy that protect them and allow them to be able to wait out periods of extreme conditions and nutrient scarcity. Telomerase, the 'immortality enzyme', is utilized for its function in restoring the length of telomeres. Telomeres are a protective chromosomal cap that normally erode with each cell division, and it's this shortening that causes DNA damage and aging in humans. Telomerase repairs this erosion and allows cells to divide indefinitely. However, because of telomerase's link to increased rates of cancer, additional copies of the gene responsible for the production of p53 protein is also incorporated. P53 is a tumor suppressor that allows damaged cells to repair themselves before dividing, which prevents the spread of cancerous cells.

Why is homunculus blood pink? Gram-negative bacteria is identifiable for its bright pink color by using the gram staining method. This is because the characteristic cell wall structure of gram-negative bacteria which makes them so resilient also causes the bacteria to display the color of the safranin. Homunculus researchers may apply a gram staining process to the circulatory system of homunculi for the purpose of identification and observation.

Relevance of gram-negative bacteria in gene cloning and military research. The most commonly used strain of bacteria used in gene cloning research is the gram-negative bacteria such as e. coli for its ready availability, ease of growth and manipulation, and simplicity. Gram-negative bacteria such as e. coli has a history in military research, in cases such as a probiotic when an army surgeon isolated a strain found in a soldier who, unlike his comrades, did not develop an illness from an infectious outbreak.

What is the zombified state of imperfect homunculi? It is the result of cell inactivation that, while it is a protective measure for the cells, the slowed or halted metabolic state causes the low-functioning mental and physical faculties that present zombie-like symptoms, and is currently difficult to impossible to reverse in imperfect homunculi due to their varying degrees of cellular instability.

Why do imperfect homunculi require compounds found in human flesh for nutrients? Plasmid stability in DNA cloned cells is often influenced by the original donor's genotype. Imperfect homunculi cells may include defects in the cell division process where the stability of the human DNA contained in the cell plasmid results in incomplete DNA replication, whereas each division causes informational gaps in the gene and interrupt protein synthesis. These gaps can be filled and repaired by taking and incorporating the required information from a healthy human cell through the process of horizontal gene transfer. Human matter must be consumed and broken down in order for the homunculus cells to initiate this process. The lack of these nutrients can cause the homunculus cells to go into a state of inactivation.

Why are imperfect homunculi vulnerable to sunlight? UV has been known to exhibit antimicrobial effects. Many bacteria, especially gram-negative bacteria, are averse to sunlight. Exposure to the UV radiation in sunlight results in the damage or solar induced inactivation of unstable homunculus cells.

Written, hopefully, as simplified and concise as possible for readability. I feel like I'm forgetting more things I wanted to address, but maybe I'll just leave it here and just make more parts if I think of it :P

[justkidneying]

Why do people get red eyes in photographs?

This is due to how light reflects once it enters the eye. The back of the eye is highly vascularized. When light enters the pupil and reflects, red light is what is reflected (from the blood). This is why "red eye" cameras flash twice. The first flash causes the pupil to constrict and the second is for the actual picture.

Now onto some fun red reflex stuff. Testing the red reflex (if someone gets red eye) is important in the diagnosis of retinoblastoma, a type of cancer that happens in children when they lack retinoblastoma proteins (a type of tumor suppressor gene that stops the cell cycle). These children will not have red eyes in photographs, but white eyes instead, due to the cancer's white surface reflecting light. This is also called "cat's eye" because it looks like the white reflection of cat's eyes (called tapetum lucidum and is the reason many animals can see in the dark, as this allows light to hit the retina twice). People with cataracts will also have a negative red reflex test.

Another note about albinism (both occular and occulocutaneous types) is that albino people do not have red eyes. Their eyes are usually blue or a light lavender color. However, this means that their irises are not able to block out much light, so they may always have red eyes in photographs, even when their pupil contricts.

[wtffacts]

Elephants rarely get cancer because they have 40 copies of genes that code for the tumor suppressor protein p53 — humans have two.

[anulithots]

Random ask, can I ask what are apoptosis and caspases (in simple terms)?

I have been summoned

(my 'noorie rambles. be very afraid' tag will make so much sense now. I tried to talk about it in a way that's a way that's both engaging and simple. Lots of metaphors.)

Caspases destroy the cell if it needs to die. They dismantle the cell parts as the cell membrane turns into bubbles, containing all the damaged pieces within so that a white blood cell might disposes of them. That's apoptosis in a nutshell.

But why must the cell die you ask?

Plenty of reasons. Human embryos have webbed fingers, and apoptosis causes the webbing to dissipate. Tadpoles too, use apoptosis to rid of their tails so they can become frogs. Apoptosis opposes growth - aka mitosis - and it keeps the body in homeostasis - or a balance of sorts. The destruction to mitosis's creation.

However, what I find most interesting, what is the subject of much research nowadays, and what holds the most opportunity for angsty biology fanfics (most important/j) is that apoptosis opposes tumorigenesis. In other words, if something goes wrong, if the cell gets some notion that it might try to cheat death and live forever, if it has the inklings of an idea to hijack the rest of the body through growing its own lump of cells and draining the body of its nutrients... if it decides to throw a mutiny at the expense of peace...

Then the cellular system realizes, and it activates the caspases.

(Usually how a cell 'decides' is when something wrong happens with genetic replication, mutations and such and such. There are two labels of genes relating to this. Proto-oncogenes promote cell growth and avoid apoptosis - these are the creation genes, the ones that wish to achieve the heights of production and throw all caution to the wind. Whereas tumor suppressor genes are... tumor suppressors. They are the little 'angel on the cell's shoulder' that says 'you've done wrong, now commit cell death and accept your fate'. When a proto-oncogene mutates, it becomes an oncogene. Basically, the genes that said to grow for the sake of the body now says to grow at the expense of the body, the 'devil on the cell's shoulder' won... and now it'll try to cheat death)

Caspases are a type of enzyme, which is a subset of proteins. I like thinking about it like this: enzymes are witches, spell crafters. Proteins in general function like worker bees, but enzymes are the ones who actively create and destroy, the ones that change the way the universe manifests so life can exist. They utilize reactants from their environment - materials which they are named after, such as proteases that cleave other proteins - to either create larger, energy storing molecules (endergonic reactions), or break down large, energy storing molecules to release energy (exergonic reactions).

(One type of enzyme that I like is called kinases, they basically initiate things, they tell the cell 'it's okay to do things' or 'this will be dangerous, let's not do that', or 'oof this cell doesn't have the proper genes, that could be a problem, how about we destroy everything so this doesn't become a big issue?')

When the cell needs to die, the caspases activate.

Humans have 14 caspases. I wish I knew what all of them are, but the pub med articles I read do not have a whole list of them like a pokedex from pokemon (at least that I have read so far, after ap testing there's one article I want to read that seems to have ANSWERS to a lot of my questions)

So imagine this, the cell has lots of caspases floating around in the cytoplasm/water jelly environment. These beings of death in huge numbers in a perpetual slumber, just floating around, until the cell decides it needs them to destroy its existence, and it activates them.

(ALTHOUGH some of my questions refer to the "caspase-dependent non-lethal cellular processes", so far what I've been able to find is that if the cell needs some repair to the cytoskeleton/structure of the cell, then it activates a few caspases to destroy parts of it, so that the repair may start.)

There are two types: inflammatory caspases (if I remember correctly, this is caspase 1,4, and... a few others I'll have to check) and apoptotic caspases. What we're interested in are the apoptotic caspases. Initiator caspases get activated first. The way I story-fy them/see them in my head is as the older sibling types who condone violence. If the cell needs to die because of an external signal - a message from far away to destroy itself, to which it must oblige - then caspase 8 activates. If the cell needs to die because of an internal signal - something inside isn't right, and what a havoc it would be to pass that on through replication, so the proteins decide the fate of the world it lives in, and it choses death for the sake of the wider body- then caspase 9 activates.

Both these initiator caspases cleave (meaning 'cut', these inactive beasts are not yet 'complete', so they need further modification after activation to work properly. If the cell were to create caspases fully functional and finished, the large number of caspases would kill the entire cell, so they don't finish, they subdue the ones behind their death, and make sure to regulate their slumber.) their 'younger, violent siblings': caspase 7 and caspase 3. The doll I have is a caspase 3.

(I've found more information on them than caspase 7... although.. the one article I found.... it should have information on them all, the amount of searching I've done for those sorts of answers... but alas... I need to read the material for the ap bio exam... which does not include caspases.... one day...)

Caspase 3, as far as I could gather, destroys the cytoskeleton. The cytoskeleton supports the entire cell, acting as the 'tent poles' that keep the floppy cell membrane from collapsing. Collapsing, however, is exactly what the caspase 3 wants. It dismantles the whole thing, along with activating and inactivating a slew of other proteins. (it's an assassin basically.)

And with this, the caspases bow, for the cell is separated within these small little 'blebs' (they look like bubbles) and the cell is destroyed.

OH AND LAST LITTLE THING!

If something inhibits the caspases, the cell goes through with necrosis, which is basically instead of becoming little bubbles, the cell membrane ruptures and the cell 'guts spill out'

THANK YOU SO MUCH FOR THE ASK!! <3 <3 I got to blabber about caspases and it gave me happy sparkles.

ALSO, here's the doll I made for caspase 3:

[didanawisgi]

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and COVID-19 infection has led to worsened outcomes for patients with cancer. SARS-CoV-2 spike protein mediates host cell infection and cell-cell fusion that causes stabilization of tumor suppressor p53 protein. In-silico analysis previously suggested that SARS-CoV-2 spike interacts with p53 directly but this putative interaction has not been demonstrated in cells. We examined the interaction between SARS-CoV-2 spike, p53 and MDM2 (E3 ligase, which mediates p53 degradation) in cancer cells using an immunoprecipitation assay. We observed that SARS-CoV-2 spike protein interrupts p53-MDM2 protein interaction but did not detect SARS-CoV-2 spike bound with p53 protein in the cancer cells. We further observed that SARS-CoV-2 spike suppresses p53 transcriptional activity in cancer cells including after nutlin exposure of wild-type p53-, spike S2-expressing tumor cells and inhibits chemotherapy-induced p53 gene activation of p21(WAF1), TRAIL Death Receptor DR5 and MDM2. The suppressive effect of SARS-CoV-2 spike on p53-dependent gene activation provides a potential molecular mechanism by which SARS-CoV-2 infection may impact tumorigenesis, tumor progression and chemotherapy sensitivity. In fact, cisplatin-treated tumor cells expressing spike S2 were found to have increased cell viability as compared to control cells. Further observations on gamma-H2AX expression in spike S2-expressing cells treated with cisplatin may indicate altered DNA damage sensing in the DNA damage response pathway. The preliminary observations reported here warrant further studies to unravel the impact of SARS-CoV-2 and its various encoded proteins including spike on pathways of tumorigenesis and response to cancer therapeutics.

[letthestorieslive]

Scott McCall's Guide to Become a Vet

Rating : G Chapters : 1/1 Word Count : 1,384 Characters : Scott McCall, Menace the black cat Relevant Tags : A Bit of Angst, A Sprinkle of Past Trauma, Scott McCall-centric, Scott McCall is a Sweetheart, And a Student at UC Davis School of Veterinary Medecine, study session

TSG, the flashcard reads. “Easy,” Scott says aloud, “there’s two categories of tumor suppressor genes: caretaker and gatekeeper.” Scott flips the card and allows himself a satisfied smile as his answer matches the one on the card. He tosses it to the success pile before looking down at the next one.

Read on ao3

For Scottuary 2024

[importantwomensbirthdays]

Ruth Sager

Ruth Sager was born in 1918 in Chicago, Illinois. Sager was a geneticist whose research challenged the widespread view that all genetic information was located in the nucleus of the cell. Later in her career, at Dana Farber Cancer Institute, she conducted research on tumor suppressor genes. Sager was elected to the National Academy of Sciences in 1977.

Ruth Sager died in 1997 at the age of 79.

[residents-of-the-darkforest]

I have a malfunctioning tumor suppressor gene. (PTENÂ). It's linked to autism, ADHD, and things growing in and on my body where they aren't supposed to be. I got a three hour scan on my leg which was really really really not fun but it identified a lump there that is benign. There are about 40 thyroid nodules in my thyroid, probably gonna get my thyroid out eventually. Nobody else in my family has this mutation (though my mothers family has a history of thyroid disease). It's classified as rare!

oh holy wow!

[moonstruck-stormy]

May have RSV(respiratory syncytial virus), will be going back to the doctors tomorrow for a test bc I was only tested for Covid (there’s a rsv outbreak in my state apparently among Covid and the flu)

It sucks to admit that I’m sickly. My friend is familiar with the disorder I have bc his aunt has it too, and he said she’s sickly like me. And I was like ????.

It didn’t process even as a former bio major that the lack of one of the nervous system tumor suppressors can influence my immune system’s capabilities.

I just thought it was normal to get sick cyclically. February, May, July, November again and again. I used to get repeated sinus infections every single February. It took a lot of care to not catch Covid.

Ik I shouldn’t expect my neurologist to tell me everything about my disorder, but everything is like loosely connected that it’s like “what doesn’t this disorder do?”

(I know the answer which is it doesn’t kill me directly but like if someone with nf1 dies of cancer would you also attribute the lack of neurofibromin 1 as a contributor?)

I should be more proactive and tell her things that seem innocuous, but I don’t know what’s abnormal or not, and I don’t want to make a fuss over nothing.

NF1 isn’t even a disability under the law eyes of the law because half the people with it don’t even display symptoms.

Genetics are so confusing, man.

Polyploidy but only half of the time, genetically dominant but can skip a generation only sometimes. A mutation, but they can predict where on the very large gene that nf1 affects got mutated. What the hell?

So uh, I hope I don’t have RSV, bc apparently for the very sickly it can last weeks up to a whole month possibly more.

Sorry for the vent I’m gonna draw to feel better

[scraffles]

p53

during shadowkeep through season of the dawn the now *insanely* relevant 'Unveiling' lorebook was released. one of the lorebooks is titled p53.

p53 is a protein of proton weight 47,000 and it is responsible for the cessation of potentially cancerous cells. the voice in the darkness/ winnower posits that it is necessary for life to function, but is also a bomb waiting to detonate:

"Would you tolerate a bomb in your body, waiting to detonate if you deviated from the needs of society?

However, without p53 as an enforcer, the body's utopian surplus of energy becomes a paradise for cancer. Cells cannot resist the temptation to steal from that surplus. Their genetic morality degrades as tumor suppressor genes fail. The only way to stop them is by punishment."

the voice ends the tab positing the question "Is p53 an agent of the Darkness, or the Light?"

this is a very interesting way to look at p53. and poses to us a concept-- that a thing must necessarily inhibit life in order for more, greater life to continue to exist. now allow me to bring in another, separate concept.

In the 9th entry, "The Wager" , the voice in the dark/winnower states the insanely raw line "You are the gardener's final argument." But more importantly, it states "That wandering refugee [Traveler/Gardener]* chose to make a stand, spend their power to say: "Here I prove myself right. Here I wager that, given power over physics and the trust of absolute freedom, people [you, guardian] will choose to build and protect a gentle kingdom ringed in spears."

i posit that the voice is incorrect, or rather incomplete. it is not that p53 exists as an agent of darkness' will; i instead posit that p53 exists as the aforementioned "ring of spears" against the *true* darkness: cancer. Cancer, by virtue of existence, kills. It is the only thing it knows how to do (though this is framed incorrectly perhaps; cancer only knows how to duplicate, but by duplicating it drains necessary resources, which result in death. to say a cancerous cell is birthed to kill and then die is merely skipping the middle of the syllogism). That sounds, familiar! In "The First Knife" the voice states "And I had only one purpose and one principle in the game. And I could do nothing but continue to enact that purpose, because it was all that I was and ever would be." Seems a little damning, no? But I do not disagree with p53's classification as an element of darkness. It is a bomb. But am I not a bomb? Do I not kill? Have I never snuffed out a consciousness? Contained within my cellular structure is indeed p53.

I posit that the ring of spears is necessarily darkness.

In the final page of the lorebook, I think the Queen of the Reef describes heaven (or at least some place akin to it), and not here. She states, "

Given the choice to live in any world, any world at all… we would need a little Darkness in it, I think, to keep the balance true. But not so much as we would need the Light…"

Understanding this as an ideal, and not a description of reality as fact, the point comes into focus. The light in its current form, exists. To exist is to prove your existence to use the words of another. I think, understanding this ring of spears as a concept of darkness, the Gardener makes its argument. necessarily we must prove that we exist. because to not do so equates to death.

it means that you must prove your right to live against forces who are very eager to demand proof.

That ring of spears, it is starting to drip with epistemological proof.

The final shape is the paring back of all that can be. That which remains when all that can be removed, has been removed. That which remains after it has been winnowed; after the garden has been tended to. That beautiful, final shape of the garden. Of the flowers and the hedges, the full completion, perfected. In layman's terms, it is the extermination of all life that cannot prove its existence. That cannot prove its *right* to live | exist. That is the philosophy of the final shape. Of the Darkness. or at the very least, all of our enemies right now :)c .

Let us pare back of the darkness what we need. That epistemological proof. That right to exist. That ring of spears.

p53, nuclear weight of 47000, is an element of the darkness;

however, to understand p53 as an *agent* of the darkness is to misunderstand its purpose. That is why I believe the voice is incorrect.

To understand the ring of spears as an agent of the darkness is to misunderstand its purpose.

~~~~~~~

*[the familiarity conjured by 'wandering refugee' seems to directly refer to the Traveler, as opposed to the ideological Gardener which really makes me doubt if this is the winnower, and not some force beyond (maybe this is the witness speaking?). then again the nonchalance the voice brings to the table, "my man oryx", for example, suggests power, almost? i dont know how to properly describe it. the way that this voice speaks to us is this bizarre realm of nonchalance and it almost even feels like condescension at points which feels almost like the point but i dont understand the point that it is trying to make]

...is the name of this lore book supposed to be a pun on 'the veil'...?

also on the wikipedia page for p53 it says

and that feels pretty on the nose

[twinkl22004]

Tumor Suppressor p53 Protein , Victor McKusick, Mendelian Inheritance in Man, 1966.

Here I present: “Tumor Suppressor p53 Protein”, Victor McKusick, Mendelian Inheritance in Man’, 1966. INTRODUCTION. Tumor Suppressor p53 Protein encoded by the TP53 gene, is the most frequently mutated gene in cancer. There is evidence that the tumor protein p53-binding protein-2 (TP53BP2) gene is on cytogenetic location 1q41  and genomic coordinates1:223,779,893-223,845,947 .  The screenshot of…

[colinwilson11]

The cGAS-STING Pathway: A Key Immune Surveillance Mechanism

The innate immune system provides the first line of defense against invading pathogens like viruses and bacteria. One of its key mechanisms for detecting microbial infections is the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway. This cellular surveillance pathway plays a critical role in detecting foreign DNA from invading microbes and mounting appropriate immune responses.

How It Works

When microbial DNA enters the cytosol of host cells, it is recognized by the cGAS enzyme. cGAS has the unique ability to bind to DNA and produce the second messenger cyclic GAMP (cGAMP) from ATP and GTP. cGAMP then acts as a ligand to bind and activate the endoplasmic reticulum-associated adaptor protein called STING.

Activation of STING leads to its association with tumor necrosis factor receptor-associated factor 3 and 6 (TRAF3/6). This triggers a downstream signaling cascade involving the protein kinases TANK-binding kinase 1 (TBK1) and interferon regulatory factor 3 (IRF3).

Phosphorylation of IRF3 by TBK1 causes IRF3 dimerization and translocation into the host cell nucleus. There, IRF3 induces the expression of Type I interferons (IFN-α and IFN-β) and other proinflammatory cytokines that signal the presence of invading pathogens to other cells and recruit additional immune defenses.

Role In Antiviral Defense

The cGAS-STING Pathway plays a critical role in the host defense against various DNA viruses like herpes simplex virus 1, cytomegalovirus, Epstein-Barr virus, vaccinia virus and HIV. Upon viral DNA entry in the cytosol, cGAS binds and activates STING to induce Type I IFN production. This initiates an antiviral state in infected cells and neighboring uninfected cells to limit viral replication and spread. Mice lacking cGAS or STING exhibit impaired IFN responses and increased susceptibility to infection by these DNA viruses.

Protecting Against Cancer

Aside from fighting infections, the cGAS-STING Pathway also acts as a tumor suppressor mechanism by detecting aberrant genomic DNA in cancer cells. Many cancer cells have disruptions like broken DNA strands that could lead to cell death if sensed by the immune system. However, cancer cells often develop ways to evade this cGAS-STING surveillance.

Studies have shown that loss of or reduced expression and activity of cGAS or STING promotes tumorigenesis in various cancer types like colon cancer and prostate cancer. At the same time, therapeutically activating the cGAS-STING Pathway seems to stimulate antitumor immunity and enhance the effectiveness of cancer immunotherapies in mouse models. This highlights the pathway's potential for developing new immunotherapeutic strategies against cancer.

Role In Autoimmune Disease

While the cGAS-STING Pathway protects against infections and tumors, its overactivation can also lead to inflammatory and autoimmune conditions. Defects that cause constitutive STING signaling have been linked to autoinflammatory diseases. Genetic mutations that make STING hyperactive and uncontrollable result in a group of rare hereditary inflammatory syndromes known as STING-associated vasculopathies with onset in infancy (SAVI). Patients with SAVI exhibit symptoms resembling systemic lupus erythematosus due to excess Type I IFN production.

Meanwhile, environmental and endogenous cytosolic DNA from dying cells have been shown to aberrantly trigger the cGAS-STING Pathway and IFN responses during conditions like systemic lupus erythematosus or Aicardi-Goutières syndrome. Figuring out ways to modulate cGAS-STING activation or signaling may yield new therapeutic approaches for these diseases.

Pharmaceutical Applications

Given its crucial contribution to antiviral immunity and cancer immunosurveillance, the cGAS-STING Pathway represents an attractive target for pharmaceutical intervention. Small molecule drugs that activate cGAS or STING are being developed as potential antiviral and anticancer agents. STING agonists administered alone or in combination with checkpoint inhibition immunotherapy show promise in treating solid tumors in clinical trials.

Moreover, cGAS or STING inhibitors may offer new ways to treat autoinflammatory conditions caused by overactive cGAS-STING signaling. Researchers continue working to refine drugs that can selectively modulate different points along the pathway for optimal therapeutic benefit while avoiding side effects. As understanding of this defense mechanism deepens, more opportunities may arise to harness it against an array of diseases with immunological underpinnings.

The cGAS-STING Pathway serves as a critical surveillance system helping our innate immune defenses detect cytosolic DNA. Its ability to sense microbial as well as aberrant self-DNA makes it an important regulator of antiviral immunity, tumor suppression, and inflammatory balance. Ongoing investigations into modulating cGAS-STING activation hold promise for developing new immunotherapies targeting infections, cancer, and autoimmune disorders.

Get more insights on this topic:   https://www.ukwebwire.com/role-of-cgas-sting-pathway-in-detecting-cytosolic-dna/

Author Bio:

Alice Mutum is a seasoned senior content editor at Coherent  Insights, leveraging extensive expertise gained from her previous role as a content writer. With seven years in content development, Alice masterfully employs SEO best practices and cutting-edge digital ing strategies to craft high-ranking, impactful content. As an editor, she meticulously ensures flawless grammar and punctuation, precise data accuracy, and perfect alignment with audience needs in every research report. Alice's dedication to excellence and her strategic approach to content make her an invaluable asset in the world of  insights. (LinkedIn: www.linkedin.com/in/alice-mutum-3b247b137 )

*Note: 1. Source: Coherent  Insights, Public sources, Desk research 2. We have leveraged AI tools to mine information and compile it

[gsuniversityofficial]

Types, Risk Factors, Symptoms, and Treatment of Brain Tumor

Brain tumors are complex and varied, impacting the central nervous system in diverse ways. They can occur in any part of the brain and affect various functions depending on their location, size, and type. Understanding the types, risk factors, symptoms, and treatment options for brain tumors is crucial for early diagnosis and effective management.

At GS Super Speciality Hospital, we offer comprehensive care for brain tumor patients, leveraging advanced medical technologies and expert neurology and neurosurgery teams to provide the best possible outcomes.

Types of Brain Tumors:

Brain tumors are categorized into two main types: primary and secondary. Each category includes various tumor types with distinct origins and characteristics.

 

Primary Brain Tumors:

Primary brain tumors originate directly in the brain or surrounding tissues. Common types include:

Gliomas: Arising from glial cells that support and protect nerve cells, gliomas include:

Astrocytomas: These tumors develop from astrocytes, a type of glial cell. They are classified into grades I-IV, with higher grades indicating more aggressive and malignant forms.

Oligodendrogliomas: Tumors that originate from oligodendrocytes, which are responsible for producing myelin, the nerve cell's protective covering.

Ependymomas: Develop from ependymal cells lining the brain's ventricles and the spinal cord. These tumors can affect cerebrospinal fluid flow.

Meningiomas: These tumors start in the meninges, the protective membranes surrounding the brain and spinal cord. While often benign, they can cause significant symptoms depending on their location and size.

Medulloblastomas: Primarily found in children, medulloblastomas are highly malignant tumors that arise in the cerebellum, which controls coordination and balance.

Pituitary Tumors: These tumors form in the pituitary gland, which regulates hormones throughout the body. They can disrupt hormone balance and lead to various systemic symptoms.

 

Secondary Brain Tumors:

Secondary brain tumors, or metastatic brain tumors, result from cancer cells spreading from other parts of the body. Common origins include:

Lung Cancer: The most frequent source of brain metastases, lung cancer cells can spread to the brain.

Breast Cancer: Another common origin of brain metastases, often affecting women with a history of breast cancer.

Melanoma: Skin cancer that can spread to the brain, making early detection and treatment crucial for managing overall prognosis.

Understanding these tumor types is essential for diagnosis, treatment planning, and managing the impacts of brain tumors on overall health.

Risk Factors for Brain Tumors:

Several factors can increase the likelihood of developing a brain tumor, although not everyone with these risk factors will develop the condition. Understanding these risk factors can help with early detection and prevention. Key risk factors include:

Genetic Factors:

Family History: Inherited genetic conditions can heighten the risk of brain tumors. Examples include:

Neurofibromatosis: A genetic disorder that leads to the growth of benign and malignant tumors on nerve tissues.

Li-Fraumeni Syndrome: A rare genetic disorder that increases susceptibility to multiple cancers, including brain tumors.

Genetic Mutations: Certain mutations, particularly in tumor suppressor genes, may predispose individuals to brain tumors.

Environmental Factors:

Exposure to Radiation: Previous exposure to radiation therapy, particularly in the head or neck area during childhood, significantly raises the risk of brain tumors.

Chemical Exposures: Some studies suggest that long-term exposure to industrial chemicals or solvents may increase the risk of brain tumors. However, evidence remains inconclusive.

Other Factors:

Age: Although brain tumors can occur at any age, they are more frequently diagnosed in children and adults over the age of 60.

Gender: Certain brain tumors are more common in one gender than the other. For example:

Meningiomas: More common in women.

Gliomas: More prevalent in men.

These risk factors can serve as a guide for understanding susceptibility but do not guarantee the development of brain tumors.

 

Managing Life after Treatment:

Post-treatment care is essential for ensuring long-term health and quality of life for brain tumor survivors. Effective management includes:

 

Regular Follow-Up Appointments:

Tumor Monitoring: Routine imaging and assessments to check for any signs of tumor recurrence.

Side Effect Management: Ongoing evaluation to address and manage any lingering or new side effects from treatment.

 

Rehabilitation Services:

Physical Therapy: Helps restore movement, strength, and coordination, improving daily functioning and mobility.

Occupational Therapy: Aims to enhance the ability to perform everyday activities and adapt to any changes in physical or cognitive abilities.

Speech Therapy: Supports recovery of communication skills and cognitive function, particularly if affected by surgery or treatment.

 

Psychological Support:

Counseling: Provides emotional support to help patients cope with the psychological impacts of brain tumor diagnosis and treatment.

Support Groups: Offers a community of individuals with similar experiences, providing shared understanding and encouragement.

These strategies ensure that patients receive comprehensive care and support to facilitate their recovery and maintain a good quality of life after treatment.

Symptoms of Brain Tumors:

Brain tumor symptoms can vary significantly depending on the type, size, and location of the tumor. Early recognition of these symptoms is crucial for prompt diagnosis and treatment.

 

General Symptoms:

Headaches: Persistent or worsening headaches, particularly those that are more severe in the morning or become progressively worse over time.

Nausea and Vomiting: Unexplained nausea and vomiting, often occurring without any apparent cause, and worsening as the tumor grows.

 

Neurological Symptoms:

Seizures: New-onset seizures or changes in existing seizure patterns are often one of the first signs of a brain tumor.

Cognitive Changes: Memory loss, confusion, difficulty concentrating, or changes in problem-solving abilities.

Speech or Vision Changes: Trouble speaking, understanding language, blurred vision, or sudden loss of vision.

 

Physical Symptoms:

Weakness or Numbness: Weakness, numbness, or tingling in the arms or legs, usually on one side of the body.

Coordination Issues: Difficulty with balance, coordination, or walking, making everyday tasks more challenging.

Personality or Behavioral Changes: Changes in personality, mood swings, increased irritability, or even aggression.

Diagnosing Brain Tumors at GS Super Speciality Hospital:

In the Top 10 private hospitals in Uttar Pradesh at GS Super Speciality Hospital, advanced diagnostic tools are used to confirm the presence and nature of brain tumors, ensuring accurate treatment planning.

 

Imaging Tests:

Magnetic Resonance Imaging (MRI): Provides high-resolution images to locate and analyze brain tumors.

Computed Tomography (CT) Scan: Offers a detailed view of the tumor’s size and impact on surrounding structures.

Positron Emission Tomography (PET) Scan: Assesses tumor activity and potential spread.

 

Biopsy:

Surgical Biopsy: Tumor tissue is sampled during surgery.

Needle Biopsy: A needle extracts a small tissue sample for analysis.

 

Other Diagnostic Tests:

Lumbar Puncture: Examines cerebrospinal fluid for cancer cells.

Genetic Testing: Identifies specific genetic mutations linked to the tumor.

 

Treatment Options for Brain Tumors:

Treatment for brain tumors is highly individualized, aiming to effectively target the tumor while preserving brain function and overall health. A comprehensive treatment plan may include one or more of the following options:

Surgery:

Surgery is often the first line of treatment for brain tumors, aiming to remove as much of the tumor as possible while minimizing damage to surrounding brain tissue. Surgical options include:

Craniotomy: This procedure involves removing a portion of the skull to access and excise the tumor. The extent of removal depends on the tumor’s location, size, and type.

Stereotactic Surgery: A minimally invasive technique that uses precise imaging guidance to target and remove the tumor with high accuracy, reducing damage to healthy tissue.

 

Radiation Therapy:

Radiation therapy uses high-energy rays to destroy cancer cells and shrink tumors. It is often used in conjunction with surgery or as a primary treatment for tumors that cannot be surgically removed. Types include:

External Beam Radiation: Radiation is delivered from outside the body using a machine that targets the tumor.

Stereotactic Radiosurgery: This non-invasive technique employs focused radiation beams to treat tumors with extreme precision, often used for small or inoperable tumors.

 

Chemotherapy:

Chemotherapy involves using drugs to kill cancer cells throughout the body. This treatment can be administered orally or intravenously and is often used in combination with surgery and radiation. It is particularly useful for malignant tumors and metastatic brain tumors.

 

Targeted Therapy:

Targeted therapy involves drugs that specifically attack cancer cells based on their molecular and genetic profiles. These therapies can be more effective and have fewer side effects than traditional chemotherapy. They are used alone or alongside other treatments.

 

Immunotherapy:

Immunotherapy harnesses the body’s immune system to combat cancer cells. Treatments include:

Checkpoint Inhibitors: Drugs that help the immune system recognize and attack cancer cells.

Monoclonal Antibodies: Lab-made molecules that bind to cancer cells and mark them for destruction by the immune system.

 

Supportive Care:

Supportive care focuses on enhancing the patient’s quality of life throughout treatment. It includes:

Pain Management: Medications and therapies to manage pain.

Anti-Nausea Medications: Drugs to alleviate nausea and vomiting caused by treatments.

Cognitive and Emotional Support: Psychological support and therapies to help patients cope with cognitive changes and emotional stress.

These treatments are often combined to achieve the best possible outcome and are tailored to the specific characteristics of the tumor and the patient’s overall health.

Why Choose GS Hospital for Brain Tumor Treatment?:

10 Best Neurology Hospitals in Uttar Pradesh like GS Hospital stands out as a leading institution for the diagnosis and treatment of brain tumors, offering unparalleled care through advanced technology, expert medical teams, and a patient-centered approach. Here’s why GS Hospital is the top choice for brain tumor treatment:

Advanced Technology:

GS Hospital utilizes the latest technology to ensure precise diagnosis and effective treatment of brain tumors. The facility features:

State-of-the-Art Imaging Systems: Advanced MRI, CT scans, and PET scans for accurate tumor detection and monitoring.

Cutting-Edge Surgical Equipment: High-resolution microscopes, neuronavigation systems, and intraoperative imaging tools for precise tumor removal and minimal invasiveness.

Expert Medical Team:

The hospital boasts a multidisciplinary team of specialists dedicated to brain tumor care:

Neurosurgeons: Skilled in complex brain surgeries with a focus on preserving neurological function.

Neurologists: Experts in diagnosing and managing neurological symptoms associated with brain tumors.

Oncologists: Specialists in radiation and chemotherapy tailored to brain tumor types.

Radiologists: Professionals adept at interpreting advanced imaging and guiding treatment decisions.

 

Personalized Treatment Plans:

One of the Best Neurosurgery Hospitals in UP like GS Hospital provides individualized treatment plans that are:

Tailored to each Patient: Plans are based on the tumor’s type, location, and stage, as well as the patient’s overall health.

Collaborative Approach: Treatment strategies are developed through consultations among specialists to ensure comprehensive care.

 

Comprehensive Support Services:

In addition to medical treatment, GS Hospital offers extensive support services:

Psychological Support: Counseling and mental health services to help patients and families cope with the emotional impact of a brain tumor diagnosis.

Rehabilitation Services: Physical, occupational, and speech therapy to aid in recovery and enhance quality of life.

Counseling and Education: Resources and guidance for navigating treatment options and managing side effects.

 

Research and Innovation:

The hospital is at the forefront of medical research and innovation:

Ongoing Research: Participation in clinical trials and studies to explore new treatments and improve patient outcomes.

Access to Latest Therapies: Availability of cutting-edge therapies and experimental treatments as part of research programs.

 

Patient-Centered Care:

GS Hospital is dedicated to providing compassionate and patient-centered care:

Holistic Care: Emphasis on addressing the physical, emotional, and psychological needs of patients and their families.

Informed Decision-Making: Ensuring patients are well-informed and actively involved in their treatment decisions.

By combining advanced technology, expert care, personalized treatment, and comprehensive support, GS Hospital offers a holistic approach to brain tumor management, striving to achieve the best possible outcomes for its patients.

Conclusion:

Brain tumors are a serious and complex condition that requires prompt and effective management. Understanding the types, risk factors, symptoms, and treatment options is crucial for early diagnosis and successful treatment. At GS Super Speciality Hospital, our team of experts is dedicated to providing the highest level of care for brain tumor patients, utilizing advanced technologies and compassionate support to achieve the best possible outcomes.