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La conversación también debe incluir el acceso a revisiones, información médica confiable y atención oportuna. Compartir información responsable puede ayudar a generar conciencia.

¿Qué barreras de acceso a la detección y atención del cáncer de mama consideran que deberían atenderse con mayor urgencia?

#SaludPública

I was reading this paper on penile cancer, and at one point they say, (LR=local recurrence)

This finding aligns with previous fi ndings by Lee et al. [12] who reported PeIN in the surgical margin as a predictor of LR in a large cohort of 319 patients. Positive surgical margins for invasive tumour were not associated with LR. Notably, patients with positive margins who did not receive additional treatment did not have a higher risk of LR compared to those who did, suggesting that LR may more likely refl ect new tumours arising in the remaining predisposed epithelium, rather than actual residual disease.

I don't understand, why would patients with positive margins receive no additional treatment? Doesn't that just allow the remaining cancer to continue spreading?

Please help me https://doi.org/10.1080/17474086.2026.2715445

Hi all, I made a post before asking about the reasons why cancer research is more focused on cure instead of prevention and early detection. From what I understood from the replies is that the word cancer is an umbrella term that includes many types and isn’t a single thing, I also understood that it’s “very challenging and difficult” to conduct the prevention study because various (environmental) factors might be causing it and it would difficult to isolate these causes and that it also requires generational studies.

Okay so now I just have another thought on this, and apologies if it may be a dumb question, but I was wondering, could AI ever be used in future research studies to facilitate these research barriers? Such as understanding environmental factors?

I’d really appreciate answers from researchers and medical practitioners. Thank you.

Immunotherapies and kinase inhibitors do not break the same kind of thing. We keep seeing it in the structure of the networks themselves.

When we map a disease signalling network and ask, for every interaction, whether an alternative route exists around it, a consistent split shows up.

The edges targeted by immune checkpoint blockade, PD-1, PD-L1, CTLA-4, have no alternative route at all. Remove them and nothing in the network carries the signal around. We found this in all four tumour networks where we looked: melanoma, renal cell, bladder, triple-negative breast.

Targeted kinase inhibitors sit on the opposite kind of edge. The interactions they block are embedded in redundant structure, with a detour already present in the wiring.

What makes this more than an oncology curiosity is that the same contrast appears outside cancer. In psoriasis, the biologics that block a ligand (anti-IL-23, anti-IL-17, anti-TNF) hit edges with no bypass, while the transduction inhibitors (TYK2, JAK) land on the redundant hub. Ligand versus transduction, not immunology versus oncology.

The limit, and it matters: structural coverage is not efficacy. Among those psoriasis biologics, all of them hitting edges with no alternative route, clinical response rates range from 12 to 91 percent. Structure tells you where a network can be severed. It does not tell you how well a drug does it, and it says nothing about timing.

For the clinicians here : does this map onto what you see, durable response where the network has no detour, and escape where it does?

I’m helping organize OncoHeart 2026, an academic conference in Boston about the effects of cancer treatment on heart health. Through dialogue, we aim to give patients and caregivers the chance to learn about current research and speak directly with experts, while scientists and clinicians can learn from patients’ experiences and priorities. Please comment or DM if you are interested in attending!!

If cancer is using proteins to send the instructions into healthy cells dna then with all these peptides that we have now days that are literally just modified proteins, can't we just do that same thing by taking a healthy cell (this healthy cells would be picked based on how resistant it is to cancer and with no mutations, basically pick the best cell they can find) from the person that has cancer and putting those dna instructions from the healthy cell onto a modified protein peptide and maybe if needed attach that strand of dna to a mRNA that would then go into healthy cells and cause no issues cause the instructions are the same but then when those instructions go into the cancerous cells wouldn't it literally make the cancer cells turn themselves back into healthy cells because you literally put the instructions of turning into a healthy cell into the nucleus through a protein or even just by sending those instructions it could start the process of apoptosis. Peptides are basically just specifically picked pieces of protein, I believe they are going to have a major type in the future of medicine. This concept could work for any type of cancer and things way beyond cancer. This could be done for a ton of things. This would be attacking the cancer cells in the exact same way the cancer is attacking your healthy cells. Then you would just inject this sub q every day.

I knew nothing about cancer a hour ago. I'm currently sitting on my kitchen floor with 50 papers in front of me from researching cancer. Please voice your thoughts on my theory cause this has not been tested and I have literally 2 hours of research on cancer in my whole life, im not a scientist, im not even in medicine, im just a regular guy who likes to use his brain.

Also, how do researchers know they can’t prevent or cure cancer if there isn’t enough research in prevention and early detection research in the first place?

I did some quick search on this topic and I found that there’s a gap in research funding areas:

“14% of European cancer research papers have a focus on prevention research.” “Less than 4% of funders show interest in primary prevention” (Schmutz et al., 2023).

In the UK “Prevention accounted for 3% of the funding, detection and diagnosis 5%” (Mayor, 2006)

In a global study of cancer research funding it says: “It has been suggested by researchers that prevention and early detection are key to cancer control globally. However, despite this, our analysis reveals that only a relatively small proportion of research investment is directed at cancer detection and diagnosis.” (Alan et al., 2023).

Is there a reason why funders aren’t interested?

Dear All,

I hope this message finds you well.

I am currently working in the field of psycho-oncology and am planning to pursue a PhD in Singapore. As an international applicant, I am eager to connect with professionals who can offer guidance regarding the academic and research environment, job opportunities, and the overall living experience in Singapore.

I would greatly appreciate any insights, recommendations, or contacts that could help me navigate this transition and make informed decisions.

Thank you in advance for your time and support.

Please DM if you want to share personal experience.

Scope in future? Neet pg 26 aspirant btw

Dear Oncologists/Pathologists/Cancer Biologists of Reddit. Medical student here, I’m quite struggling with keeping the specific cancer pathogenesis pathways in my mind, memorising the genes that are found in the most cases etc. What is the best way to study cancer genetics, common genetic abberations found in specific subsets of cancers, thanks a lot!

I'm an EM doc, but have a family member (recent college grad with LS degree) who's looking at jobs as a pharma rep - esp in oncology.

Are reps still relevant, and do they do anything really helpful anymore? Or is the field dying out?