Full Transcript Introduction and Guest Background 0:04 This is the Doctors Making a Difference podcast, living with metastatic cancer, highlighting patients, doctors, and researchers who are fighting to win 0:12 against cancer. 0:22 Today I am pleased to welcome Dr. 0:24 Javier Martin-Broto. 0:26 Dr Martin Broto is MD, PhD, and he works at Fundación Jiménez Díaz University Hospital in Madrid. 0:33 He's been active in the medical oncology research and patient care, has done a lot in this world and has made a tremendous difference in the research and 0:44 availability of information regarding various types of tumors, including solitary fibrous tumors. 0:49 And those who listen to this podcast a lot will know that I also have that type of cancer myself, and I'm delighted to welcome Dr. 0:56 Martin Broto. 0:57 He gave me permission to call him Javier. 0:58 So Javier, would you mind introducing yourself more thoroughly to our audience? 1:03 Yeah, absolutely, Peter. 1:05 It's my big pleasure to be here with you. 1:08 And yeah, this is Javier Martin Broto, medical oncologist devoted to sarcoma care and research for more than 30 years. 1:16 I finished my oncology residency 31 years ago. 1:23 So my pleasure is to to here and replying all the questions or topics you want to talk about that. 1:30 Yeah. 1:30 Just briefly, how did you end up getting into oncology? 1:34 You know, a young man studying in college. 1:37 How did, you ended up in this research field? 1:39 Because again, many people listening are physicians or maybe they're residents in training or medical students and are considering a career. 1:49 I finished my oncology residency in 1994, the residency as medical oncologist, time flies, oh my God. 1:58 I was involved in sarcoma care maybe since January 1994. And yeah, during this time I tried to be transformative, I triggered the activation of the Spanish 2:12 Sarcomas Group in this year. 2:14 in 1994. And honestly, the way we ended in the medical oncologist election is hard to say because there are many, many factors that can influence in this election, 2:27 in these choice. 2:29 Maybe one of them is to avoid to give up to hold the knowledge about the medicine because medical ecologist is a specialty that renounced to the overall 2:44 knowledge about the medicine. 2:46 You need to have the knowledge of internal medicine, for instance, but internal is very competitive and maybe medical oncology is more innovative in some 2:57 way that requires research. 3:00 And I don't know the kind of. 3:03 details can influence in the election. 3:05 And yeah, intensive care as well is the same concept of not renouncing to all the knowledge of the medicine, but it's more technical speciality. 3:17 So medical oncologist maybe was more fit with me, with my scope. 3:24 And maybe this was the reason, but yeah, in the end, there are few little details because in medical school, you are not aware about how every single specialty 3:37 is or is about. 3:38 So in then there, are a few details that maybe take importance in this election. 3:46 But I will select medical oncologist again for me. 3:51 Yeah. 3:52 Well, you've done great work in this field. 3:54 Like you say, for over 30 years. 3:56 And obviously you stayed in it and you have been able to advance. 3:59 You have done many publications.
How Javier Martin-Broto Entered Oncology 4:02 As it pertains to solitary fibrous tumor, that means a lot to me and to others who are suffering with this disease to have someone who is so committed 4:11 and dedicated to learning about that disease and trying to develop better treatments. 4:16 Yeah, thank you for what you're doing. 4:17 I appreciate you sticking with it and making a difference for all these years. 4:21 That's a tremendous accomplishment. 4:24 Yeah. 4:24 Thank you. 4:25 This is a part of our task because we understand the medical oncology as not only caring patients, but also to research and also, 4:38 to teach. 4:38 But research means that you will be transformative in some way. 4:44 and research not only in focusing on clinical research, that means that new trials are activating in your site, but also in the preclinical setting where 4:56 you can discover new relevant biological processes within one specific disease and maybe you check the efficacy of different treatments. 5:09 Disqual research is very, very convenient in the context of medical oncology. 5:15 So this is a part of our specialty. 5:18 This is the question. 5:20 Maybe I began working in clinical research back in 1996 and moved into proclinical research in 2008. Since then, been leading The clinical team focus on 5:35 sarcoma research and right now we have around 40 projects going on in the preclinical setting with molecular biologists and technicians and pre-docs as well. 5:49 So I can imagine definitely medical oncologists without research. 5:54 And that research has to cover everything translational, proclinal, clinical, the whole perspective. 6:02 And our work obviously is always dively to help patients. 6:08 And we have designed more than 30 clinical trials in sarcoma and always pushing to make a real difference in clinical practice. 6:18 This means that new treatments or new strategies are putting on the table in these clinical trails. 6:26 SFT was one of the rare diseases within the sarcoma field. 6:31 There are more than 100 entities. 6:34 But SFT for sure was an unmet need because we required new treatments. 6:40 I think the first ever conducted clinical trial in Sft was designed by our team in two different cohorts. 6:49 So exploring the efficacy of antiangiogenesis, anti-angiogenic pathopany. 6:55 It's the 1st line of antigenics. 6:58 In two different cohorts, the formerly typical SFT and the formally called malignant SFTs. 7:05 In these two cohort when the patients had metastatic spread, we tested the efficacy of pathopanid and we essentially we have learned two main messages. 7:17 The first was that At the time of the diagnosis, the prognostic subset of SFT determines the behavior at the times of metastatic spread. 7:31 I mean, for instance, one patient diagnosed with low-risk Sft if five years or ten years later developed metasthesis. 7:44 behaves more indolent than those diagnosed at the localized disease time as a malignant, as high-risk SFT. 7:55 So this was important because the median progression free survival of the cohort typical was more than 10 months.
Sarcoma Research and Early SFT Trials 8:03 And for the so-called cohort malignant, which is bad nomenclature, fortunately improved recently by WHO definitions, had a medium progressive resurveival 8:18 in this high-risk operation of five months. 8:22 Another important message was that anti-angiogenic seems to be more important than chemotherapy agents and because the figures we achieved in terms of 8:33 median progression free survival and even median overall survival were by indirect comparison better than what we can achieve with chemotherapy. 8:44 And another message was that for those patients achieving at least stable disease, we can make some rotation at the time of progression with other anti-angiogenic agents. 8:58 And this was beneficial for the patients. 9:01 This was the three messages. 9:03 Yeah, I just want to make sure I'd summarize because I think those are all really interesting. 9:08 First, you found that Pesopanib and other antigenics were more effective overall than traditional chemotherapy. 9:16 And then I think you found, again, it used to be categorized into malignant versus non-malignant, but you've found that the behavior of the disease, 9:24 depending on what it was at the time of diagnosis, modified a little bit later on. 9:28 In other words, there was something that was a high-grade, high risk tumor was more likely to spread or become malignant rather than a low- grade tumor 9:36 at time diagnosis. 9:37 Is that correct? 9:38 It's absolutely correct. 9:41 And the change was very convenient because there is no considered benign tumors in the context of SFT. 9:48 So the most correct definition is low risk or high risk, but even low-risk can develop metastasis spread. 9:56 This is why we needed to know the behavior in their advances for those initially diagnosed low risks Sft. 10:05 Yeah, well, and that's an interesting characterization, too, because older literature that I've read on solitary fibrous tumor describes it as largely 10:14 a benign process. 10:15 And now the more recent studies say high risk or low risk based on mitotic rate, amount of necrosis within the lesion, the size of the original tumor. 10:25 And those factors kind of influence the likelihood of malignancy. 10:30 And I think you said, as it goes on, if somebody starts off with a high-risk tumor with high mitotic rate, high necrotic, 10:36 all the World Health Organization classifications, they're more likely to have metastatic disease. 10:42 When you design treatment, you know, design studies around it, have you found that the anti-angiogenics, like Paisopanib, 10:49 do they have an equal rate of effectiveness on those tumors, or does it vary quite a bit based on the original type of tumor and their grading? 10:57 Yeah, we took the advantage of explore several details in this prospective trial. 11:04 And one of the important message was the detection of efficacy of these compounds. 11:12 One important consideration is that with these responses with antiangiogenics in these contexts are very uncommon. 11:21 But on the contrary, choice responses are frequent within the context of antiangiogenics. 11:28 Choice responses means that the density of the tumor changes because of effect of an anti-angiogenic treatment. 11:37 And this can be measured by radiologists with a kind of unit called Hansville units. 11:44 So this can be measured. 11:46 And this was important as well because we could quantify the impact of the antigenic agents in the tumor. 11:55 So, this this is important. 11:57 Some correlation can't be obtained between the response and the PFS, but it's true that maybe this correlation requires a higher number of patients to 12:10 be more robust. 12:12 But yes, we detected this kind of response in both contexts, in high mitotic SFT or low mitot Sft. 12:22 It's true that in the specific subset of the differentiated SfT, anti-angiogenic agents are not working, so this required chemotherapy instead of antigenesis. 12:36 So, de-differentiating ones didn't respond as well, but the majority of others did respond better to anti-angiogenic agents than anything else. 12:43 And, like you said, I didn�t realize that you, at least in clinical studies, could judge the effectiveness of the antiangiogenetic like pesopanib by the 12:53 Hounsfield units or by, in other words, by density of tumor rather than just the absence or presence of tumors. 12:59 Do you see that happen? 13:00 Do ever see the tumors will regress or do they just become less dense with the anti-angiogenics? 13:07 Yeah, less than the change that we can observe outside. 13:12 I mean, because it's darker in the CAT scan, the lesion comes darker after the treatment, and this can be measurable, obviously. 13:22 Yeah. 13:23 And summer shrinkage you can also detect, but it is more frequently with density changes. 13:30 With this specific treatment. 13:33 It's not the best treatment, obviously, but it's more than double than the chemotherapy can demonstrate in the context of advanced SFT. 13:43 And I think it is a benchmark. 13:44 We have now a bench mark of activity in terms of medium of progression free survival for each cohort and also for overall survival with this strategy of 13:56 rotating anti-angiogenic agents. 13:58 But obviously we continue with the research and maybe New biological processes are important in the safety control or treatment.
Anti-Angiogenic Therapy in Solitary Fibrous Tumor 14:09 So yeah, we are investigating in different areas now. 14:14 Well, another one I think I had read is Bevacizumab versus Paisopanib and other angiogenics. 14:21 I thing a lot of your work had worked on Paysopani, but a lots of patients also take Bevaccizomab. 14:26 You mentioned you have to rotate them. 14:27 Do you find a difference between the effectiveness or does it seem to matter which of the angiogenics are used initially? 14:34 Yeah, initially we thought that maybe Sunitinib, which is probably more potent anti-angiogenic agent than pathopony, could be more effective, 14:45 at least in some ultra rare tumors where antiangiogenesis is important. 14:51 For instance, in Velasoparsarcoma, the first ever conducted randomized clinical trial in this ultra rare tumor was conducted with Hediranib, 15:03 which is an anti-angiogenic agent. 15:06 And in these contexts, Henedinib demonstrated higher activity compared to other antiangiogenics agents. 15:14 But it's difficult to say, and maybe Bebacitumab with the mosolamide is comparable in terms of efficacy with or sunitinib. 15:26 So I think the most important question of focus here is that we have seen that patients are progressing after treatment, 15:36 but in those patients that at least you achieved an stable disease, After the rotation with another different antiangiogenic, 15:46 you can also observe a choice response. 15:50 So this is important because the notation is the key question. 15:55 It seems that for some reason, anti-angiogenesis is an important treatment way in SFT. 16:04 So we have patients we treated with thopanib and then maybe partial response was achieved. 16:11 And then, maybe in eight months, some leashes progress. 16:16 Then we rotated to zoonetini furnaces and we do some efficacy or some signal of activity. 16:23 For instance, another choice response, and maybe six or 10 months later, we should change to another antiangiogenesis, anti-angiogenic agent, 16:36 for instance. 16:37 And this is interesting because it seems that it was not cross resistance between antigenic agents. 16:46 So this was important. 16:48 That's an interesting finding because you would think it would develop resistance to the class of drugs, but what you're finding is as you rotate patients 16:56 between anti-angiogenics, depending on what their density of their tumors are, you are still seeing a response. 17:01 And one of the challenges I think about as a patient with solitary fibrous tumor and on the physician side of it is how do we find agents that not only 17:11 are palliative or slow down the progression of disease but start to reverse it? 17:16 And I noticed you had studied, you published something called predictive gene signature study earlier this year. 17:21 It said predictive genes signature for the efficacy of Paisopanib. 17:25 And, I thought that was interesting, a predictive model that you could use to try to predict which type of tumors would respond. 17:31 I wondered if you can tell us more about that research. 17:35 Yeah, we are engaged with prediction as well. 17:38 We are very happy with the seven gene signature of prediction for immunomodulation using anti-PD-1 compounds in a wide series of sarcoma treated with antiantigenic 17:50 plus antiPD1. 17:52 And this was initially obtained by dynamic changes over time comparing the week six versus baseline. 18:02 So those genes that were modulated in this time were important for us because this means that these genes were impacted by the treatment. 18:14 And then after we tested this seven gene signature, which is very, very nice validated in another series at the baseline. 18:25 and we observed that is predictive. 18:28 I mean, there are two different populations. 18:32 this signatory is able to distinguish two different populations and is validated with the SARC series. 18:39 The SARCs series is imposed by patients enrolled in pembrythoma in several sarcoma subtypes. 18:47 And so we are very happy with this signature because it's validated. 18:51 So for other signatures, we require more validation and maybe we cannot make a robust statement around that because sometimes validation is hard to find 19:03 a similar series with transcriptomic and with the same genes explored in our signature. 19:10 But yeah, in the end, it is very important to have predictions about the efficacy of one specific drug. 19:19 And for that, the best way is to obtain dynamic changes over time. 19:25 This required more effort by the patient because this means biopsy at baseline and biopsies, in this case, at week six. 19:34 But in the end, this change over time is critical because you are ruling out those genes that are more important in prognosis, 19:44 inherent of the biology of tumor. 19:47 And you're focusing on those gene that they're modulated by treatment. 19:52 And then after this dynamic signature, you can check if a baseline is enough to be predicted. 20:00 And this was the case for this signature of immunomodulation. 20:04 So we are very happy with this signator. 20:07 For other signators, we still require validation with independent series to observe that. 20:14 So in this sense, for sure, in SFT, we must continue investigation because the immunomodulation in the monosar 1 seems to offer some activity in SFT. 20:27 But in monasar 2, which means six different cohorts based on the signal of activity we have detected in previous study, plus two new cohorts of chemoimmunotherapy. 20:40 But one of these cohort with antiangiogenic tests, anti-PD-1, was a solitary fibers tumor. 20:48 And unfortunately, after the interim analysis was not enough, the median progression free survival we obtained with immunomodulation to continue up to 20:59 the second part.
Predictive Gene Signatures and Immunotherapy 21:01 We are very convinced that maybe we have to modulate firstly macrophages. 21:07 in the context of SFT. 21:09 Sft contains maybe the greatest proportion of micro features in my compartment compared to other sarcoma. 21:18 And most of them are M2 microfeatures. 21:22 This is a research line of our team as well. 21:26 We have investigators devoted to micro-feature polarization and modulation with CSFR1 inhibitors. 21:35 So I think we require this kind of modulation before any other immunomodulation with anti-PD-1, for instance. 21:43 So this is an interesting fact that we are considering. 21:47 And yeah, in some sarcoma, my environment is cold in the majority of sar comas. 21:53 And we required some in-plane activation with several strategies. 21:59 To get the more macrophages active. 22:02 Yeah, because in sarcoa in general, the half of the mass of tumor is constituted by macophages. 22:11 But specifically in SFT, this amount of macaphages is huge. 22:17 So this is important to take into consideration. 22:19 And obviously these tumor-associated micro-phages are M2, which means that are polarized towards tumor growth. 22:29 Then these M-2 microphage facilitate the cold microenvironment, prevent the immunomodulation attack to the tumor. 22:40 So it's important to modulate firstly these M2 polarized microphages before any immunomodulation treatment in the SFT context. 22:51 This is one of our learning messages after this investigation. 22:57 But there are other lines of research which are very, very promising and very appealing in SFTs. 23:03 I just want to summarize for a second. 23:04 That's quite interesting. 23:06 You've done a lot of work on antiangiogenic agents, and it sounds like the microenvironment around the solitary fibrous tumor does have a lotta macrophages, 23:15 requires an inflammatory response to recruit more macophages. 23:19 And you wanna create an environment that can be destructive to the tumors rather than promoting of the tumor. 23:25 So there's work being done around that micro environment with macraphages I noticed, published an article or a study, the Immunosarc 2 trial update and 23:34 I think you said you had multiple cohorts and solitary fibrous tumor was not included in that most recent publication, is that correct? 23:42 Yeah, it's included in the investigation that, as I mentioned, in Immunosac 2 trial, the specific cohort of SFD unfortunately had to be stopped in interim 23:54 analysis because we didn't achieve the minimum of progression-free survival to continue to the second part. 24:02 In some cases, we detect a signal of activity with Sunitinib and Ivoluma. 24:07 It's true, but then we refocus our investigation and probably the fact of immunomodulation detected with these compounds is because this amount of microfetches 24:20 in the context, in my environment, is of SFT. 24:24 So this is one of the important research lines. 24:27 We have to obtain some promising findings in the upcoming months because I think this could be positive. 24:35 Right now we have drugs that are able to modify the polarization of macrophages in some way. 24:42 Some drugs called R1 inhibitors. 24:46 Benzeltinib, bimicotinb, mactutumab are examples of this family of tumors that are being registered for TGCT, which is a kind of benign tumor in the joints. 25:00 Tumor, you know, this is the nocinovial gene cell tumors are very sensitive to this kind modulation of CSF, CS-FR1 inhibition. 25:13 This is their modulation microfeatures. 25:16 And this is important because we can modulate that. 25:18 This research line definitely will be important. 25:23 Because we continually to think that important immune modulation in SFT, because, we have published the peripheral inflammatory signature is prognostic, 25:34 very prognostic in advanced Sft. 25:37 I mean, this kind of peripheral signature, by the ratio between platelets and lymph cells or between neutrophils and leaf cells. 25:51 And this means that cytokines has influence in SFT. 25:57 So definitely this is important, but we have to maybe find the key signaling pathways that will allow the efficacy of anti-PD-1 compounds, 26:11 for instance. 26:12 So far, it's not possible. 26:14 But there are more promising research lines in SFT, and if you want, I can share some of them. 26:22 Well, that's interesting. 26:22 Like you said, there's a lot of work around antiangiogenesis. 26:26 and a lot of work on the microenvironment around solitary fibrous tumor. 26:31 And I guess that was my next question. 26:33 Where do you see the field of research going in the future? 26:36 Are there other promising modalities that might provide hope for people with solitary fibers tumor or other sarcomas? 26:44 We have the privilege and the big pleasure to work with Dallas research team and through them we have tested the relevance of bed inhibition in the context 26:58 of SFT. 26:59 And in the proclinical models, bed inhibition is working in SFT.
Macrophages, Microenvironment, and New Research Directions 27:04 So this is something that is promising in this disease. 27:09 And unfortunately, so far, we were unable to find a pharma company prone to investigate in SFT with these compounds. 27:19 But again, we are fine in tuned the results of these kinds of compounds. 27:24 And for me, this is something that is very promising, obviously, and know all the bad inhibition is useful for safety treatment. 27:35 but those compounds that are able to inhibit the pan-bed receptors, which is hard to explain now, but not all the bed inhibition is okay. 27:46 But some of them is very convenient in the SFT context. 27:50 And another research line, I think this will bring hope and bring new activity in context of Sft is the inhibitions of alternative splicing. 28:01 which is very, very disruptive and very innovative in oncology and in solid tumors at least. 28:07 And we are conducting now a clinical trial with Thirtubivint, which a inhibitor of some splicing factors. 28:18 For many reasons, we think that some specific translocation-related sarcomas are sensitive to this kind of inhibition. 28:29 So in proclinical setting, we have seen very important, I would say the most important activity I have detected in the pro-clinal setting in SFT is with 28:40 alternative splicing inhibitions. 28:42 which is very important. 28:43 And in some patients included in the clinical trial, we have activated this summer. 28:50 We have detected a shrinkage of the, of tumors. 28:54 So, which isn't very, very convenient. 28:58 It's too early to withdraw conclusions, but hopefully in ESMO meeting we will be able to communicate the results of this phase two trial. 29:12 This phase two trial is enriched by SFT patients. 29:18 Maybe we have included in these four or five months 15 or 16 patients with Sft. 29:25 And yeah, our experience so far is very good. 29:31 So we need more time to have the whole perspective of the activity. 29:36 But this is definitely one For me, one of the most helpful research lines in the context of SFT. 29:45 It's exciting to think that there's other things. 29:47 Most of the stuff I read about sarcomas and then solitary fibrous tumor in general is more palliative to slow the disease, 29:55 but not to eradicate the diseases. 29:57 And so when you see trials going on where you can start to see tumor shrinkage, you know, where it reduces in size, that's very promising. 30:04 I also think it's wonderful that you're already at the clinical trial stage. 30:08 There's a lot of preclinical work that goes, give these trials to patients and publish that data, I think that moves the field along tremendously. 30:18 Yeah, initially we expected that for us committing, maybe we could be able to share this data, but the deadline for this is January 28th. 30:30 And this will be very too early for communicating this activity and safety as well of steer tubing. 30:38 So we should wait for a small, that definitely this something that we can check and, um, Preclinically, as well, we can make some tests in a specific patient, 30:52 for instance, through the disaggregates. 30:56 So, disagregates of the tumor is important because you can check, you contest several drugs for this patient. 31:04 And the interesting thing of these disaggregates is that you have the microenvironment there. 31:10 It's not about tumor cell culture, it's about the disagregate which contains all the tumor cells plus the macroenvironments. 31:21 So the translational research to the patient maybe is more, I don't know if this word exists in English, we say extrapolable in Spanish, 31:32 but it's more robust, the conclusion you can find. 31:36 And then this is something that we can do as well in a patient with progressing sarcoma, We can check what kind of drugs can be more active in this context. 31:47 And we can check this kind of new drugs we are testing and we're considering promising in these disease. 31:55 So I think, yeah, there's arguments for hope and sometimes we have some strategies that can work, especially for those consider bulky tumors where surgery 32:10 is not possible because the size In some cases, we have treated these patients with trapectin plus radiation therapy. 32:19 We have a substantial experience with this strategy and we have seen responses in the context of SFT. 32:28 So today is one strategy that can work. 32:33 And we even have patients with brain Sft treated with trabectin plus radiation therapy with a shrinkage of maybe 80% of the tumor. 32:47 achieved with this combination. 32:50 So it's true that in general, the dissemination of SFT in the vallices is through different metastasis and then it is more difficult to apply that.
Future Treatments and Patient Advice 33:00 But sometimes the problem is big mass that should be reduced in size in order to obtain a good disease control. 33:09 And then we can offer this trabectidine-plus radiation therapy as well. 33:16 Well, I want to thank you for what you're doing. 33:18 I know as we wrap up our time here, those who have listened to this will find that there is hope. 33:23 There's a lot of research being done on solitary fibrous tumor, other sarcomas, and I appreciate you. 33:28 You're one of the people who's done a lots of that work. 33:31 Do you have any final thoughts of things, of a message you would want leave to patients who might be listening to these? 33:36 Because again, most of podcast listeners are doctors, but there are people have this and what other message would you want them to know? 33:44 Yeah, maybe the first message is you are not walking alone. 33:48 There are a lot of community around you, doctors, but also advocacy patients, patient groups. 33:57 So this is important. 33:59 To share your situation is as important as well in order to be encouraged by the experience of others and doctors. 34:08 And so this important, And maybe the second message is obviously to be sure that the doctors that are in charge of your care are expert in sarcoma. 34:26 So I think this is important as well because sarcoma patients should be treated by MDT, by multidisciplinary teams experting in Sarcomas. 34:37 not only medical oncologists, but also radiation oncologist, pathologist radiologist surgeons, etc. 34:47 This is important as well. 34:49 And these are the two main messages. 34:53 And then to be sure that you can also have access for innovative procedures, innovative treatments. 35:02 And so this is something that is also important to consider. 35:06 I think these are the message. 35:09 I want to thank you again for taking the time to do this. 35:12 Thank you for the research you're doing. 35:14 Look forward to seeing the publications on the clinical trials you are doing, and I'm really interested to see where the field goes. 35:21 And again, thank for you and for your research team for what you doing and, I hope you'll keep in touch. 35:34 Thanks for tuning in to the Doctors Making a Difference podcast. 35:37 And thank you for what you do to help your patients and your community. 35:40 Your work truly helps so many people. 35:42 We produce this content to have the tools you need to stay in medicine and to highlight the amazing work being done by physicians around the world. 35:49 Please note that while I am a physician and many of the guests on this program are also physicians or other professionals, 35:55 the discussions on the podcast do not represent my employer or any professional organizations to which I belong. 36:02 This podcast is for your information and entertainment only, and should not be taken as professional advice. 36:08 You should seek appropriate professional advise pertaining to your own situation. 36:12 Please check out more of our content on our website, DoctorsMakingADifference.com. 36:16 Also, please follow, like, or subscribe on your podcast player or YouTube channel, and give us a five-star rating. 36:23 It really helps to spread the message. 36:24 Finally, if you'd like to be a guest on the podcast, Or if would like nominate someone else to a be guest, Please visit the website or email admin at Doctors 36:34 Making A Difference dot com. 36:35 See you next time.
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