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ONCO MS-7 - Shared screen with speaker view
Matthias Fischer
15:55
Heyho!
Durjay Pramanik
16:15
hello ..
Oleg Demin
27:16
Question 1 to Jessica: Why is 3 of CTL proliferation is equal to 7? What happened if decrease/increase the number?
Oleg Demin
29:55
ERROR CORRECTION: "# of CTL proliferations" NOT "3 of CTL proliferation"
Oleg Demin
34:29
Question 2 to Jessica: PDL1 expression on cancer cells, mDC and endothelial cells is regulated by IFNg. Do you have effect of IFNg into account?
Durjay Pramanik
36:29
Question : Could there be an effect of diet plan (suggested to patients) that might change the proliferation rate of CTL? Therefore, explaining some of the variability of tumor response in different patients?! Thanks. Nice presentation.
Segun Oke
39:30
Nice talk
Stacey Finley
39:42
thank you, Jessica. enjoyed your talk
Russell Rockne
40:07
Very nice work Jessica thank you for joining the session
Jessica Leete
43:21
Oleg: The number of PDL1 receptors per tumor cell is a parameter in our model. Currently it is set to the average number we see in our tumor type, but we are exploring how treatment response changes as the number of PDL1 per cell changes. And it is something we definitely want to include in our virtual populations later on. So while IFNg is not explicitly modeled, it would affect that parameter.
Jessica Leete
47:31
Durjay: I am unaware of how diet may change T cell proliferation, but that is a great question! The proliferation time is a parameter that our model output is looking sensitive to though, so I hope we can get a greater understanding of just how sensitive the model is to it and how much we can expect the proliferation time to vary between patients as I get into the virtual population part of the project.
Oleg Demin
52:24
Thank you Jessica! Good work!
Mohit Kumar Jolly
52:39
Can this approach help identify whether the enrichment of subpopulations is due to induction (drug-induced switch) or expansion (pre-existing higher fitness)?
Andrea Bild
53:08
Is there often co-occurrence of populations with different signaling states, suggesting cell interactions?How variable are the signaling states within populations overall?
Heiko Enderling [he,him]
57:15
Very beautiful data. In the combination experiments with sustained tumor inhibition, are the tumors fully necrotic or do they contain viable cells ?
Heiko Enderling [he,him]
01:03:49
Sandy needs a SMB baseball card !
Stacey Finley
01:04:32
^^
Arne Traulsen
01:23:21
Sandy, you moved from quite complex to quite simple models in your career! If we selected the best simple models to extrapolate, do you anticipate a standard way to do this that does not need re-thinking the model all the time? SO the clinicians can use this as a decision support on their own?
Segun Oke
01:25:44
Great talk, Sandy!
Daniel Glazar
01:25:58
Great talk! :)
Amina
01:26:21
Nice talk. Thanks Sandy!
Alexander Anderson
01:26:31
Great question Arne
Alexander Anderson
01:27:19
I think a fairer summary as we have become more data driven we have developed simpler models dictated by that dat
Alexander Anderson
01:27:29
But you point it still valid
Alexander Anderson
01:27:50
Is there a more automated way to reduce model complexity
Alexander Anderson
01:28:30
This is beyond my mathematical skills but I’d love to discuss it further if this is something you are interested in
Alexander Anderson
01:30:38
Andrea yes! We should discuss, Maxi Strobl will present our new Ovarian cancer model at this meeting: http://schedule.smb2021.org/ONCO/ONCO-CT07.html
Kristin Swanson
01:42:51
Did you seek to identify any sex differences in your ecotypes? Particularly with the known sex differences in response to immunotherapies.
Alexander Anderson
01:44:47
Ecotypes are a cool idea! Did you ever try to quantify them spatially? I can imagine the same ecotype having very different functional behavior depending on the spatial associations!
Andrea Bild
01:45:44
Exquisite analyses Andrew. If the majority of cell types can reflect a diversity of patient outcomes across the data, and ecotypes can predict outcomes better than biomarkers that don’t consider ecotypes, do you hypothesize that the majority of tumors function collectively to resist therapy (ie are ecosystem in some cases more important than cancer cell states)?
Durjay Pramanik
01:48:00
Thank you. It was a very nice series of talks.
Stacey Finley
01:48:24
great talks! thank you for an excellent session
Amina
01:48:31
Thank you Russ!
Amina
01:48:41
And Andrea!