This is missing a lot of critical features seen in apps like Complete Anatomy.
a) Proximal/Distal Attachments
b) innervation
c)Arterial Supply
d) Actions of Skeletal Muscles. Having the same description for all skeletal muscles is amateurish
e) Similar issue with brain as well, no mention of functions of lobes, gyri, etc
Additionally the striation of the muscles are poor quality.
The models are lifted from an open source 3d model of human anatomy.
I am one of the 3D modeler's working on complete anatomy and I agree, It's a nice demo but it feels half baked. There's no real love in it. I feel like so many of the AI projects are like that, shiny but lacking polish and love.
That's odd. This was content that was still on the MCAT when I took it last year. I even remember keeping the formation of objection permanence occuring ~0-2 years of age on my flashcards.
It’s far from perfect in newborns (containers take some time to understand, and in general infants have weak short-term memory). I also wonder how much effort goes into updating MCAT questions with new scientific developments, especially when there is limited clinical significance - an infant who struggles with object permanence likely has serious neurological/cognitive problems across the board.
You're mostly correct but immunotherapies do work for a many different type of cancer. The issue is differences in tumor biology plays a major factor. The even bigger caveat is that given a sufficient amount of tumor mutational burden (TMB), immunotherapies are found to be effective for any solid tumor. Granted most patients don't have the sky had TMBs needed for it to be effective
I believe he got just got either Ipilimumab and Nivolumab as a combo therapy or Pembrolizumab. He's a researcher who focuses on neo-adjuvant (use therapy before resection) therapy in melanomas. It was a good gamble to try the same paradigm in Glioblastomas
It's neo-adjuvant (treat prior to surgery) with a three mAbs: Ipi + Nivo, which is a well established combo of immunotherapeutics for many solid tumors, rounded out with relatlimab which I'm less familiar with (LAG-3 inhibition). Neoadjuvant use of immunotherapies is established concept and is utilized in clinical practice for non-small cell lung cancer and colon cancer. This is the first time I've seen a use of 3 immunotherapies used at once: Ipi + Nivo isn't the most tolerable treatment regimen. Other novel aspect is use of neoadjuvant therapy in GBM.
Don’t mean to hijack this thread, but I don’t think HN has DMs. Read some of your comments and as a person with cancer would love to pick your brain a little to develop my mental model further (and of course wouldn’t expect anything for free.) Drop me a line at [my HN username] [at] nearby.org if open to discussing more. Thanks!
Do they give immunotherapy before, after or instead of chemo? Asking because I heard what it is after in some cases and that puzzled me as chemo usually hits immune system.
No chemo. The entire idea of this regime is to hit the tumour with immuno to get the reaction. They want lots of tumour cells and for it to be "treatment naive" - Richard hadn't even had corticosteroids, which dampens immune.
Once they primed his system they excised as much as possible and kept the immuno going while doing a course of radiation.
Profs Long and Scolyer work with melanoma where chemo is rarely used these days.
That was a concern in the early days of development of anti PD(L)-1 agents - that chemo and even steroids would harm the T-cells you’re trying to activate.
Yet there are settings where a deliberate combination of anti PD-1 with chemotherapy is the standard of care. And there are other types of immunotherapy where a combination with chemotherapy is advantageous too.
From what I read (in a book written by Scolyer), the treatment didn't involve chemo. It was along the lines of:
1. immunotherapy
2. Surgery to remove the bulk of the tumour.
3. More immunotherapy
4. Radiation therapy
5. A course of vaccine customised to the genome of the cancer
• Prostate cancers are known to have a wide spectrum of outcomes.
• Stage IV (metastatic) disease tends to have genetic testing. These panels tend to be on the order of a few hundred genes to 1000s of genes.
• Classically prostate cancer is driven by androgen receptor upregulation. Disease progression is often due to the disease overcoming treatment with antiandrogenic such as enzalutamide.
Correction: enzalutamide was designed to overcome castrate resistant prostate cancer. abiraterone would have been more appropriate to bring up here.
• Upon review of NCCN guidelines: there are two main genetic indicators for targeted therapies. Both of these mutations are indicated for germline and somatic contexts: BRCA1/2 for parp inhibition and dMMR/MSI-H for pembrolizumab
o Note that there are some somatic mutations with HRD pathway that are indicated for treatment. But that is only if they are somatic
• This study aims to figure out the etiology of the disease in an evolutionary manner. That is what are the key events that lead to oncogenesis.
edit note: the word that escaped me was epistasic given that we are looking into the nuts and bolts cause and effects of different mutations.
edit note 2: I'm going to be honest, most of the time I've read about prostate cancer is in the metastatic setting and thus it has already become castrate resistant. Abiraterone is also meant to aid in sensitizing castrate resistant prostate cancer. Let's just say androgen deprivation therapy for now. On the other hand, I hope this was instructive in showing how important AR is as a pathway for prostate cancer
• Quick thought: this could be useful if this matches with molecular screening in earlier stage disease. If we can reliable map out which chain of events (tumor suppressor loss of function mutations/ gain of function mutations for oncogenes, chromosomal level mutations) lead to more aggressive disease, we can inform changes in surveillance and earlier/ more aggressive treatment.
• Granted this isn’t too out there, tissues cores are taken out to begin with to get initial snapshot into how aggressive disease (it’s how you get the Gleason score after all).
• Regarding switching pathways, that’s not too crazy given neuroendocrine transformations exist in prostate + lung cancer
Personally, I think confabulations would be a better term. To the best of my understanding, these AI rely on a model similar to the reconstructive theory of memory in humans. The connotation of the word confabulation indicates no maliciousness while highlighting the erroneous nature of the action.
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