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Today we are on our to welcome Dr. Lacey McIntosh

0:46

for a lecture on Imaging response patterns in

0:49

the modern era of cancer treatment, Dr. McIntosh currently

0:52

serves as the chief of the oncologic and

0:55

molecular Imaging division of the University of Massachusetts Medical

0:58

School.

1:00

She completed her Radiology residency at the University of Massachusetts Medical

1:03

School and a fellowship in cancer Imaging with

1:06

a focus on PET CT at Dana Farber,

1:09

Kansas cancer institute at Women's Hospital in

1:12

Boston.

1:14

Her interests are in clinical trial tumor assessment criteria Precision

1:17

oncology and novel PET

1:20

CT tracers at the end of the lecture join Dr.

1:23

McIntosh in a Q&A session where she will address questions

1:26

you may have on today's topic.

1:28

Please remember to use the Q&A feature to submit your

1:31

questions so we can get to as many as we can before our time is up

1:34

with that being said we are ready to begin. Today's

1:37

lecture Dr. McIntosh. Please take it from

1:40

here.

1:41

Hi everyone. Thank you for having me today and thank you

1:44

for registering for the conference very excited

1:47

to give this today and kind of

1:50

give some some of my perspective on how we

1:53

need to think about cancer Imaging, you know,

1:56

in today's modern era of kind of

1:59

new and exciting treatments. So that's what

2:02

we'll be talking about today.

2:07

It's just some disclosures. I do some clinical trial reading

2:10

and Consulting.

2:12

An outline of what we're going to cover today. We're going

2:15

to talk about Imaging assessment in general kind

2:18

of specifically looking at different response

2:21

criteria. You know how these

2:24

were created how these are used limitations and

2:27

using certain criteria and how

2:30

they've kind of changed over time. We're going

2:33

to review classes of drugs and have these

2:36

can result in different response patterns. We're

2:39

going to look at pitfalls and challenges associated

2:42

with you know, some of

2:45

the response criteria and some of

2:48

the newer treatments and then also talk a little bit about clinical

2:51

context.

2:54

So what I can say to start with imaging assessment

2:57

is that you know, what we

3:00

do in clinical trials is really kind of Highly regulated

3:03

and very specific which is

3:06

not necessarily equivalent to what we're doing in routine clinical

3:09

practice every day at the workstation, you know

3:12

in the clinical trial session setting it's

3:15

very specialized. We have Central readers who are all kind

3:18

of reading the same patients throughout the clinical trial blinded

3:21

to clinical data. We're prospectively

3:24

selecting Target lesions, and

3:27

we're kind of comparing them throughout the course of treatment to look

3:30

at how things have changed since the Baseline and

3:33

the nature which is where things look the best that kind

3:37

of assessment can be challenging in routine

3:40

clinical practice where you guys all

3:43

know as you know, either residents or practicing Radiologists that

3:46

we have lots of challenges where the baseline

3:49

or serial exams or not always available, especially if

3:53

you're working.

3:54

Kind of a larger Center where patients are sent to you, you know,

3:58

we are combining our objective measurements of

4:01

lesions and kind of subject assessment, you

4:04

know, we integrate clinical data into

4:08

our assessments tumor markers how

4:11

the patient's doing overall a lot

4:14

of times the information that we're trying to provide especially at

4:17

staging has to do with you know tnm staging

4:20

so, you know a t staging

4:23

of a lesion which is giving the largest measurement in any

4:26

Dimension maybe different than how we're

4:29

using recessed or clinical trial assessment, you

4:32

know an attractable way. So yeah,

4:36

these are not necessarily equivalent, but I think it's very important

4:39

to kind of understand how the

4:42

clinical trials are run and look at the different response assessment

4:45

criteria so that you can apply those principles into

4:48

your routine clinical practice and you know

4:51

kind of use the concepts as

4:54

you can in the setting that you have.

4:56

So I do want to share this resource. I have this as one of my home

4:59

pages that opens up anytime. I open up my browser, but

5:02

it's the cancer.gov NCI drug

5:06

dictionary and this is wonderful. You can type in any

5:09

drug you can use the the generic or the trade name

5:12

and it will pop up with just a short

5:15

paragraph on the mechanism of action and you know,

5:18

there's new drugs that come out all the time. So I use this

5:21

frequently to kind of understand what kind of drugs patients

5:24

are on because that can be really helpful in determining what

5:28

you expect to see for response patterns, which may

5:31

be atypical with some of these newer treatments.

5:35

So a big part of you know,

5:38

I think accurately staging or restaging

5:41

patients is knowing what to expect.

5:44

Right? So for patients

5:47

who are on traditional chemotherapies full of

5:50

fox anything Platinum based, you know,

5:53

the things that have been around for a long time when you

5:56

think about the mechanism of these drugs, these are

5:59

really cytotoxic and they're designed to kill cancer cells

6:02

are actually any kind of rapidly metabolizing cell,

6:05

which is why patients often lose their hair because hair

6:08

follicles cells are you know, regenerative frequently

6:11

turning over same thing

6:14

with sometimes in the skin and the bowel. So those

6:18

kind of you know are explaining the toxicity

6:21

is a little bit with targeted therapies,

6:24

which will go into more depth about,

6:27

you know, examples of these but these drugs

6:30

tend to be more cytostatic where they are designed

6:33

to actually help.

6:35

Cancer cell growth so, you know, they're inhibiting angiogenesis

6:38

or stopping the cell

6:41

cycle to inhibit proliferation things

6:44

like that. So, you know

6:47

for these assessment.

6:49

Criteria, you are not

6:52

necessarily looking for dramatic changes in size.

6:55

So we'll talk about that more but you know

6:58

and for you know therapy there's a couple

7:01

of different types passive inactive or the the way that

7:04

I like to category categorize these but when

7:07

you think about the mechanisms of

7:10

how these act you can kind of imagine how these might

7:13

manifest differently when the cancers are

7:16

responding to them. So in general for like

7:19

an outline, I like to think about, you know, when you're thinking about

7:22

traditional chemotherapy and these cytotoxic

7:25

treatments recess which is a size based

7:28

criteria, which we'll talk about in a second is you know,

7:31

the one that you're going to want to use here for the targeted

7:34

therapies, since you know size may not always

7:37

capture all of the response. There's

7:40

some other criteria like choice or mask that

7:43

we're gonna think about and you know

7:46

with immunotherapy we are all we're gonna be thinking about

7:49

all

7:49

Of these plus, you know some immune related response

7:52

criteria. So we're going to talk about all these in-depth but

7:55

you know, just an overview I think

7:58

you know, it's good to know what drugs patients are

8:01

on because then you kind of know what to expect. How should patients

8:04

be responding. How should their tumors be changing on

8:07

Imaging?

8:08

So I mentioned a couple but these

8:11

are kind of your traditional chemotherapy agents.

8:15

you know, you can see there's like tons of different examples

8:18

here and how they act, you know

8:21

on different portions of like the cell or

8:24

the cell cycle, but the overall

8:27

you know, I think for Radiologists what's really important to know is

8:30

that these are cytotoxic and so these are designed

8:33

to kill cancer cells. Everything should get

8:36

smaller.

8:37

For targeted chemotherapy. This is

8:41

a little bit different you can see there's all you know variety of different

8:44

targets that we can design drugs for whether it's

8:47

you know, an endothelial growth factor

8:50

inhibitor or you know

8:53

parp Inhibitors. All of these drugs that

8:56

have Target these different regulations systems for

8:59

for cancer. And so I think

9:02

about these more as psychostatic and

9:05

so, you know size measuring size

9:08

alone is not always going to give you all the information that

9:11

you need.

9:13

Um, so one good hint that I like to you know,

9:16

give is that if anything ends in an IB,

9:19

you know synonyms seraphinib

9:22

imaginib. Those

9:25

are some common ones. Those are usually going to be in this targeted category

9:28

and they're usually tyrosine kinase

9:31

Inhibitors. So you can see again just

9:34

exhaustive list of all these different drugs for all

9:37

of these different targets that really the end goal is to

9:40

kind of slow down or stop cell proliferation and

9:43

angiogenesis.

9:45

So one thing that comes up with these is resistance

9:48

these drugs tend to work very

9:51

well at the beginning and then patients, you know can develop

9:54

resistance after a certain number of you know,

9:58

treatments or time on treatment and you

10:01

know, that may be due to mutations and drugs have

10:04

to get changed. But again kind of knowing just

10:07

broadly about how these drugs work

10:10

and what they should look like when they're being used.

10:14

So for Passive cancer immunotherapies, so

10:17

these terms are targeted but they're not the tyrosine kinase

10:20

Inhibitors. So really what we're talking about here is

10:23

kind of immune mediated but not actual T

10:26

Cell killings. So some good examples are

10:29

like bedesses you have which is avastin as

10:32

the trade name, which is a monoclonal antibody to to veg

10:35

F and then trust who's a

10:38

map is another one that's antique her two and retucks. The

10:41

map is commonly used philipomo, which is against the Monopoly antibody

10:45

against the cd-20 antigen. So these are going

10:48

to inhibit cancer cell growth by blocking receptor

10:51

sites and signaling proteins, and they basically

10:54

induce death by tagging these cancer cells

10:57

for removal by the immune system.

11:00

So I make this these distinctions between passive

11:03

and active cancer immunotherapy. This

11:06

is kind of the ones we just talked about here. And then you know,

11:10

the active is more T cell

11:13

mediated killing of the actual tumor cells. So

11:16

this is where we give drugs that

11:19

allow the immune system to actually recognize and kill

11:22

cancer cells. Usually we're

11:25

doing this by turning off mechanisms that cancer cells use

11:28

to evade detection and kind

11:31

of slow down the immune response. So I

11:34

love this graphic. I think it's really nice and clear

11:37

and explains kind of how these drugs work. So if

11:40

we're using the pd1 or PDL one

11:43

pathway, this is programmed death

11:46

is what PD stands for but normally what

11:49

we have is here's our tumor cell. Here's

11:52

our T cell and this interaction here between

11:55

the blue parts are is the pd1 and the

11:58

PDL one and basically this is

12:00

adaptive mechanism that the tumor cell has that's able to

12:03

shut off the T-cell it, you know, once this binding

12:06

occurs, it kind of makes the tumor cell invisible to the

12:09

T cell and it can just kind of go along doing, you know,

12:12

go along and its business doing whatever it wants when we

12:15

give patients these, you

12:18

know immune checkpoint inhibitor drugs, which are either targeted to

12:21

the PDL one or the pd1 side.

12:24

We block this this

12:27

Binding from occurring and we

12:30

allow the T Cell to see the tumor the

12:33

tumor cell and kill it as well. There's a

12:36

kind of a similar mechanism that happens over here

12:39

the graphic on the right between the Androgen presenting

12:42

cell and the T Cell

12:45

which allows it to kind of present it and so

12:48

similarly when we give these drugs. We not only enable The

12:51

Killing but we also enable the antigen presentation

12:54

which you know enhances the T Cell response.

12:57

So that's probably didn't expect this from a

13:00

radiology lecture, but it's really interesting and it's it's good

13:03

to know about because it helps you understand what you're

13:06

seeing on the Imaging and why it may be atypical.

13:10

Um, so in addition to the pd1 pdl1 pathway

13:13

ctla 4 is another pathway that

13:16

ax very similarly. If you block this interaction, you're

13:19

able to allow T cells to

13:22

kill tumor and also enhances the

13:25

antigen presentation.

13:29

So one of the side effects of this active cancer

13:32

immunotherapy is that we can get unwanted activation

13:35

of the immune system. And so there

13:38

can be a wide range of toxic effects. So it's just something

13:41

to kind of be aware of that. You don't want to mistake these findings for

13:44

progression.

13:46

So moving on to you know kind of an overview

13:49

of the different cancer response criteria. So these

13:52

are used when a patient has started out chemotherapy, you

13:55

know, whatever class we just talked about.

13:58

To be assessed at Baseline and then

14:01

at interval follow-ups and these may be

14:04

different depending on which clinical trial in clinical

14:07

practice patients are usually imaged every three months or

14:10

three to six months and you know that may space out

14:13

the longer out. They are from their diagnosis and depending on

14:16

what kind of treatment they've had. So generally they're

14:19

kind of classified. If you look in this left-hand column into

14:22

different response categories. So CR stands

14:25

for complete response PR stands for

14:28

partial response SD is stable disease and

14:31

PD is Progressive disease so you

14:34

can see these are just kind of a group of examples

14:37

recess one point

14:40

one is kind of the the new version

14:43

of the newest version of recessed and that's one of

14:46

the you know more commonly used response assessment

14:49

criteria, but if you look down the column and

14:52

you see, you know, kind of where how these descriptions

14:55

are, they're really only focused on size, right?

14:58

So a complete response would be a

15:01

disappearance of all lesions a partial response would be a 30%

15:04

decrease in the sum of longest Dimension and we'll

15:07

talk about kind of how this is done in a second.

15:10

Skip down to Progressive disease which

15:13

is a 20% or more increase in the sum of the

15:16

longest Dimensions or any new lesions and then

15:19

stable disease is kind of in between these two. So if

15:22

you are not meeting parcel response

15:26

and you're not meeting Progressive disease, so I think this is

15:29

kind of important to look at this distinction because you

15:32

may have like a little bit of response or

15:35

you may have a little bit of increase in size. But as long

15:38

as you're not meeting, you know that criteria of progression,

15:41

you know, that's actually considered stable.

15:44

So that's a point. I like to you know,

15:48

kind of highlight in terms of terminology. It's something

15:51

that I see where sometimes residents

15:54

or other Radiologists May document a

15:57

very slight increase in size of a finding, you know,

16:00

even in just you know millimeters, but if they put

16:03

in their impression like, you know progression of disease

16:06

that is actually not necessarily the right

16:09

use of that term

16:11

Um a more accurate or kind of better way to

16:14

describe that might be like a mild or a minimal increase

16:17

in size of you know, a particular finding or

16:20

very slight increase in tumor burden or things like

16:23

that. But I tend not to use the word progression unless it's

16:26

actually meeting this criteria, um,

16:29

you know, if there's new lesions or if there's actually like a 20% or

16:32

greater increase, so unless you're actually gonna like do that calculation or

16:35

it's very obvious. You need to be kind of careful about

16:38

your terminology.

16:40

So we kind of touched on recess, but you can see Choi which

16:43

we'll talk about a little bit talks about

16:46

size. But it also talks about attenuation revise Joy

16:50

very similar and then Mass criteria

16:53

also looks at attenuation immune response

16:57

criteria has some different thresholds and then has

17:00

some requirements for follow-up for confirmation, but

17:03

there's a lot of information on this slide, so don't

17:06

worry about about this. We're going to go through all of these things

17:09

together.

17:10

Um, there can be some types of diseases that

17:13

are very difficult to quantify, you know,

17:17

for instance peritoneal carcinomatosis. So

17:20

for a lot of these GYN or peritoneal base

17:23

tumors or you know, gi gi cancers

17:26

that have disseminated to the peritoneum. You can

17:29

imagine that when you have like military

17:32

Or sheet, like disease that it's very difficult to

17:35

measure that right and it's difficult to measure it in a reproducible

17:38

way. So there's some other

17:41

response assessment, you know such as the peritoneal cancer

17:44

index which is more kind of it's a way

17:47

to try and quantify this unquantifiable disease.

17:50

So you give scoring based

17:53

on how much tumor you see and where you see

17:56

it the whole, you know, the abdomen and pelvis or divided up into these segments,

17:59

so

18:01

Um, so recess 1.1 has evolved from

18:04

The Who criteria and then recess 1.0

18:07

which we don't really need to learn much about these because they're

18:10

not used anymore. But basically if you have measurable

18:13

disease you have to have at least one centimeter of

18:16

disease on CT and a non-notal lesion.

18:19

If your disease is within lymph nodes

18:22

and the they have to be a little bit bigger where

18:25

the short axis has to be at least 15 millimeters

18:28

to be considered a Target lesion, or at least

18:31

10 millimeters to 15 millimeters to be considered a non-target

18:34

lesion, and then we kind of

18:37

already talked about what the definition of progressive disease was, which

18:40

is you know, 20% is kind of the the threshold

18:43

there. So the way that we do this is we basically

18:46

look at a baseline exam and we can select up

18:49

to five lesions. You can have up to two in

18:52

any single organ and then you

18:55

basically just measure them in one dimension

18:58

and then you add all of those up.

19:01

And you come up with a number and then that number is kind of

19:04

calculated at each visit and you look at the differences and that's how

19:07

you classify patients into their different response assessment categories.

19:10

So

19:12

we kind of all disease needs to be documented. And

19:15

so, you know, you fill up your target slots,

19:18

you're up to five lesions and then everything else in excess

19:21

of that or that's not really measurable kind

19:24

of falls into this non-target lesion definition. So it's

19:27

kind of like you're following things and attractable measurable

19:30

way with the targets. And then with the non

19:33

targets is a little bit more qualitative where you're you know,

19:37

things like plural effusions or sides or peritoneal disease,

19:40

you're giving a little bit more of a subjective kind of

19:43

a little bit more leeway and determining is this

19:46

better. Is this worse? Is it about the same because it's

19:49

hard to measure right. So yeah,

19:52

that's pretty much it. I think we've

19:55

kind of reviewed all this stuff. So here's an example finally some

19:58

Radiology, right finally some Imaging. So this

20:01

is a patient who has colon cancer

20:05

with metastasis to the liver. And so these two top

20:08

images A and B are measured at the Baseline

20:11

so you can see you have

20:12

Two dominant lesions here. You're only allowed up

20:15

to to two per organ. And so if you take

20:18

4.6 centimeters, which is the longest access measurement.

20:22

Here and add it to your 5.4. Then

20:25

you get a 10 centimeters is

20:28

your sum of diameters at the Baseline so

20:31

images C. And I guess

20:34

also see it should be our measuring

20:38

3.3 centimeters and 2.7 centimeters. So

20:41

when we add those up we get six centimeters. So

20:44

how we would classify this using resist is

20:47

that we've had a you know greater than 30%

20:50

decrease in the sum of diameters. We have 40% here

20:53

that this would be a partial

20:56

response. So when when

20:59

your drug Works in a way

21:02

that lesions should decrease in size, this is a really really

21:05

good way to kind of classify how patients

21:08

have responded.

21:12

So limitations, we've touched on some of these already a

21:15

little bit. So non-measurable disease, we've all seen this

21:18

like peritoneal like taking or you

21:21

know, just kind of the linear like blanketing of

21:25

disease throughout the omentum and that's really hard to measure even

21:28

if you can measure it on one exam or you're going to be able to

21:31

measure it the same way on the next exam because you know,

21:34

it's kind of a mobile organ. It can be it can be really challenging. And so

21:37

when you are trying to designate a Target

21:40

lesion or something that's you know to be tracked over

21:43

a series of images or a series of time points, you

21:46

know, peritoneal disease may not be a good candidate for

21:49

that mesothelioma similar

21:52

thing. This doesn't grow in a spherical or mask

21:55

like fashion this kind of grows in

21:58

a more grind like morphology. And so, you know

22:02

when it's growing in that circumferential pattern, it's

22:05

how do you put a longest access measurement on this?

22:08

So we have some modifications where for musicalioma we

22:11

pick

22:12

Couple of places and we measure the width of it instead, but

22:15

that's another topic from today. But

22:18

some other limitations anybody who's read

22:21

lymphoma cases, you know that even when disease

22:24

has totally responded you can have residual soft tissue

22:27

or masses that persist after therapy. And if

22:30

you're using CT alone, it can be really hard to tell you know

22:34

has my patients disease gone away. I still

22:37

see lymph nodes are not as big as they used to be. Are they

22:40

still active cancer or is this treated disease which is

22:43

why pet, you know is really so important in lymphoma because you

22:47

can actually, you know, you kind of incorporate the

22:50

metabolic response as well as the

22:53

as well as the anatomic response.

22:56

So for targeted therapy, like we talked about this is you know

22:59

kind of accent a site of static way. And so really what's

23:02

happening at the cellular level is we are

23:05

stopping cell growth, right? And so if

23:08

we don't appreciate huge changes in size

23:11

in our tumors are we really capturing the

23:14

response that's going on there. We need to look

23:17

at more than size here.

23:19

So for things like just carcinomas other

23:22

soft tissues sarcomas, you know,

23:25

so certain tumors, but also, you know certain therapies. We really need

23:28

to look at density and kind of the inner character of the tumor.

23:32

Um, some drugs can cause an intraumeral Hemorrhage, you

23:35

know, which is actually part of the treatment

23:38

response and you can imagine that might cause some swelling

23:41

or growth of tumor that if

23:44

you're only looking at size you're going to miss classify that

23:47

you know as possibly an increase in

23:50

tumor burden or even progression if it's significant enough.

23:53

When we have long lesions

23:56

that respond showing cavitation, if

23:59

you're measuring the outer margin of

24:02

these lung lesions, it's probably not going

24:05

to significantly change overall, but you may have cavitation

24:08

and if you're using size only resist-based

24:11

measurements, you're not going to capture

24:14

that response, right? And then immunotherapy is

24:17

it's has its own sets of challenges, which we're really

24:20

kind of dive into later. So here's an example. This is

24:23

a patient metastatic colon cancer.

24:25

Sir, and says you mad or trade name is

24:28

avastin and this is the monoclonal antibody to vegf. So it's

24:31

very classic that you see cavitation in

24:34

response to this drug. But you know,

24:37

if you're looking at this knowledgeable and you measure this as seven

24:40

millimeters and then on your six week follow-up and measures one

24:43

point five you if you're only looking at size,

24:46

right you're gonna classify this as progression. This thing is

24:49

more than doubled in size. But in fact, this is a response.

24:52

So this is showing that recessed and

24:55

size based only is not always, you know, the right

24:58

thing to choose or not always reflective of

25:01

what's actually going on.

25:04

So this is particularly important for gist, you

25:07

know metastatic just to the

25:10

liver and if they've never been on any sort of tki and that

25:13

live it's very classic for these to have a mixoid

25:16

degeneration Hemorrhage necrosis as part of

25:19

their response patterns. And so while you may

25:22

not see significant changes in size or you may actually even see increase

25:25

in size you can you usually appreciate a

25:28

dramatic drop in density. Sometimes you

25:31

have lesions that like kind of up here

25:34

or become more well seen

25:37

and this may be due to

25:40

the fact that they were actually kind of a cult on the previous Imaging and

25:43

now you're seeing them because they're in a product. So this

25:46

is something important to be aware of because you don't want to misinterpret these

25:49

for Progressive disease whether you're calling an increase

25:52

and size of something that's existing or actual new

25:55

lesions. So if it's not

25:58

clear what's going on, which sometimes it's not special with like Hemorrhage

26:01

PET CT is another tool you

26:04

Use to kind of help figure out what's going on.

26:07

So here's a nice example, you know, we have

26:10

Baseline Imaging here up in

26:13

the top left and we've got a lesion that's 2.8

26:16

centimeters and illusion that is 1.7 centimeters. So

26:19

we add these up and this is 4.5. When we

26:22

look on the post treatment first follow-up time

26:25

Point. These lesions have gotten bigger right 3.9 centimeters

26:28

and 2.9 centimeters. So when we

26:32

add these up 6.8 we have a more than 50% or a

26:35

50% increase here. And so if we're using size

26:38

alone, you know, we would

26:41

we would say this drug isn't working. Right? This is like the cancer

26:44

is growing through the drug. That's what we mean when we say

26:47

progression.

26:48

Um, but when we look at these, you know,

26:51

Mr. Images of these same lesions, we can see that

26:54

these are T1 bright, you know

26:57

not having enhancement in these areas that this

27:00

is actually just intertumeral hemorage and we go

27:03

back and look at the CT if you can appreciate this area is so

27:06

much less dense than it was here. So what we're

27:09

seeing on the Baseline is like enhancing solid tissue. It

27:12

happens to be less enhancing than surrounding liver. This

27:15

is enhancing tissue on the follow-up that

27:18

we we actually have pockets of like not enhancing tissue, which

27:21

we know from the MR is into tubal Hemorrhage and so

27:24

the amount of actual like persistent enhancing

27:27

tissue is much less than it

27:30

was on the Baseline. So this is actually an excellent response to therapy.

27:34

Hugs, so this is an example of you know, how size

27:37

alone is not enough to characterize what's going on,

27:40

especially with certain tumors and especially with certain

27:43

drugs.

27:44

So as a result, you know

27:47

this criteria called the toy criteria was created. It's

27:50

been modified. But you know,

27:53

you can see that the definitions of how you classify a

27:56

patient's response or a little bit different right? So this

27:59

decrease in size of 10% So this is a

28:02

low earth threshold that was what was required for recess which

28:05

was 30% or a decrease

28:08

in tumor attenuation by 15% or

28:11

greater. And so

28:15

You know, we're looking at more than just partial response

28:18

which I mean sorry more than just size

28:21

which is really important. We also obviously have to have no new

28:24

lesions and no obvious progression of non-measurable disease. So

28:27

stable disease will

28:30

kind of skip because that basically is just something that doesn't fit PR or

28:33

PT, but for PD you have to have a size increase of

28:36

10% but all so it's

28:39

not, you know changing in attenuation that would

28:42

classify it as a PR. The other thing that

28:45

Joy highlights is these new intraumeral nodules or

28:48

increase in size that existing inch or

28:51

two moral nodules. You can imagine if you're looking at a very heterogeneous

28:54

lesion that has intraumeral nodules, you

28:57

know, if you've given overall size you're not

29:00

really going to be class.

29:02

Specifying these so here's an example of this where this patient

29:05

had been treated for metastatic gist and

29:08

their lesions were like very low density almost kind of like liquid

29:11

fluid looking and on a follow-up, you know,

29:14

the overall illusion definitely hasn't increased in size

29:17

is measuring exactly the same but we have these new

29:20

kind of enhancing soft tissue nodules

29:23

within the tumor. They're usually along the wall, you

29:26

know, that's where they tend to occur but

29:29

really important to look for these when you're reading follow-ups

29:32

on you know, patients with treated

29:35

disease or you know to follow these if patient

29:38

has these at the Baseline

29:40

So you can see a follow-up was done in these it

29:43

definitely all increase in size. And you know, if you're using

29:46

size assessment alone of the entire lesion, you

29:49

are going to miss all of this, right but when you're looking at

29:52

the character of the lesion, there's definitely progression and

29:55

increase in tumor burden here a pet

29:58

was done here which, you know kind of confirm that this is all active disease,

30:01

but we we know that right from the morphology and the

30:04

character of what's changing.

30:06

Um, so yeah, this has been you know,

30:10

modified and revised and everything but this the

30:14

newest criteria include what we talked about with

30:17

the decrease in size and the decrease in attenuation

30:20

or sometimes these do act like they're supposed to and they

30:23

just decrease in size. So they've kind of accounted for that as well.

30:29

Um, so here's some more limitations of recess.

30:32

This is a case of metastatic renal

30:35

cell carcinoma and this patient was on serafinib, which

30:38

is a tyrosineke is inhibitor. They ID gives you

30:41

that clue so it acts on a bunch of different targets here.

30:44

But what it does is it basically induces the cell

30:47

to disassemble itself and then

30:50

be cleared from the system. So when we

30:53

look at the Baseline here, you can see there's you know,

30:56

a few to multiple lesions in the

30:59

liver. This one has a nice hyper enhancing

31:02

kind of irregular thickened rim,

31:05

and then internally, there are probably some

31:08

cystic components but there's also some hypo enhancing

31:11

soft tissue as well when we

31:14

look on the image on the right that's labeled D.

31:17

This is a follow-up exam. And when you first look at this, right

31:20

probably what stands out to you is that looks like there's more

31:23

lesions and so oh no is this patient progressing through the

31:26

treatment? Is it not working? I see more lesions when I saw

31:29

Chord, it would be easy to miss classify this as Progressive disease,

31:32

right but when you actually look at the character of

31:35

the lesions that the dominant lesion in the left lobe no

31:38

longer has that enhancing a regular Rim. If you

31:41

look at the internal density, it's almost you know

31:44

certain the almost. The entire thing is kind of this liquid

31:47

fluid density. Now, they're you know, there is still some enhancing tissue

31:50

in the middle and maybe a septation but and when

31:53

you look at these other kind of newly apparent lesions,

31:56

they all are very low density. So what this

31:59

is actually showing us is that we have

32:02

a response in the tumors that we know about and we also

32:05

have a response in lesions that we're probably previously a

32:08

call there was more disease and we could even appreciate on the previous

32:11

exam. And so this is actually really excellent response to

32:14

therapy, but you can imagine that if

32:17

you're using recess or only thinking about size that

32:20

you're you're

32:21

Not going to come to that conclusion as

32:24

easily.

32:26

So Mass criteria is one that's specifically used

32:29

with metastatic renal cell carcinoma. And

32:32

so instead of using your crpr

32:35

SD and PD categorizations. They kind

32:38

of talk about these in a different way of a favorable or

32:41

unfavorable response, but,

32:44

you know similar to Choi they're looking at

32:47

You know, they're looking at size but they're also really looking

32:50

at character and you know attenuation of

32:53

lesions. So you don't have to know any

32:56

of these in depth. I mean, it's good to be familiar with

32:59

recess 1.1 but really

33:02

my intent and talking to about these

33:05

guys is to

33:08

You know kind of understand the concepts and just being

33:11

able to apply those at the workstation.

33:15

Um, so we kind of talked about this.

33:18

And so if you're using recessed, this is just

33:21

you know results from a study showing that less than

33:24

half of medicine renal cell patients could achieve an

33:27

objective response by recessed criteria. And so you

33:30

can imagine that if you are developing new drugs for metastatic

33:33

renal cell carcinoma, and your data

33:36

is showing that less than half of your patients can

33:39

achieve an objective response. Like that's not going to look like

33:42

your drug is working very well, right? And so that's kind of

33:45

why they come up with these alternative assessment patterns

33:48

to really kind of it's important to be

33:51

able to capture response. And so

33:54

that is you know, very very key for

33:57

the development of all of these different criteria is

34:00

to kind of find the best way to capture

34:03

response. So yeah,

34:07

I mean if you are calling something stable Disease by

34:10

recessed

34:12

You know you you may not be really capturing the

34:15

clinical benefit that they're getting from the particular drug.

34:21

All right. So for immune related response criteria, um,

34:24

these thresholds are a little bit different, right? So

34:27

CR is the same disappearance of all lesions PR

34:30

this requires a 50% or more

34:33

decreased in the bi-directional measurements. So this is measured into

34:36

Dimensions where as recess. It's

34:39

just one.

34:42

It's um, and then PD is

34:45

a 25% or greater increase in by

34:48

a directional measurements. These are a little bit, you know different from what

34:51

we were staying for but when we call PD,

34:54

especially early in treatment, we because

34:57

of this phenomenon of pseudo progression, which we're

35:00

going to talk about shortly. We need reassessment on an additional

35:03

scan which can be performed. No sooner than four

35:06

weeks.

35:07

So we'll talk about student progression in a second. But

35:10

we're going to review the immune checkpoint inhibitor

35:13

response patterns. So, you know,

35:16

there's like four patterns that are kind of recognized with

35:19

these drugs. Number one is really easy because it

35:22

is you know, what you expect to see when a

35:25

patient's on chemotherapy. So we see a decrease

35:28

in tumor size no evidence of new tumors, you know

35:31

after the completion of treatment and so kind

35:34

of any criteria that you use this is going to look like a response,

35:37

right? So either it shrinks or it

35:40

goes away what we expect to see so this is an example of

35:43

metastatic melanoma patient was on it the

35:46

limit and this is Baseline and 16 months.

35:49

So there's still some residual soft tissue here, but

35:52

you know, it's definitely increased by any measure of

35:55

response assessment. We're going to call this a response.

36:00

Um, so pattern number two is where you basically just

36:03

get like long-term stability. Sometimes you

36:07

get long-term stability and then an eventual response and sometimes

36:10

you just get long-term stability, so

36:15

This is an example of metastatic melanoma also on epilepsy

36:18

lab and this is at two four and

36:21

seven months after treatment completion. So really kind of

36:24

Not changing much.

36:27

So the third pattern is one of the

36:30

phenomenon that's described as pseudoprogression. And

36:33

so what we see here is that existing tumors

36:36

appear to increase early on

36:40

in treatment and then they're followed by an eventual decrease

36:43

and sometimes you know complete disappearance. And

36:46

so there's a lot of examples of

36:49

melanoma here because that's where these drugs were kind

36:52

of first introduced and most extensively studied. So you're

36:56

gonna see a lot of examples of melanoma here, but here we have,

36:59

you know, the subcutaneous knowledge will which on baseline

37:02

or sorry this is three weeks.

37:05

Four weeks seven weeks 13 months

37:09

and twenty. Sorry. The first one is the Baseline and

37:12

then three weeks four weeks seven weeks seven months 13 months

37:15

and 26 months, but you can see between the

37:18

first and second time Point. There's a significant increase

37:21

in size of this soft tissue. And so

37:24

if you are reading this by really

37:27

any criteria, there's no significant decrease in the density.

37:30

You're going to call this progression and say, oh no, this drug

37:33

isn't working a patient's cancer is growing while they're on the drug, but

37:36

you can see by the next time Point labeled C

37:39

that there's a little bit of a decrease in size, and

37:42

I don't know if you guys can appreciate it, but there's also a

37:45

decrease in density.

37:46

And then moving down to De andf, you

37:49

can see Progressive decreased in size

37:52

of this finding to where it's like almost not even seen anymore.

37:55

And so this is really rare

37:58

this only accounts and like three to ten percent of cases. But

38:01

what we postulate this is

38:04

due to is, you know, there's two mechanisms one is

38:08

that we have true continued growth during the

38:11

time that it takes to mount an immune response, right these drugs

38:14

take time to basically train the

38:17

immune system to kill so number one is

38:20

that it's actual tumor growth, but it's it's just

38:23

because the immune system hasn't kicked in yet. The second

38:26

thought is that you get

38:29

actual immune cell infiltration into tumors and

38:32

you know with or without a team and so you're you're

38:35

tumor may be actually like under attack

38:38

and swollen and undergoing like

38:42

cell death before it starts to actually

38:45

like turn around.

38:46

So we have like histopathologic confirmation

38:49

of both of these phenomena in these settings.

38:52

So it's something that you know, you have

38:55

to definitely keep in mind if you are looking early on

38:58

there's no specific set like

39:01

time criteria of when

39:04

pseudo progression can occur, but it's

39:07

most commonly seen I think in the first 12 to

39:10

15 weeks of treatment.

39:11

So if you are reading a cancer

39:14

case on a patient who you know is using an

39:17

immune checkpoint inhibitor. It's really

39:20

important to know when was that treatment started because if

39:23

you are in that first 15, you know

39:26

12 to 15 weeks and you've seen an increase in size. You

39:29

don't want to necessarily call it progression and take

39:32

a patient off a drug that might benefit for them. What you what you

39:35

need to say in those scenarios. Are we need another time

39:38

point we need to figure out where this is headed. Is this going

39:41

to continue to increase in size or we in one of these scenarios

39:44

where it's actually going to turn the corner and start responding. So

39:47

there are case reports that

39:50

show super progression occurring out as far as like 50 weeks. So

39:53

it's really, you know, like the drugs don't they don't

39:56

read the books. They don't necessarily follow the

39:59

guidelines, but you know, it's very important

40:02

to think about early on and that's why you know

40:05

that second time point is required to

40:08

kind of give confirmation.

40:11

Um, so here's another example. We've got

40:14

a patient with metastatic breast cancer. So pretreatment. You

40:17

can see she's got this long lesion on the right which by

40:20

time point B on week 12 again. We're

40:23

really early in treatment has definitely decreased in size

40:26

like nearly doubling right and then we go back at

40:29

week 20 and this thing has nicely decreased in

40:32

size both compared to the Baseline and the interim.

40:35

So this is a really nice example of super

40:38

progression for a patient on an anti-pedial One

40:41

agent on the graphic

40:44

below. This is a sorry a liver

40:47

lesion and a patient with metastatic lung cancer and you know

40:50

the middle graphic B on treatment week

40:53

seven like this thing has exploded right and it's not

40:56

like it's just decreased intensity by any response criteria

40:59

that you use Joy recess Mass. Whatever. This looks

41:02

like an increase in tumor, which very well

41:05

may be we may be kind of in that scenario where the drug

41:08

hasn't kicked in yet and we have

41:11

tumor growth and so on week 15

41:14

we can see that this is you know declared itself in the direction

41:17

of response and it's you know, definitely decreasing in

41:20

size. So again, this is an anti-pd-1

41:23

agent but this phenomenon of

41:26

student progression can be very very confusing because it looks exactly

41:29

like progression.

41:31

So here's another one. This is again metastatic. Melanoma.

41:34

You can see Progressive increase in size over the first three.

41:39

First three images on the top and then you can see it the first

41:42

one on the bottom row on the left. We have like

41:45

a significant drop in density followed by a decrease

41:48

in size.

41:51

Here's another metastatic. Melanoma on epilemon map

41:54

and you can see these soft tissue lesions in both thighs

41:57

actually with the arrowheads and on the middle time

42:00

Point definite decrease in size and

42:03

enhancement in number of nodules that area

42:06

that was previously kind of cystic and

42:09

necrotic is now kind of filling with soft tissue and

42:12

then time Point C like gone.

42:15

So these are

42:18

just some really really nice examples from the literature of pseudo

42:22

progression.

42:24

Here's another one Hodgkin's lymphoma on pembrolizumab.

42:27

And so even though the patient

42:30

in this case met criteria for Progressive disease,

42:33

their performance status was so good that they kept them

42:36

on the drug, but you can see from the myth images

42:39

on the top that this dominant.

42:42

That lesion in the mesentery in the right of our quadrome

42:45

mesentery has like, you know progressively increased up

42:48

until cycle 4 12 weeks and then at 24 weeks

42:51

is like magically gone. It's it's really

42:54

cool. Some of the disease in the chest had kind

42:57

of you know, gotten better. If you look in the left upper lobe these

43:00

findings had had gotten a little bit better. So one

43:03

question I get from clinicians a lot from oncologists is

43:06

how do you tell the difference between progression and pseudo progression

43:09

and the short answer is that we can't we

43:12

need more time points, right? We need the follow-up confirmation to

43:15

figure out which direction it's headed but something that

43:18

always makes me really think about pseudo progression

43:21

and you know, really kind of

43:24

lean that way is if there's a mixed response,

43:27

right? So if we have some disease that is getting better.

43:30

It makes me

43:33

wonder if you know, okay is someone

43:36

is some disease responding and some just has a lot had

43:39

long enough to actually start turning around yet. So

43:42

Short answer is you can't tell but I think about

43:45

it more when I see at least some of the disease responding.

43:51

Um, so the fourth pattern is where we don't

43:54

just see an increase in size of

43:57

disease that we know about but we actually see new

44:00

lesions. So this is an example metastatic melanoma

44:03

patients on epilepsy lab so you

44:06

can see this area of subcutaneous tissue in the left hip there's nothing going

44:09

on here. But on the follow-up at time point B,

44:12

we have a new or newly apparent soft

44:15

tissue nodule which then goes away

44:18

at you know, 24 weeks. And so what this

44:21

is thought to represent is that it may

44:24

not necessarily be like a new lesion, but it's kind of

44:27

blooming or blossoming of a site of micro metastatic

44:30

disease that we just couldn't resolve on on

44:33

our original Imaging because

44:36

it was just too small.

44:39

Here's a case of metastatic lung cancer on Pembroke and

44:42

Baseline three

44:45

months. They had a you know, a clear increase in

44:48

size of this right adrenal metastasis. Um,

44:51

but, you know, we were kind of in that first three month pattern. So

44:54

we said let's give it a little bit more time and at six months the lesion

44:57

is like pretty much gone just a tiny bit of warmth left

45:00

in that lateral limb.

45:03

Here's some examples. I just wanted to show you in other organs. We've

45:06

done a lot in like the liver and the lung and the subcutaneous tissues.

45:09

But here's one of the patient with metastatic

45:12

lung cancer and on immune

45:15

checkpoint inhibition and on week 8,

45:18

they have a new lytic lesion in the right iliac bone.

45:21

So that's kind of

45:24

confusing right but we're at week eight. So we don't really

45:27

know what to make of it follow up week 17 we can

45:30

see that this thing is getting sclerotic which you know

45:33

indicates that there's an interval healing and

45:36

this thing is responding. We also have

45:39

a lymph node here in the right and the right

45:42

external iliac station, which was like totally totally

45:45

normal pretreatment resolves by

45:48

week 12. This is a patient with metastatic melanoma. And

45:51

then this one here on the bottom see I

45:54

think this is the same patient, but they had like

45:57

new lyric lesion in this lumbar vertebral body

46:00

and right transfers process which then

46:03

You know become sclerotic by week 23, so I

46:06

think you know in most cases patients aren't

46:09

being imaged this early in treatment. These are

46:12

from kind of clinical trials and early development week

46:15

eight is very early to image most people wait

46:18

three months for the first Imaging time point but sometimes

46:21

patients come into the ER sometimes they're sick

46:24

they get Imaging early for whatever reason so really

46:27

important to have this on your radar and to also

46:30

think about at that first time point of three months

46:33

when you see changes because we don't really know which way they're headed

46:36

yet.

46:37

So how do we know what's actually going on? So history

46:40

is really really important and you guys

46:43

know that's always a struggle to kind of get and

46:46

depending on how good of

46:49

a functioning electronic medical record you have

46:52

it may be easy to get or it may not but you

46:55

know things that I always want to know when I'm

46:58

reading a cancer patients Imaging who's undergoing treatment

47:01

is you know, what treatment is the patient on and then

47:04

I kind of know what response patterns I'm

47:07

expecting to see right if they're on cytotoxic treatment.

47:11

Every like traditional chemotherapy everything should get better. There's a

47:14

really no circumstance in which anything can get worse

47:17

and a response be happening.

47:20

If they're on immune checkpoint inhibitor, that's a totally different story. Right

47:23

things can look a little bit worse before they get better. Also if

47:27

I know they're on a targeted therapy or a tki I

47:30

really need to focus on the character of the tumors as

47:33

well as the size.

47:35

So how long have they been on it? You know this

47:38

is really important for the immune checkpoint of hippers. Like we talked about with

47:41

considering student progression. Um and which

47:44

comparison to use as a new Baseline. So these cancer

47:47

treatment regimens can be really complicated patients

47:50

can go through multiple lines of therapy. And

47:53

so in order to give the clinician the information

47:56

that they need you need to know. When was this new treatment started

47:59

because if you just pick a study that's like two years old that may

48:02

be from two treatments, you know regimens previously

48:05

like you need to kind of go through the medical record

48:08

figure out when was this drug started and this is

48:11

actually something to be really challenging because sometimes with insurance approval

48:14

or if a patients getting on a trial their Baseline

48:17

Imaging or what you think is their Baseline may

48:20

not actually line up when with when there's treatment

48:23

was started. And so sometimes you see changes but

48:26

you say the CT was done two months before the

48:29

patient started their treatment. I don't know if this growth that

48:32

occurred was actually prior to starting

48:34

Therapy and now disease is stable or is

48:37

it actually just growing through, you know, whatever treatment they're

48:40

on so knowing kind of where your

48:43

Imaging lines up with your treatment

48:46

is really important.

48:48

And so if you see a parent worsening of

48:51

disease while patients are on immune checkpoint Inhibitors, you

48:54

know, you really need to think about

48:57

student progression and you need follow-up Imaging

49:00

before you can really make a decision.

49:04

So yeah, just to kind of recap you

49:07

don't need to know the specifics if you know, I think it's good

49:10

to be familiar with recess because it's the most commonly when

49:13

used one but it's just

49:16

I think conceptually nice to know about these different

49:19

response assessment criteria. So size, you

49:22

know recess really only considers size

49:25

toy and mask kind of consider size and

49:28

morphology, you know and immune

49:31

response related response criteria. Think about

49:36

You know all of those things, but also, you know may require

49:39

some additional time points, especially early on.

49:42

So again, knowing what

49:45

to expect so know what drugs the patients are on and you

49:48

know kind of know which Concepts to use for looking for response.

49:53

Um, so just some pitfalls. We only have a few minutes left,

49:56

but one thing I want to point out are these sarcoid

49:59

like reactions so particularly with the

50:02

immune checkpoint Inhibitors, you can kind of you can

50:05

get this overdrive of the immune system. And

50:08

so it's very common to see things like thyroiditis colitis patients

50:11

get rashes. We don't usually appreciate those on

50:14

Imaging but pneumonitis. These are really kind of important things

50:17

and so you don't want to miss classify those as Progressive disease

50:20

and you also want the clinicians to know

50:23

because in rare cases and humanitis can be fatal patients

50:26

may be very symptomatic. So it's good to have on your

50:29

radar but I'll show you one example, we have this patient with

50:32

a left axillary melanoma and

50:35

she underwent treatment where you can see that the the

50:38

lesion went away, but she actually showed up with a right axillary

50:41

lymph node hot on pet and her follow-up exam.

50:44

So this ended up getting a biopsy and

50:47

it showed you know changes consistent with sarcoidosis

50:50

not casing illness.

50:53

Um, so she went on for her next follow-up time point and she

50:56

had kind of a more classic presentation of what we see with these

50:59

sarcoid-like reactions, which is usually kind of media style and Hyler

51:02

activated lymph nodes, but you

51:05

can see it on CT too. Obviously they get big

51:07

Here's a case of kind

51:10

of like a mild pneumonitis after this patient

51:13

had metastatic lung cancer, which was on pembrolizing lab.

51:17

So you can see these changes here in the right upper

51:20

lobe left lower lobe patient was stopped

51:23

on their therapy and

51:26

given steroids and you can see that it went away.

51:29

So really important thing to put on the clinicians radar.

51:32

They want to know kind of what it looks like how much of the long

51:35

it's involving. You can see kind of more minor changes here and here as

51:38

well.

51:40

But yeah, those are kind of important to not mistake for

51:43

for PD. So take home points know

51:46

your cancer know how it behaves we didn't talk much about that because

51:49

that's more of like a staging thing and today's really focused on

51:52

like restaging but know the treatment the class

51:55

of drug how long they've been

51:58

on it what the side effects are like be careful

52:01

about terminology, you know progression really

52:04

refers to a specific set of criteria. So

52:07

if you're if you're saying that make sure that's what it really means because

52:10

what the clinician sees when they see progression is

52:13

this drug is not working and we need to change it.

52:17

So understand limitations and size only assessment and

52:21

use all of your tools get all

52:24

the information you can out of the medical record sometimes additional

52:27

findings like, you know, tumor markers can be

52:30

really helpful to not sway you but confirm,

52:33

you know what you're thinking and then

52:37

lastly student progression is rare. You can

52:40

suggest it up front but it's only kind of confirmed retrospectively

52:43

when you have your follow-up time

52:46

points, but there are lots of patients on these drugs

52:49

every day at every hospital. So this isn't just

52:52

something you need to know how to make Center Community Hospitals use

52:55

these drugs all the time.

52:56

So that's all we have time for. Thank

52:59

you everyone for logging in and I'm

53:02

going to check out.

53:06

Let's see the Q&A box here.

53:10

So, let's see. How do you see the clinical impact of AI

53:13

on ecologic monitoring real world

53:16

application like volumetric data, not just radionomics and

53:19

academic like markers that need extensive validation.

53:24

So

53:25

yeah, I mean, I think these response assessment

53:28

criteria have been developed as a way

53:31

for us to track lesions, you know

53:34

their conventionally done in one or two

53:37

dimensions on axial slices. And this

53:40

is a you know, a difference of how things are done at the workstation

53:43

versus like, you know at a clinical trial Reading Center.

53:46

Those aren't always as necessarily as

53:49

reflective as like, you know, T stage or things

53:52

like that. So it's it's really kind of a reproducible way

53:55

to track something. And so I think AI can

53:58

definitely enhance that um, some clinical

54:01

trials do like to use volumetric assessment

54:04

and you know, they

54:07

Sometimes we'll look at recess 1.1 but then they'll

54:10

also create additional criteria to look at

54:13

and follow and see how those line up and you know, that's sometimes how

54:16

new response that response assessment are validated or

54:19

kind of created is they're done

54:22

in parallel with older older systems. So I

54:26

think you know practically the way

54:29

that we do it to be able to read lots of patients over lots

54:32

of time points is in a way that's simple but I think that

54:35

can certainly be enhanced by by AI, you

54:38

know as well as metric assessments, maybe more kind

54:41

of comprehensive and reflective then just,

54:44

you know, unilateral or by dimensional measurements which

54:47

have been designed more for practicality.

54:51

All right and suspected pseudo progression

54:54

in which time do we say next CT to

54:57

exclude City progressions? It's a great question. So I think

55:00

the guidelines tell us to not do it sooner than

55:03

four weeks because if you do it standard

55:06

four weeks, you're likely to just see the same thing and be in the same position so

55:09

I often will

55:13

say in my fall of recommendations no sooner than

55:16

four weeks, but in conversations with with clinicians,

55:19

they usually like to just give it

55:22

one more cycle of treatment. And so if they

55:25

are particularly worried about a patient

55:28

because the one thing that you have to kind of keep in

55:31

mind in addition to student progression is hyper progression,

55:34

which we didn't really talk about today, but that's like we're patients

55:37

just hyper progress on a particular drug and

55:40

you want to catch that sooner rather than later. So, you

55:43

know, if a patient is out there three months follow-up appointment

55:46

and it looks like there's you know worsening of

55:50

disease and we don't know if it's

55:51

Aggression or suited progression? Sometimes they

55:54

say I'm surprised that the Imaging looks like this because the

55:57

patient is doing great. They feel so much better. Their symptoms are

56:00

improved. They're doing more than you know,

56:03

we say well maybe this is super progression. Why don't you

56:06

give it another cycle? And so they'll actually wait like three months before they do another

56:09

scan. But if they're like, you know, the patients

56:12

deteriorating like they're not doing very well, they feel horrible. Um,

56:16

then, you know, they may image closer to like

56:19

four six or eight weeks from from that time point

56:22

so I think

56:24

You know, the the guidance is no less than four weeks,

56:27

but I think how far you go out kind of really depends

56:30

on the clinical picture of the patient, which unfortunately we

56:33

don't really usually know and that's kind of up to the clinician to

56:36

the side.

56:37

Okay, next question what might be the

56:40

clues to stop a drug or biologic therapy During the period of

56:43

time when pseudo progression is possible. Well, maybe

56:46

the clues.

56:48

To stop during the time.

56:50

Yeah, so this one we've kind of talked about that.

56:54

You know, if if you are suspecting a

56:57

hyper progression and that's not something that we suspect radiologically

57:00

we just are more objective in

57:03

that, you know things look worse things look better. Um,

57:06

but you know, if I get the clinical information not a

57:09

patient is like doing very poorly then, you

57:12

know, then I think more about hyper progression

57:15

and that's really when the drug should be stopped. You know,

57:19

and it sometimes it can be hard to tell like are they having

57:22

are they doing poorly because their disease

57:25

is continuing to grow and they are hyper progressing

57:28

and their cancer is making them

57:31

feel poorly or are they feeling poorly

57:34

because they're having toxicities and side effects from the drugs

57:37

and one interesting point.

57:40

Is that patients who develop these

57:43

toxicities they actually tend to respond. And

57:46

so if you see somebody that's developing thyroiditis

57:49

or pneumonitis or they have like rashes

57:52

that may actually tell you

57:55

that the drug is working very well and that they are going to be somebody

57:58

who responds so I think that's

58:01

a little bit we have to rely on our clinical colleagues to

58:04

kind of kind of tell us, you know,

58:07

if they're feeling poorly what do we think? It's

58:10

what do we think it's due to, you know, in addition

58:13

to us being able to detect those other talks to cities.

58:17

Um, okay next one.

58:21

So recessed is absolutely approved by oncology, or

58:24

is it instill in trial or research state? So recess

58:27

1.1 is definitely established. It came

58:30

out several years ago and that's being routinely

58:33

used in clinical trials. That's it's used

58:36

in research, but rhesus one point one is

58:39

like absolutely validated.

58:42

Um, all right, somebody said can you discuss the features of

58:45

Legato criteria? I would love to that's like a whole

58:48

separate a whole separate topic. That's

58:51

really a Lugano is an assessment criteria that is used

58:55

in lymphoma. And there are

58:58

pet features that you look at versus CT

59:01

features. And that depends is

59:04

your lymphoma fdg Avid, then we use the pet

59:07

criteria or is your lymphoma not fdg, then

59:10

we use CT based criteria, but there are some

59:13

similarities where you pick certain Target lesions

59:16

and you follow them over time. Those are

59:19

assess a little bit differently measure long and short access

59:22

you multiply them by each other and then you come up with, you know,

59:25

some of perpendicular products which are

59:29

then compared and the thresholds for how you categorize patients

59:32

response are a little

59:35

bit different than racist one point one, but the using the

59:39

pet we kind of talk about

59:41

Little criteria, which is a five-point Scale

59:44

based, you know relative to background

59:47

tissues relative to liver and we kind of classify the

59:50

metabolic behavior of lymphoma and

59:53

look at assessment response assessment based

59:56

on improvements or worsening in SUVs. So

60:00

that's like the two minute the two-minute version of

60:03

it, but it's it's kind of totally separate than

60:06

the ones we talked about today the ones we talked about today are really

60:09

for solid tumors and don't really address lymphoma.

60:14

I think

60:16

That is all we have. So yeah all

60:19

we have time for at least. Thank you guys for having

60:22

me and yeah, it's a

60:25

great platform to to be able to share these lectures and

60:30

I am happy to be here.

60:32

Dr. McIntosh, thank you so much for your lecture today and thanks

60:35

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60:38

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61:09

Thanks everybody.