I’m unsure where to even start to learn more about this, so I’ve just been asking AI. Unsure if it’s true:

Biological Factors Contributing to the Lower Risk of Metastasis in HRAS-Mutated Pheochromocytomas

1.	Nature of the HRAS Mutation and Its Pathway:
•	HRAS is an oncogene that is part of the RAS/MAPK signaling pathway, which primarily regulates cell growth, proliferation, and differentiation. Mutations in HRAS (such as HRAS p.Q61R) result in continuous activation of the RAS pathway, leading to increased cell proliferation.
•	While HRAS mutations promote cell growth and proliferation, they do not typically activate pathways that are crucial for tumor invasion, metastasis, and epithelial-mesenchymal transition (EMT), which are necessary for cancer cells to spread to distant sites.
2.	Tumor Differentiation and Cellular Characteristics:
•	Well-Differentiated Tumor Cells: HRAS-mutated pheochromocytomas tend to be well-differentiated, meaning they retain many of the characteristics of normal adrenal medullary cells. Well-differentiated tumors are generally less aggressive and less likely to gain the ability to invade surrounding tissues or metastasize.
•	Lack of Epithelial-Mesenchymal Transition (EMT): EMT is a biological process in which epithelial cells lose their cell-cell adhesion properties and gain migratory and invasive capabilities. HRAS mutations do not typically drive EMT, which is a key step for metastasis in many cancers.
3.	Low Proliferative Activity:
•	Low Ki-67 Index: HRAS-mutated pheochromocytomas often have a low Ki-67 index, which indicates a low rate of cell proliferation. Low proliferation rates are associated with slower tumor growth and a reduced likelihood of acquiring additional mutations that could drive metastasis.
•	Indolent Growth: Because these tumors grow slowly, they have fewer opportunities to invade nearby tissues or spread to distant sites. Slow-growing tumors are also less likely to undergo the genetic and epigenetic changes necessary for metastasis.
4.	Lack of Angiogenesis and Hypoxia Pathway Activation:
•	Minimal Impact on Hypoxia-Inducible Pathways: Unlike VHL and SDHB mutations, which lead to stabilization of hypoxia-inducible factors (HIFs) and subsequent angiogenesis (formation of new blood vessels), HRAS mutations do not typically activate the hypoxia pathway. Without significant angiogenesis, the tumor’s ability to invade nearby tissues and spread through the bloodstream or lymphatics is limited.
•	Reduced Vascular Invasion: Tumors with less angiogenesis have fewer new blood vessels that cancer cells could invade and use as pathways to spread to other parts of the body.
5.	Absence of Genomic Instability and Epigenetic Alterations:
•	Stable Genomic Profile: HRAS-mutated tumors tend to have a more stable genomic profile compared to those with SDHB mutations, which often display significant genomic instability. Genomic instability can lead to more aggressive tumor behavior and a higher likelihood of metastasis.
•	Lack of Epigenetic Changes: HRAS mutations do not typically cause the same degree of epigenetic changes (such as CpG island hypermethylation) seen in SDH-mutated tumors. These epigenetic changes in SDHB-mutated tumors can lead to a more aggressive phenotype and a higher risk of metastasis.
6.	Somatic Nature of HRAS Mutations:
•	Non-Germline Mutation: HRAS mutations in pheochromocytomas are almost always somatic (occurring only in the tumor and not inherited). This means they are not associated with familial cancer syndromes that predispose to multiple tumors or more aggressive behaviors. As such, the biology of these tumors tends to be less aggressive and more localized.
7.	Clinical Presentation and Course:
•	Localized Tumors: Clinically, HRAS-mutated pheochromocytomas typically present as solitary, localized tumors without evidence of metastatic spread. This presentation is consistent with their relatively benign behavior.
•	Better Prognosis: The combination of factors—well-differentiated cells, low proliferative activity, and lack of invasive and angiogenic capabilities—leads to a better prognosis and a lower risk of both local recurrence and distant metastasis.

Conclusion

HRAS-mutated pheochromocytomas have a lower risk of metastasis because the mutation primarily drives cell proliferation without significantly influencing pathways involved in invasion, angiogenesis, EMT, or genomic instability. These tumors are generally well-differentiated, have a low Ki-67 index, and lack aggressive characteristics such as hypoxia pathway activation or significant epigenetic changes. Consequently, HRAS-mutated pheochromocytomas tend to behave in a more indolent manner, with a focus on localized growth rather than distant spread. This distinct biological profile contributes to the overall favorable prognosis for patients with HRAS-mutated pheochromocytomas.

Hi everyone

Quick note that I’m not well versed in genetics so I might be getting some things wrong. Does this mean Armenians are genetically closest to Western Europe? If so, how did this end up happening?

Thanks in advance.

Hello, just wondering bar ireland/denmark/Germany for industry jobs in europe, what other places are suitable for finding industry jobs?

Also, I know a lot of people are saying Ireland is a great place to find industry jobs for genetics graduates but I want to know where they're getting that information? I've lived there for a couple years and it really doesn't seem to be the case? Only jobs there seem to be manufacturing (which seems to be just a fancy factory worker) type jobs, other jobs available are higher in seniority (senior consultant/manager) type positions. Where are people finding these industry jobs in Ireland? Or am I missing out on information somewhere that I should be aware of.

I was under the impression that if you got your whole genome sequenced, this would necessarily include information about your karyotype. Then I saw that karyotyping seems to cost a similar amount to genome sequencing, even though it appears to involve only taking a microscope image of a cell culture, compared with all of the complexity involved with breaking up the dna and doing the reads and then aligning and calling etc.

So, why is this? Is karyotype information lost in standard genome sequencing analysis? What if your sample is XXY or something, how would you know to work this out and take it into account during alignment?

I was thinking about these two disorders and it got me thinking, is the issue found on chromosomes 21/15 or on the sex chromosomes?

Hi, I was wondering for a long time, if intellectual abilities are hereditary. I inherited bipolar disorder from my grandfather's sister (don't know how it called, so I'll call her auntie). My grandfather told me about this only after I got diagnosed. Auntie was a true genius. She was a mathematical programmer in the 70s, studied game theory, wrote poems and was simply the greatest person I, sadly, never knew personally. I've always been called genius, I got used to it quickly. I'm really good at math, logical thinking, languages and, coincidentally, board games. Once, my grandfather told me I have same traits as auntie and it got me thinking, if I got all this, if I already have bipolar disorder, from her

So apparently if this study is true, could challenge the central dogma of inheritance in that there's such a thing as protein-based inheritance?

https://x.com/matt_eroglu/status/1830643437802008835
https://www.nature.com/articles/s41556-024-01494-9

I heard that you can lose an ancestors DNA to the point they don't show up on a DnA test in any traceable way but does this mean they play no role in your DNA or does it mean the role they play in your DNA is too small to trace at least with current technology?

Unfortunately, for my thesis I am stuck with the most unhelpful supervisor available and all he does is nods his head every time I have a question. And so, I am on my own and to guide me all I have is a previous students thesis on a similar topic. All I was provided with are samples of two unrelated patients (autosomal recessive nonsyndromic deafness) and the samples of their family members. These two patients have mutations in different genes as confirmed using WES. So, my sample size is just 1 for each mutation and I am to use these samples without any positive or negative controls, other than the family members of the patients. There are chances that the mutations aren't even novel, and without controls all of this is useless. I have already wasted enough time dwelling on this, I cannot give up on this research due to my scholarship, so am I going nowhere with this or is this publishable stuff?

I’m trying to show some people I know (African American) that they’re NOT Native American and have mostly West and Central African DNA (and even more European dna than Native American) I have compiled some myself but I just want to make sure I have a lot of good quality, credible evidence. If this type of post is not allowed, feel free to remove!! @mods

WHY IS THIS WRONG

I have started my A levels and I want to set my path from now on to get a good job in the genetic industry. What courses should I be researching for genetics. Can someone list all the possible courses and I will research them to see if it interests me. Personally I don't like anything to do with plants and agriculture. I prefer human and animal biology.

Whats the analysis details on a bioinformatics level and how confident is it?

Hello, since i am studying in a field related to the sub reddit, i thought i would ask my questions here.

I’m a 22 year old student who will graduate with a master in applied and fundamental genetics, my grades could be considered pretty low but my ranking is actually okay-ishly high (12th over 200 students by the end of my bachelor’s, and 5th out of 170 during my first year of masters). I’ve done a couple of short time internships in two different labs, one in a diagnosis and research institute, and another in a medical lab.

I am pretty lost when it comes to what to do in the future, i’ve been looking into a variety of stuff but i’m still very unsure and it’s causing me quite a lot of anxiety.

I was wondering if anyone could possibly share their experience, or advise me on what I could possibly look into or expect to do in the near/far future?

Thanks a lot in advance.

It seems the consensus is that humans and chimps only have a few percent difference in DNA. Another consensus seems to be that due to neanderthal DNA, people evolved in Europe and Asia have about a 1.4% difference to sub Saharan Africans. Obviously genetics is extremely complex to put it mildly, but is there any scientific reason that this difference isn't more widely discussed and studied? Or is it only due to societal pressures and the fear of being labeled negatively? Similar to the lack of discussion on the "out of Africa" theory. Namely the new and in my humble opinion, scientifically valuable, fossil discoveries in Turkey that put that theory into doubt. I am interested in my species origins and evolution, as a great deal other topics. To me, the truth, free of bias, is the most important aspect of science and knowledge as a whole. Again, strictly in my non genius opinion, it seems facts have been taking a backseat to convenient and popular ideas as of late. But that statement is beyond the scope of this question even though discussion on it is as welcomed as any in good faith. Thank you all in advance.

Hey so I just had the most random thoight and now Im curious.

So quick history, Im gay and likely to adopt if kids are ever in my future. My old brother is straight and married but due to some concerns at birth turns out my brother is sterile.

My brother kept this under wraps from me and really expressed it to my mom who let it out of the bag. Without knowing anything I had offered my sperm thinking, "Well then my brothers kids would be my brothers kids, thered really be no difference,".

Obviously that isnt true after the little research I had done, and my brother had gone through IVF with his wife and now have 2 lovely twins.

My question is how similar would it had been compared to my sperm to his? And can we measure repeatable variants in DNA? I look at my aunts son who looks exactly like uncle. My brother looks exactly like my dad and I look like my moms father. So obviously theres repetition but where and how does this all work?

Is homosexuality hereditary in any way? If not, then is homosexuality not genetic? What is the gay gene then?

Am I specifically allowed to pay tribute to a proffessor whom has passed within the name?

ex: the "person" transcript

Can a publisher reject my paper if I do that? And would that change if the proffessor being named is politically involved?

Hi, I'm not a geneticist, just curious. Can anyone explain how a species can change the number of it's chromosomes? I don't mean how two chromosomes combine, but if two sets of chromosomes do combine, like in our ancestors, from 24 pairs to 23 pairs that had to happen in one individual. So how did that 1 individual with fewer chromosomes than it's parents find a mate and go on to have billions of descendants? It's always baffled me why it didn't have sterile offspring like the horse-donkey cross.

Thanks.

Would it be feasible to use genetic engineering technology to not only increase one's intelligence, but increase it beyond what is naturally possible?

I’m a black woman with no recent admixture. I remember seeing pics of myself as a baby and noticing that my hair was once wavy or looked a little straight-ish. By the time I was two it was definitely curly though. Is this common? And if so why does it happen?

Hello, I'm wondering type of job titles are in the genetics industry that isn't bioinformatics/data/lab technician type job roles. What other types of roles are there? What are some good paying roles? I'm trying to have a clearer aim for my career however very few job listing's exist for genetics graduates where I'm from and they're all senior roles.

How many of these job titles would require a phd? I'm trying to decide if I should do a masters or phd, as I have the option to do a PhD immediately after graduating my bachelors, but opinions have been mixed on whether I should take that route due to the sheer difficulty and how it might make me overqualified for entry level roles. Also because some people think it's not worth it since I only want to go into industry and not academia.

Sorry for all the questions, all this career stuff is really stressful and I'm at a loss for what to do

I don't know if it's even possible to know this information, but I had to try and find out. Doesn't need to be exact obviously, but just a general ballpark on how close to average these numbers of variants are. Thank you!

1410 variants on ADGRL3,
63 on MTHFR,
205 on CYP2E1 and
118 variants on CYP3A4

439 on FOXP2

101 on SLC6A3

They're not even using Hamming codes! ROFL

My dad passed away last year of June 2023 due to stroke complications. He’s had a pretty bad health throughout most of his 30s,40s up to 70s. Fighting high blood pressure constantly and always having to go to the doctor. He was also an alcoholic and also diabetic.

So now I realized I’m dealing with the same thing. Even though I try to change my life for the better with much more healthy habits. I don’t drink at all only on special occasions. I eat healthy minimizing refined carbs and I work out literally 3-4x a week lifting and light cardio. Keeping away from seed oils and just eating clean.

I’m suffering high blood pressure that no meds can lower. I’ve tried basically 15 types of meds. Did all sort of test CT aniogram, Calcium score, echocardiogram, renal aorta ultrasound and all came out normal. My dad doest not have a manly body as he’s thin with a pot belly and pointy chest. Guess what? I also inherited the same arms and torso like an exact carbon copy of it. Hate it, makes me feel so insecure. No amount of lifting and working out won’t get rid of it. I feel like he’s very estrogen dominant. So I’m really trying not to suffer the same faith. So far my brothers and sisters are healthy. My brother did not inherit his body and his health.

Despite all my efforts of working out and eating clean. I’m always at the doctors, I don’t feel good anymore, I’m depressed and always dealing with floating spells, dizziness and fatigue.

Hello, all.

I was looking around to see whether Landoltia punctata has had its full genome sequenced and ran into some mixed results. I found some sources that suggest it was (others that said its transcriptome was), but was unable to access the full genome. I was left to wonder if it was just the length and C/G:A/T radio that was evaluated, but I'm just not sure if I'm looking at the right databases. If it has been sequenced, does anybody know to what extent it has been studied?

Thank you all in advance for your help! If you have any specific questions, don't hesitate to ask