EPIC EHR

Our hospital is moving to EPIC EHR (from Cerner) starting in Sept. All the nurses did EpicU but we are all so nervous about the change.

I'm one to be highly organized during my workflow with a sheet that I typically fill out for each patient. For reference, the picture is the worksheet I would use when I used Cerner.

For those that currently use EPIC, do you have any advice?

Are there any activity tabs you find yourself in the most? For example Rooming or Flowsheets?

I currently follow an oncologist for my blood clotting disorder. I do not have cancer but my primary care says it's best to follow with them instead of a hematologist. They just prescribed me 100mg enoxaparin every 12 hours because I am 5 weeks pregnant. I was taking Eliquis 5mg 2x daily but oral anticoagulants aren't good to take while pregnant. I have a prothrombin gene mutation F2 heterozygous, not the worst but not a blood disorder I like having especially for the rest of my life. Is 100mg of enoxaparin to much for me or is is safe to take? I get nervous about trying new medications.

Hi, I am a first year university student and recently I have been in researching on cancer tumours. I found out that maybe there's a way to solve on the problem of antigen-loss escape in cancer immunotherapy. I was thinking about whether asynthetic/foreign protein antigen (E) could be engineered not only to act as a target for CAR-T cells, but also to be functionally coupled to an essential cancer-cell process. The idea is that if cancer cells retained E, they would remain vulnerable to CAR-T recognition, but if they lost or suppressed E to escape immune recognition, they would also lose an essential function and therefore have a significant fitness disadvantage.

I’m aware that synthetic tumour antigens and cancer-specific dependencies have already been investigated separately, so I’m trying to determine whether combining these concepts in this way is actually feasible or whether there is a fundamental biological limitation that I’m overlooking.

Would anyone be willing to give me your thoughts on whether this is a reasonable hypothesis to investigate further, and perhaps point me towards any areas of literature I should look into?

Also please don't shit on me :( I am new to this and I am trying to broaden my knowledge.

Thank you!

(Mod approved post)

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I’m hoping to get some insight from oncologists, doctors, nurses, podiatrists, or anyone with experience in oncology.
I’m a **Foot Health Practitioner (FHP) in the UK**. For anyone unfamiliar with the role, we are trained foot-care professionals who assess and treat a range of common foot and nail problems and provide preventative foot care. Our training includes anatomy, physiology, pathology, infection control and other relevant aspects of healthcare. However, we are **not doctors, and we don’t diagnose or treat systemic medical conditions**.
I have several patients who have cancer and are either undergoing, or have undergone, cancer treatment. I’d like to improve my understanding of what can happen to the feet as a result of **cancer itself and/or cancer treatments**, so that I can provide safer and more appropriate foot care to my patients and recognise when something may need to be referred back to their medical team.
One thing I’ve found quite difficult when researching this is that searching things like *“cancer and feet”* tends to bring up information about **cancers that originate in the foot** (melanoma, sarcoma, etc.). That’s **not** what I’m asking about.
I’m interested in the systemic effects of cancer and its treatment on the feet.
For example:
What changes can chemotherapy cause in the feet?
What about radiotherapy, immunotherapy, targeted therapies, hormone therapies, steroids, etc.?
How can cancer-related peripheral neuropathy present in the feet?
Can treatment affect sensation, temperature perception, pain, balance or gait?
Can cancer or treatment cause swelling/lymphoedema in the feet or lower limbs?
What skin and nail changes should a foot-care professional be aware of?
Are there particular treatments where patients are more vulnerable to skin breakdown, infection, ulceration or delayed healing?
Are there things that a Foot Health Practitioner **should avoid doing or take particular precautions with** while someone is undergoing treatment?
Are there particular symptoms or changes in the feet that should prompt us to advise a patient to contact their oncology/medical team?
I’m **not looking for anyone to diagnose an individual patient**, and I appreciate that treatment and precautions will vary depending on the cancer, treatment regimen, blood counts, medications and overall health.
I’m really asking from a **professional education and patient-safety perspective**. I want to understand what is happening systemically so that when I’m treating someone’s feet, I have a better understanding of what their body may be going through and when something is outside my scope and needs medical input.
I’d particularly love to hear from **UK oncologists, oncology nurses, podiatrists or other healthcare professionals who regularly work with cancer patients**, but I’d also be very interested in experiences from other countries.
Thanks in advance — I’m essentially trying to make sure I’m doing the best and safest job I can for my patients while staying within my scope of practice.

Female 33

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Have you read the recent news about personalised mRNA vaccines for melanoma? I saw that the Moderna/Merck vaccine showed positive results in a Phase 3 trial, and I was wondering whether this could pave the way, in the relatively near future, for personalised vaccines for other types of cancer as well.

In particular, do you know if there are already any studies or clinical trials involving BRCA1/BRCA2-associated cancers?

I’m interested in understanding whether this technology could also be applied to these types of cancer, or whether being BRCA1/2-positive is not particularly relevant to this kind of approach.

Billionaire Vinod Khosla recently wrote a JAMA article on "Will Autonomous AI Exceed AI-Aided Physicians as the Best Medical Care?" Clickbait titles aside, AI is already outpacing physicians at many medical tasks. It can synthesize more trials, guidelines and literature than any of us can keep up with. It's very good at knowing the evidence.

But I don't think this is the same as practicing medicine. Patients often come with incomplete histories, comorbidities, prior toxicities, family dynamics, financial constraints and preferences that may not become obvious until halfway through the visit.

Sometimes, the most important piece of information just isn't in the chart. A colleague notices that the patient who said he tolerated his last cycle "fine" is now walking more slowly into the room. Or that his daughter is now answering questions the patient used to answer himself. 

When we're at tumor boards, we don't expect our colleagues to recite NCCN. Instead, we're seeking the judgment that comes from treating hundreds of patients: when to dose reduce, when to wait, when to stop, and when the technically "correct" treatment isn't right for a particular patient.

In medicine, there isn't always a single objective function. One patient prioritizes survival, while another prioritizes independence. And another just wants to feel well enough to attend her daughter's wedding.

I think Khosla has it wrong. The most interesting question isn't whether AI will beat physicians, it's what happens when physicians have AI and the accumulated judgment of other experienced physicians. AI knows the evidence, but that doesn't mean it knows what to do with the patient sitting in front of you.

What do you know from clinical experience that you’ve never seen in a guideline?

We have a family friend who is a survivor and my daughter decided to fold 1000 paper cranes in honor of our friend and donate it to our local cancer center. Sharing with all of you to share the hope!!!

I’m trying to work out whether I’m simply rediscovering an established concept under different terminology.

Several well-described observations seem to fit together:

- oncogene inhibition can cause survival and pro-death signals to decay at different rates (“oncogenic shock”);

- dynamic BH3 profiling can detect early treatment-induced changes in apoptotic priming;

- targeted therapy can rapidly induce adaptive rescue mechanisms, including pathway reactivation or new dependencies on anti-apoptotic proteins such as MCL-1 or BCL-xL.

This made me wonder whether treatment response in oncogene-addicted cancers could be viewed as a temporal competition between loss of survival signalling, apoptotic vulnerability, and adaptive rescue.

The hypothesis would be that sensitive tumours have a larger or longer transient vulnerability window after driver inhibition, while resistant tumours either fail to enter that state or escape from it more rapidly.

If so, I would expect:

1. early temporal features after driver inhibition to predict later cell death better than baseline pathway activity alone;

2. sensitive and resistant models to differ in the duration or magnitude of this transient state;

3. the optimal timing of a second intervention to depend on when adaptive rescue emerges, rather than necessarily favouring simultaneous combination treatment.

I realise that none of the individual mechanisms here are novel. What I have not been able to determine is whether they have already been explicitly integrated and tested as a general predictive framework based on temporal dynamics across oncogene-addicted cancers.

So I’d particularly appreciate input from people working in oncology/cancer biology:

Is this already a recognised framework under terminology I’m missing?

And if not:

What is the strongest biological reason to expect this model not to generalise?

I’m not an oncologist or cancer biologist, so I’m primarily looking for missing literature or a good reason to falsify the idea rather than trying to claim novelty.

I just landed a job working in supportive oncology. It is a new program in a growing oncology department. Essentially it’s everything outside of actual cancer treatment that supports the patient and their Families. I’m hoping to connect with people who are already doing a similar job, or working a system with an established supportive oncology program. I’d love to connect.

I'm a high school student trying to train a model that predicts early stage ORNJ (Osteoradionecrosis of the Jaw) based on patient data. For that, I'm trying to encode a scale for a patient's T stage and N stage.

So far, it's obvious that I can put T0-4 and N0-4 on a 0-4 scale. However, to my current understanding, I'm not sure where to put TX and NX.

I know that X means the tumor/spread for T and N respectively means they cant be assessed. But what does that mean exactly in terms of size/spread? Does it mean that X is so big/spread out that it cant be measured? Or does X indicate more of like a null/missing value where it can't be measured for some other reasons. If it's the latter, what are those potential reasons?

I really appreciate your time answering a simple question like this one :)

I’m looking for oncology research groups that may need help with ongoing projects, particularly manuscript writing or literature reviews. I’d be very interested in contributing to a project and gaining research experience, with the possibility of contributing to a publication.

John’s Hopkins announcing most ovarian cancer starts in the fallopian tubes. While many in the medical community seem to be aware - this is news to most of the public. talk to your PCP!

https://www.pbs.org/newshour/show/how-new-findings-on-ovarian-cancer-origins-may-help-reduce-risk

My colleagues are divided on how much weight ORR should carry in accelerated approval decisions. I don't think there's one right answer.

If you're talking about replacing an established 1L regimen that delivers a real OS or QoL benefit, I think the burden of proof should be high. Evidence of an OS or patient-outcome improvement is hard to argue against, especially when a new option adds toxicity or cost.

But this changes in diseases with few options such as r/R T-cell lymphoma. Romidepsin and belinostat got accelerated approval off ORR data, and pralatrexate followed a similar path. Romidepsin's confirmatory trial missed its OS endpoint and the approval got pulled. I think that's an interesting test case rather than a clear-cut argument because some patients had genuinely durable responses. Just because the drug didn't move OS in the broader population doesn't mean those patients didn't benefit. It just means ORR alone couldn't tell us who would benefit in advance.

That's the real issue. In small, heavily pretreated populations, running an RCT is often impractical. It also gets hard to justify randomizing patients to a control arm once you're already seeing durable responses in early data. So we're left leaning on ORR as a proxy even though it's imperfect. And we can't tell the subgroup that benefits from the patient who doesn't.

To me, the real questions aren't whether surrogate endpoints are good or bad. It's whether ORR is doing the job we need it to do in a given clinical context. And how much uncertainty we're willing to live with when the alternative is no option at all.

Where do you draw the line for when ORR alone is enough?

Edit: no AI was used in writing this post.

Hello , I wanted to ask if there is any oncology resident in Switzerland or Swiss oncologist who would like to share their thoughts on the specialty especially in the DACH region (work life balance, competitiveness, open spots, salary, working in private clinics or owning a praxis etc). Also do you think it’s more worth it for an international doctor to do the specialty directly in Switzerland or to go when he or she is already a board certified oncologist? (from Greece for example)