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FLINCE_Laro TRK HCP Adoption Research Interview 2018 1-29 1pm 5
January 29, 2018

Interviewer: [Pause] Alright, to start us off, we’re going to be talking about a broad range of
cancers in our time today but to start off, I’d like to understand a little bit about
the setting that you’re in, your specialization, what you are doing on a day-to-day
basis and the type of tumors you see most.

Respondent: Sure, I’m a medical oncologist, a hematologist as well, both certified in both fields
in a prior practice setting solo community-based. I’ve been practicing for 17 years
since I finished my fellowship training. I’m a general hema so I see varieties of solid
and some liquid tumors and I see an average of about 250 or 300 patients a month.
I see all types. The common tumors that I see, of course, are breast, lung,
colorectal and I see good numbers of gastric and pancreatic as well and liver, of
course, in my practice because where I practice is a large metropolitan area but
have a lot of Asian descent patients too.

Interviewer: Okay.

Respondent: [I definitely]

Interviewer: So give me a sense, you told me about 250 to 300 patients a month so in a typical
month, about how many of the patients you see would you estimate would be non-
small cell lung cancer?

Respondent: If it’s all stages –

Interviewer: Yes.

Respondent: I would say 55, at least.

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Interviewer: Okay, and colorectal?

Respondent: I would say probably about 30 to 35.

Interviewer: Okay and pancreatic cancer, you mentioned that as well. How many times are you
seeing pancreatic?

Respondent: I will say about 12.

Interviewer: Okay and then, papillary thyroid carcinoma, let’s throw that one in there.
[Laughter] How many of those would you see? Is that more like a typical year or a
typical month that that number would make more sense?

Respondent: About 10 of them a year.

Interviewer: Okay, perfect. That’s one that I’m not familiar with so I wondered how frequent it
is so I want to start out just talking about when you think about the new
treatments that have come along. This has been happening for a long time in
oncology, lots and lots of new treatments all the time. What is it about a new
treatment that comes to market that really makes it a practice or paradigm
changing breakthrough kind of thing?

Respondent: A couple of aspects of that new treatment, first is the clinical trial proved that it
significantly improves meaningful outcome. For me, the definition of meaningful
outcome will be response, survival, either disease-free or over survival so those are
the meaningful outcomes I look at but, of course, depending on what line of
treatment, the expectation may vary but [Audio Gap] will also have a comparative
arm through a Phase III trial afterwards. So that is one [Audio Gap] fundamental
will make me turn my head and say “Let’s listen about this product X,” and the
second is, of course, this is a medicine may not have all those fantastic numbers
but it is being introduced in a disease that we have not had many options except
the detrimental such as pancreatic cancer, metastatic thyroid cancer but today we
got also rare diseases of cholangiocarcinoma, gall bladder. The liver, they haven’t
got [what a good drop]. We may have a handful of them but not doing well or
haven’t got good, new powerful drug so if we have a drug that show that it works
and it is something that is also logical or realistic, can be given to most people, not
just protocol patients, that is another feature that would turn my head and say
“We haven’t had much going on. Finally, we’ve got something. Not only, of course,
will be the toxicity, as I mentioned. Afterwards, I already introduced the concept

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 of being realistic. I don’t want to have a drug such as [Infofarnex] for pancreatic
cancer [can’t present] on my patient, can’t get it. It’s still very toxic so –

Interviewer: No, say more a while on me. Okay, it’s because of toxicity that only 10% can
actually take it. There are just so many complications or difficulties around it.

Respondent: Yes, it’s just like [Cal T cell B] for [Unintelligible] B cell lymphoma. Honestly, I
don’t think I can have all [relaxation] to get [Cal T] so that baggage tagged along
with the product will also influence its ability to be adopted by myself.

Interviewer: Yes, perfect and are there specific agents that come to mind that meet that
definition for you so either they’ve got really great outcomes or they culminate in
a cancer or a treatment area where there’s real need. There’s just not great drugs
today and the toxicity is manageable enough that a bulk of the patients could
benefit from it.

Respondent: One quick good example, Abraxane, [you will switch them side to be] in the first-
line setting for metastatic unresectable pancreatic cancer. It’s certainly [Audio
Gap] study trial, would it show that it matches the potential efficacy but because
of the tolerance, the administrative style at that trial, you can give it for patients
with performance status of I or even II and the [Crosstalk] their equivalent so I
think that is a very good example. To me, it’s like a drug that is able to change the
game and be utilized fully by community physicians, not limited. Of course, in lung
cancer, the immunotherapy agent could choose for patients who have a PD-L1
expression of 50 above.

Interviewer: Yes.

Respondent: It’s a new process that is a new class, new idea, new approach and, of course,
most important, backed up by the outcome.

Interviewer: Yes.

Respondent: Even have to touch on the toxicity so that’s even wonderful so those are the two
grades. Of course, liver cancer, don’t forget. Over the past couple of months,
Opdivo is approved in the liver cancer, second line setting patient failed the first
line of NEXAVAR. That, to me, is an encouraging first step forward because for so
long, we got a treat here and there. We got [Xavaga] finally approved about a year

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 ago but liver cancer patients, as oncologists, I’m so shameful that I don’t have
much to offer but that would open discussion that I cannot talk about [Audio Gap]

Interviewer: Okay, I’m losing you. I’ve got some static in the line. Can you hear me okay?

Respondent: Yes.

Interviewer: Okay, am I on your cell phone?

Respondent: No, I just put in a speaker but if you like, I can put you back on. Is it better?

Interviewer: Oh, you know what? Yes, it’s totally better. Whatever you just did, maybe you
talked closer or something?

Respondent: Okay, no, no, no. I was lazy. I didn’t want to hold on to the headset but I put it
back. [Laughter] Okay, that’s fine.

Interviewer: No, no, no, that’s fine. Now, you’ve put me back to your face because whatever
you’re doing right now is great. I can hear you.

Respondent: Okay so let’s continue on this.

Interviewer: Okay. [Laughter] Alright, so those are great examples so the Abraxane example was
something that matched the efficacy of what was currently available and made it
much, much easier to give it to a broader group of patients, it sounds like? Perfect?

Respondent: Yes.

Interviewer: Then, in lung cancer, with KEYTRUDA, talk to me about - so in non-small cell lung
cancer, I know there are a lot of specific targets, alk-positive cancer etcetera.
Have any of those really made a big impact the way you feel like KEYTRUDA has in
non-small cell lung?

Respondent: Certainly, I think the new agents, for example [Alatinut], recently approved. I
always give credit for the very first generation. I’m not saying they’re not good.
[Laughter] Unfortunately, time goes on. I mean we have to have second and third
generation to replace our old ones.

Interviewer: Yes.

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Respondent: This is just that so first, salute to all the first line, the first generation, but like
[Alatinut], it’s suddenly from the [J. Alix] done in the Asian countries and
confirmed by the regular [Alix], the global and in America that showing that
[Alatinut] has better RCNS over response rate survival and finally got approved as a
front line treatment in November by FDA. I think that is very exciting and game
changing because now, we can certainly have a targeted agent for alk, which is
better tolerated, but the key thing is they also address the CNS relapse which we
all [got from oncol] when we use XALKORI. [We call like] yes, we treat it piece by
piece. Now, you can say “I’m just protecting you upfront” so that’s a very good
BRAF inhibitor because BRAF is not just in lung, in colorectal as well and, of
course, all the time to the melanoma is being identified to be a real existing
member that we cannot ignore and the next-generation testing will help us to
identify that in order to pick on that maybe 1 or 2% but to those patients that
response rate is 60, 70, 80% so I think that is a very exciting area that we are able
to “welcome” in lung cancer targeted agents specifically.

Interviewer: Okay, both alk and BRAF, there have been agents that really are exciting so talk
about why, I guess the difference between the impact of KEYTRUDA in lung cancer
versus the alk-positive treatment or the BRAF-positive treatment in lung.

Respondent: The difference, of course, is perspective of those therapies. We have different

mechanisms of action so the logic behind utilizing each drug is different. When I
discuss KEYTRUDA, I am focusing on the part about how the “basic biology 101”
body cell will recognize the mutation that can always happen any second in
anyone, you and I, right now but in expected normal situation, my cells, my body
would know to clip it and replace it with the proper coding but in the patient, this
mechanism fails by introducing, identifying the patient when this is playing as a
major player, we’re able to restore the nature of policy, surveying, and then pick
up those “wrong” cancer cells and phagocytosis and then cause the tumor to
strength. So I think this is a different aspect versus when we talk about BRAF, it’s a
very done to like the pieces of your music that you’re listening to. The song where
you go to the second verse, what’s happening here? It’s so specific that this note
was not played well so let’s either change the instrument. The string has to be
tightened or something very specific, not just say you have a great Maestro to
check on everyone as a whole orchestra. So I think it’s a different aspect on how
you can correct but it’s also why sometimes it’s frustrating because you’re correct.
You’re hinting that this picture is not just one. It is not individual game,

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 unfortunately. This is not like just over Australian Open, Federer versus Cilic. No,
this is a Team USA kind of game. Everybody go in. You have one plan to play this
individual set. You have doubles and then, you have mixed doubles. Together, the
score will give you which team is the winner and just happened that how you’re
going to play with the game in this scenario looking at your opponent should we
emphasize and put our number one seed to play the single but put the two and
three to pick the mixed. This is different strategy and also we don’t know why do I
have to say exclusively, fortunately now it’s not exclusive, that maybe [a male
cell] cannot be mixed with BRAF inhibitor. I don’t know. There’s no natural rule to
say that but yes, we just tend to do it because it’s a habit of doing it so I think,
talking about the differences is just whatever in the right circumstances may
produce the best but in the back of my mind is the frustration or the interesting
dilemma is they could be working as a team.

Interviewer: Yes, so how important is it to you today in these tumors to quickly and accurately
identify genetic aberrations or mutations as they surface? Like with BRAF on your
list of things to look at in non-small cell lung long before these treatments came
along and how does that happen?

Respondent: We are the generation, even though I’m much older than the younger generation,
but we’re the one that the iPhone, the internet, Instagram, you know we want it
now.

Interviewer: Yes.

Respondent: No one wants to wait. In the old days, it seemed reasonable, two weeks, things
have to take place. If you try to call someone, you text someone. You don’t get a
response. You get upset so unfortunately, my personality is the sooner the better.
It’s just because I’m older, I could say yes. I think it’s only we have to wait but of
course, time is always a very important component that if the result can come back
sooner, it’s only going to be better and I would rather choose something that can
come back sooner than keep waiting so this is my honest reply.

Interviewer: What are the implications of that? So I’m less familiar with how long these variable
tests take so are you saying that there are certain things like KEYTRUDA you can
use instantly because you can get that marker back quickly or how does that play
out actually?

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Respondent: Yes, because PDR1 testing is spot immunohisto-chemistry so it’s only 24 hours to
come back because you stain it and you look at it and the result comes. The
pathologist can report the next day.

Interviewer: Yes.

Respondent: This is how fast, [how quick] but with BRAF or [tabular] agent, it depends, again,
on the technique. If it’s alk, you use the IXC. Okay, similarly, you may take but it’s
never one day. I don’t know why but usually two or three days. If it’s PCR, again,
three or four days but if it’s a next generation, because the mutation alley is very
low, the [control] is very sensitive. That can take up to two weeks because the
logistics about how you have to prep the cell, the gene is separated from DNA
etcetera to let it grow so it’s a huge difference because of the way how it is, how
it’s set up.

Interviewer: Got it so what you are saying is that your inclination is more towards the instant
and so if there is something that has that instant test, it is really going to impact.
I’m going to be more likely to go with that first and I’ll know that information for
my next round if it took two weeks to get the information but if it’s not there,
that’s really going to impact things.

Respondent: Yes, but fortunately, I think the key opinion leaders or the “big shot,” they have to
alleviate those kinds of stress and “anxiety.” We have been talking about even
though the PDR1 may come back in a day, the genetic mutation and the [fication]
testing may not come back after four weeks, you have to wait because we know,
for example in eGFR-positive patients, treating it with PDR1 upfront or instead of
[targeted region], we may not have the best response so I’m seeing that more like
an anecdotal situation, not that they are prospective study being done but from
the experience, we learn that you just need to patient. When you grow a plant,
you have to wait for the seed to grow and a little bit sprout and then, become a
little plant. You cannot keep pulling it but –

Interviewer: [Laughter] I love your metaphors.

Respondent: Of course, I’d love to see it as soon as possible meaning that if we don’t ask,
technology will not improve and hopefully, one day, all these things can be
expedited.

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Interviewer: So to that point, are there tumor types where you feel that you are more likely to
wait for that two week test to come back and other tumor types where you’re
more likely to want to jump? Does it have to do with the specific patient
circumstances, with the tumor type or what you’ve got available if that test comes
back positive? What drives that decision, whether to be patient or not?

Respondent: Really, the one key factor to wait or not to wait is the patient’s clinical symptoms
scenario. Can the patient wait?

Interviewer: Okay.

Respondent: If someone experiences traumatic with fluid or shortness of breath or practically on

an intubator with lung cancer, we have to act on it. We have to start treatment,
meaning chemotherapy, or in lung cancer, we may have the privilege of mixing it
with the immunotherapy but if the patient is more stable, maybe coughing a little
bit, some pain, discomfort but nothing like a crisis then, I would wait because
having the final information can totally change the treatment choice.

Interviewer: Okay, how much are you staying on top of this? There’s new, potential – like with
BRAF for example, relatively more recent, I guess, in several tumor areas. Are you
being proactive in saying “I want to make sure BRAF is there,” or is that something
the pathologist is adding to panels and so you’re getting it or you really have to get
that broad next-generation testing in order to learn it? How much is that driven by
you versus driven by what the pathologist is offering you for a given tumor type?
Does that make sense?

Respondent: Yes, it does because even though I’m [feeling] with the academic hospital but
because I practice in the community, meaning that my fellow doctors, the
pulmonologists or the GI doctor when they do the initial testing or sampling,
sometimes even when they have intervention with radiologist from more like a
community based hospital, those tests don’t get done so I have to be the one who
actively had to ask specifically if I want to know the diagnosis to make sure that
the biomarkers for all of the specific tests are being conducted. Yes, I have a
[reflex] panel of pathologists. In most cases, would not have something reflex or
would call me and say “Hey, listen. I have this newly diagnosed colon cancer. Do
you want me to be at the BRAF or the MSI?,” or all those things. Rarely do I get
those phone calls unfortunately.

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Interviewer: Alright, you just referenced the MSI so I’ve got to go there. So that kind of a whole
different paradigm that KEYTRUDA has gotten approved, I think this is what you’re
talking about, across tumors, sort of a pan-tumor kind of thing.

Respondent: Yes.

Interviewer: Does that throw you for a loop or are there still tumor types that you are going to
think about that because you know it’s prevalent or how does that work? How do
you start to think about getting about that MSI test pan-tumor?

Respondent: I check it because it’s not for the frontline. It’s for the second line of patients. If
the patient, indeed, has the instability, if for colon [got checked] even in the
abdomen setting because the role of [5FDO] in abdomen setting correlate with the
MSI status so in a [Crosstalk] colon cancer at least they get checked even at the
early stage. Other than that, for the other tumor, I check it, of course, when
they’re metastatic and most likely, it will matter most in the first “relapse” and
the patient needs something for second line treatments so it’s not urgent. It’s not a
hurry and I do definitely try to order it for all of the solid tumor that I have today
and add it as part of the panel because it’s something nice to have, in case, like
the gastric, pancreatic, because if no drug is approved. I mean if there’s not many
good drugs that I can “use,” I don’t have to do it all over any more because now I
have the Opdivo but otherwise, I would try to check the MSI.

Interviewer: Okay, so you are conscious by tumor type. You just mentioned liver. You’ve got
Opdivo so you’re feeling good about your choices there. The likelihood -

Respondent: I can relax now. [Laughter]

Interviewer: You can relax, exactly. You don’t have to worry about making sure that you have
that MSI test. That’s interesting, okay.

Respondent: Because it does take time to act and even though it’s not me but my staff can
spend the time. We have so much paperwork going on every day. If you contact the
lab, sometimes you need to get the consent back from the patient. [I think it’s
just] the paperwork. It’s frustrating.

Interviewer: Yes and that’s sort of a thing that gets in the way, making you hesitate to do it.
Are there other logistical things that get in the way of you’re considering a certain
test?

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Respondent: No, the only thing is the insurance coverage if the patient was just here in the
hospital within 14 days. You can order it but that will be the only thing. I don’t
think any other things would be the key. Of course, I ordered it and they don’t
have enough specimens that the biopsy too small. They don’t have enough to share
then of course but that is not the reason I would start from the beginning to
initiate the cost of requesting it.

Interviewer: Yes, you would just learn that that was the case. What were you saying if they’re
in the hospital for 14 days, you can order it or that puts a limit on what you can
order? I didn’t understand that.

Respondent: Yes, because sometimes within a hospital, if they get a global reimbursement
pathology all those things so they don’t like us to add some tests to it especially if
it’s [coming then OSci] because sometimes those specific tests may not be done by
the in-house with the kit. They may have to send it to the reference lab and if you
send to reference lab, meaning that if it’s done within 14 days, the specimen
obtained when the patient just got admitted or discharged, the insurance company
is not going to pay for that reference lab cost so they will hold it. This is something
we learn and we have to respect.

Interviewer: We have to be conscious of, yes, exactly.

Respondent: We have to. We want to be friends.

Interviewer: Exactly, you’re going to hold it until they’re out of that inpatient setting so that it
will get covered.

Respondent: Yes, I know.

Interviewer: Okay.

Respondent: That doesn’t sound right but that’s - [Crosstalk]

Interviewer: No, not at all. I just want to make sure I understand because I haven’t heard that
before. Alright, does the prevalence of a target mutation impact your decision
whether or not to test for it? We’ve talked about some very low prevalence and
high prevalence targets. Do you feel like, in and out of itself, that has an impact
like are you less likely to test for something that’s got a 1 or 2% incidence or not so
much?

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Respondent: Well, when you just ask me, I will say no. The only thing is, for example, I don’t
test it on [all along]. If it’s [screened cells], I’ll be less likely to test for those
mutational markers because it almost doesn’t exist versus if it’s non-screened, it’s
non-small cell, even though alk, [ROS], BRAF they are like single digits or I only see
one in my life or a few handful of alk, I do that because I think it’s important to
start the ball rolling because you need the metastatic settings. I know some
colleagues they don’t but time is important. I already said it. I shouldn’t wait for
the eGFR and then do it. It’s not right for the patient.

Interviewer: Yes, got it. Now, let’s go to the product profile we’ve got here on the screen. I’m
going to come back to your screen and then pulling page two. I’ve got a Product X
here for you to take a look at. This is page one and as you saw, there are two pages
so let me know when you’re done with this page and then, we’ll flip to the second
page, okay?

Respondent: Yes. [Activity] Okay.

Interviewer: Alright, so let me show you page two. There it is. [Activity]

Respondent: Okay.

Interviewer: So what are your initial reactions to what you see here? First of all, I’m going to
change this so you have access to change the pages. Now, you see two arrows at
the bottom of the screen.

Respondent: Yes.

Interviewer: You can flip back and forth as much as you want. What are your reactions to what
you see here?

Respondent: Definitely, this is very interesting biomarker with a targetable, actionable drug
that we can utilize. A ready Product X that is simple, easy to be given. The key
thing, of course, the bottom line is the efficacy with the primary endpoint over
response of 76, even complete response being documented and looking at the other
end, it’s only 12% of progression and there’s a 93 response in patients can be made
on the treatment or surgery. That is really impressive numbers in so far as what it
can do so that is what it can do and then, of course, we talked about who likely is
going to have this biomarker detected.

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Interviewer: Right.

Respondent: It talked about the prevalence. For me, I think the breast was the key thing. [Side
Conversation]

Interviewer: Are you looking at the prevalences?

Respondent: Yes, that was the slide. It was a [solitary grand tumor]. Yes, I don’t see much but
for the breast one, it’s something that I deal with a lot. Of course, to learn what
kind of breast would be good. Is it triple negative versus triple - but is this
something that I can always consider before I need to go to even chemotherapy?

Interviewer: Hold on. Let me ask this question first. The secretory breast cancer –

Respondent: Yes.

Interviewer: They have less prevalent invasive breast cancer. Do you see that secretory breast
cancer often? What is the prevalence of that among your breast cancer patients? Do
you know?

Respondent: No, I don’t think I have a high percentage of secretory at all. Invasive, they’re the
other ones that we always will see so the tumor “type,” not the types that we’ve
often seen but for lung cancer getting up to 3.3. It’s a rare form of biomarker. It’s
not something that one will see a lot but the thing is I’m so sure you would miss it.
It could have a very strong impact. One thing, of course, if you look at it the other
way is those individuals from the list given with the high prevalence, once often
they are the ones who are very chemo-resistant versus the ones who are both
references are usually very chemo-sensitive so would they have anything to do with
it? Before, we go to the prevalence –

Interviewer: Wait, you’re making a – I’m sorry. To understand - [Crosstalk]

Respondent: Correlation about –

Interviewer: Correlation.

Respondent: Yes, of this specific “mutation,” the role that it may play in the pathophysiology,
also the tumor type.

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Interviewer: So you’re saying that if somebody got this TRK infusion, they may be especially
chemo-resistant.

Respondent: Yes, possible.

Interviewer: Right, what makes you say that? That’s interesting.

Respondent: Because of the types of the frequency that they listed like the [mammary] gland
and I know they have much experience with secretory breast but they don’t have
infantile fibrosarcoma. Fibrosarcoma is already very chemo-resistant. We know –

Interviewer: How interesting.

Respondent: Thyroid cancer also but as you go down the list, the ones that are here, they are
practically more sensitive but occasionally, we have some rare and interesting
genetic mutations. They do get associated with it so I think it’s still important to
consider especially in the case when a patient is more resistant which is really
looking to it because it goes along with the common belief that if you have a prior
mutation, that should be the one you prefer treatment approach because it just
makes sense. This is supporting it, not to prove it is indeed a causal relationship
but one thing, of course, if we go back to the testing of it is there are so many
currently available [at the cost of one night fee] and the next generation to
confirm it and then, they’re developing the companion diagnostic so I find that
maybe a bit more complicated. [Laughter]

Interviewer: Yes.

Respondent: Want me to really get to the bottom of it and of course, it will take the learning
curve to find out what it is but I think education would be the key thing for one not
to forget that just like the alk or BRAF mutation, BRAF mutation is also very low
even in lung cancer but when it changes, it really changes the whole picture. The
same thing with alk in lung cancer, they present in a very typical way. When you
find it, the patient responds very well and they can really have a great benefit so
the prevalence is just like the art of it, picking it up but it should not mean that we
should ignore it especially again in cases where it’s unusual.

Interviewer: Yes, so you’re getting into the crux of what I’m curious about here and it came
from those earlier questions. You’ve got the product where your definition of
breakthrough in some ways is you’ve got this nice efficacy. You’ve got what it

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 seems is good tolerability but then, you’ve got this relatively complicated testing
modalities, information, and these prevalences that are the range from high and
rare cancers to relatively low. How do you imagine putting those things together
and making a decision about when to test? So let’s take a couple of these tumor
types and just talk that through and I want to talk it through with the realities of
that fusion testing modalities piece there like that’s part of it. [Laughter] You
know that class will not get to the specific between fusion. A confirmatory test will
be needed but that NGS testing, there are various commercial tests that can detect
the TRK fusion and they’re getting toward a more specific companion diagnostics as
you notices. Talk me through. Let’s start with either thyroid or non-small cell lung
cancer. I’d love to talk through both of those and actually you had raised
cholangiocarcinoma as something that you were feeling like there’s an unmet
need, I believe. Rare but not quite drugs today, yes, you had mentioned that so
talk me through. How would you imagine considering and whether or not you would
test for this in each of those cancers?

Respondent: Yes, hold on. [Unintelligible] Okay, so for papillary, for thyroid cancer and
cholangiocarcinoma, I would definitely check it from the beginning when the
patient first presented with metastatic disease. The Product X is approved or
indicated in patients who have failed prior therapy or not acceptable toxicity to
the current therapy, meaning it’s the second line treatment. You’ve got to [keep
that in mind].

Interviewer: Exactly.

Respondent: I have time to wait for it so in those situations, I would definitely include that in
the initial biopsy testing to see if the IHC is there. If it is, I will confirm it with next
generation. If it is not, I’m not going to jump to the next generation in those either
yet.

Interviewer: Okay.

Respondent: I don’t think I’ll be testing fully from the beginning only because so much more is
going on plus I will have to do the next generation sequence anyway but what I
meant is when the patient relapsed regardless of the type, thyroid, cholangio or
lung cancer. Today, I would do, I hope, these testing, including Foundation I,
foundation at is liquid biopsy and so I would do a next generation sequence and
that will be the most sensitive way to pick up these infusions and I would have

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 much more sensitive way to detect it with this method. [They will be selling] the
first line. I will go to the next generation sequence testing.

Interviewer: Got it and tell me more again about why lung is different? You passed over that
really quickly [but you wouldn’t change it].

Respondent: Because lung has many more options so I don’t want to exhaust my tissue and then,
it’s just complicated and because it’s such a low prevalence. I would test for that
routine first because its IHC so I have to specifically order it. It’s not a next
generation, you check it, everything gets tested.

Interviewer: Right.

Respondent: When I have to conduct IHC, you would post more cells. You need a whole slide so I
don’t really want to “waste” my tissue unless the patient has a very atypical
[immuno refractory] to treat [Crosstalk] once again. It’s part of excess of proof or
indicator in the second line setting. Lung as well, I would rather wait till the next
line.

Interviewer: Ok so that TRK infusion that’s identified as part of some of the NGS panels today,
what’s your sense of whether pathologists would include that in a lung panel and is
there a lung panel? Is there an NGS lung panel that you are getting today at some
point in therapy that’s a standard part of what you do?

Respondent: Yes, they have those. Today, NGS, they have more like board, like foundation one
or foundation, they have big chair like 300 different genes versus if you send for
the reference lab like

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