Chapters Transcript Video Rectal Cancer Update: Short Course radiation, TNT, NOM, W&W... what does it all mean and where do we go from here? my name is Carolina Martinez. And um I am a colorectal surgeon at Tampa General. A little bit of background about myself. I did my medical school at michigan State University and then did by general surgery, residency in the University of Arizona. And then I came here to the University of South florida for my colorectal fellowship. I have the introductory slide for dr j dr Williams as well. Um And would you like to introduce yourself? Sure, I'm jay Ryan Williams. I am a colorectal surgeon here at Tampa General as well uh and also have practice in ST Petersburg. Um I did medical school at the University of Lowell and did my residency and fellowship at University of South florida. Thank you. All right. So as some of you may already be aware, marches, colon cancer awareness month. And um I have to get asked why would anyone choose to go into the field of colorectal surgery. But as we'll discuss today, we'll see why this is such a field and um that issues of colorectal cancer um need to be addressed. Um And there's also been a significant change over the last few years and the way that we view the treatment of rectal cancer and um new advances and proposed protocols on how we manage rectal cancer. So starting with a few statistics, um There are 149,000 new cases of large bowel cancer is diagnosed every year, 104,000 of these are colon cancer, with 45,000 being rectal cancer. And every year about 53,000 Americans die of colorectal cancer. Um and this accounts for about 8% of all cancer deaths. And the data that I'm going to present was obtained from the NIH National Cancer Institute's your database. Um And um if we look at the number of new diagnosis of colorectal cancer and individuals by race and gender, we can see that men are more effective than females. And we also see that african americans, caucasians. Native americans are among the highest affected, while the rate seems to be lower in asian. Um and pacific Islanders in females, we can see that colon cancer is the third most common diagnosed cancer, with breast and lung having higher incidences. And in males, we see a very similar pattern with colon cancer being the third most common diagnosed cancer and prostate and lung having higher incidences. So when we remove gender based cancer, as we can see that colon cancer is the second leading caused your second leading diagnosed cancer in both males and females. Um. Mhm, thankfully, the overall incidence of colorectal cancer has steadily decreased over the last several decades. And we think that this is attributed to improvements in both surgical and medical management, as well as a decrease in some patient risk factors. Some declines have also been attributed to screening and the increased use of politics to me during colonoscopies. Unfortunately, one thing that we also have seen um is that while we've seen that there hasn't been an overall decline in the incidence of cancer, there are also seeing an increase in the number of nuclear rectal cancer diagnosis in patients between the ages of 20 and 39. Um, in the early 1970s, the incidents in younger populations was decreasing while in patients older than 55 years, it was actually increasing, and around the 1980s, there was actually a shift in this pattern, with the incidence of colorectal cancer declining in patients Older than 55 and then starting to increase in the younger patients. Um and we again don't know exactly why this increase in younger patients is happening, but we think it could be related to diet on lifestyle, environmental factors, um and genetic factors which may play a role. Um when we look at the overall five-year survival of patients diagnosed with colorectal cancer, we can see that 64 out of 100 patients will be alive five years after their diagnosis. But more importantly, as we know, survival almost mainly related to the state of cancer at the time of presentation. Um so with patients, patients with a cancer that is localized to the colon have a much higher five-year survival at 90%, compared to those who have had regional spread of their cancer to influence, Which at that point is 71%. Unfortunately, patients with cancer that has metastasized have a 14% 5 year survival and we know that patients who are symptomatic at the time of their presentation often have more advanced disease and worse prognosis. Um So reviewing some of the risk factors associated with the development of colon cancer, I was saying that smoking alcohol, obesity, having a sedentary lifestyle, a high red meat and processed diet, family history and a low fiber diet are risk factors. Um and then some other factors that we don't necessarily always have control over which is race. Um We've seen an increase in both the diagnosis and the mortality from colorectal cancer and african americans in particular, as well as having a history. And some question whether I love you through medications or just an HIV status or transplant history, patients with HPV have an increased risk uh anal squamous cell cancer. Um As well as patients with inflammatory bowel disease, ulcerative colitis have an increased risk as well. So, um this presentation is particular focus is on the new developments in the treatment of rectal cancer. Um And this is just a very oversimplified standard of care for a rectal cancer which has been used for many years of Stage one rectal cancer patients are generally offered up from surgery. Um Stage two, stage three rectal cancer patients usually receive new activity. Chemo radiation therapy followed my surgery followed by uh folks chemotherapy and stage four rectal cancers treated with chemotherapy up front. Following a previous standard guidelines of Chemo radiation therapy. It was found that after TME resection for rectal cancer um there was actually about 15% of patients who were found to have a pathologic complete response, which means that no cancer cells were identified on the removed specimens. Um This led to the development of further studies to evaluate if this number could be improved. Whether by altering the timing of radiation and chemotherapy or just changing the sequence of the therapy. So the timing trial was one of these. Um The main objective of the study was to assess whether adding cycles of faux fox between human radiation and surgery, increase the proportion of patients achieving a pathologic complete response. Um This was a phase two non randomized trial consisting of four sequential study groups of patients with stage two, The stage three locally advanced rectal cancer. Um and each group contains 62 participants. All patients received chemo radiation upfront with five, a few. Um and uh Um radiation therapy um group one had a total missile rectal excision and um This was 6-8 weeks after Chemo or radiation patients. Between groups 2 to 4, they received 24 or six cycles of colfax respectively, between the chemo radiation and the total directoral excision. Um This is just a simplified diagram of how the groups were um separated. As we can see Group one received chemo radiation upfront followed by surgery followed by adjuvant chemotherapy. Um Groups two and three. Um As we can see the timing was separate and depending on the number of chemotherapy cycles before surgery. Um And sorry, my lights keep turning. Mhm. Um So uh looking at their some of the results, we can see that compliance was fairly good for all groups but more so for three, the longest interval between human radiation therapy and surgery was in before. And our zero resection was much more likely to be achieved in Group four versus one. With upfront surgery and complications um are 40 to 44% lowest in Group two. But more importantly, um they compared the initial clinical and pathologic response to the various treatment modalities and complete pathologic response was seen in 25, 30 and 38% of patients and groups 2-4. Um and a partial response was seen in up to 75% of patients in the treatment arms. So um the study concluded that the delivery of full fox after chemo radiation and before TME has the potential to result in a complete or partial pathologic response and increase the proportion of patients who may be eligible for less invasive treatment strategies. Um And then this transitions us to the Oprah trial which then asked, which is better doing chemo first or radiation first. Um And then it asks, does this give us a watching the option? So the Oprah trial, also known as the organ preservation and rental and carcinoma. Um is a Phase two trial which evaluates the efficacy of total neo adjuvant therapy and selective non operative management of locally advanced directive cancer. And the majority of consortium members actually participated in the timing trial as well. And they looked at the 3-year disease free survival patients with M. R. I. Confirmed Stage two or three rectal cancer were randomized into two arms. So you have your induction chemotherapy arm and then your consolidation chemotherapy where they received chemo radiation first followed by chemo. They were followed by interval evaluations with your work exam, endoscopy and MRI. Um They received four months of neo adjuvant chemo, which was either eight cycles of full class or six cycles. Okay box. And following completion of either induction or consolidation therapy, they were then re staged. Um The patients with complete or near complete response were then offered watch and wait. Um While those with an incomplete response were offered a TME reception. Um The chemo radiation regiment for moral stone Kettering was standard. Um With a total of 56th grade radiation and 28 fractions with continuous five a few infusion or cup side of me. Um Looking at the regression table that they provided um to kind of give us an idea of how these patients were were categorized. So a complete response was described as an endoscopic lee, flat white star with logic cases, no evidence of modularity or ulceration, a normal digital rectal exam. Um And these patients were washed with MRI. Studies primarily, um And their MRI should show a T. Two weighted dark T two signal with no intermediate T. Two signal and no left nodes. In your complete response demonstrated small mucosal modules or minor mucosal abnormalities of superficial ulceration or erythema around the star, possibly some in duration on the exam. And with MRI showing that there was some remaining intermediate signal um and also a partial regression of lymph nodes versus an incomplete response. There would still be visible tumor, a more intermediate than dark T. Two signal um and no regression of lymph nodes. So this is a depiction of a near complete response. We see the pre treatment uh endoscopic picture and post treatment. Um The near complete response demonstrates small modules. Some superficial ulceration with the MRI demonstrated some remaining intermediate signal. The incomplete response shows a persistent mass. And we can see here that in the clinical complete response there is a flat white star. Um Some Thailand dictations, there's no evidence of ulceration or no regularity. Um And these chinese are also consistent on MRI. The patients who were found to have this clinical complete response were then followed every three months for three years and then every six months thereafter. So um 324 patients were enrolled in the study and they were randomized to the two groups as I mentioned. Um the preliminary results were recently released and the secondary objectives that they looked at um included comparing disease free survival, organ preservation and distant metastases free survival and the rates between the two arms. Um uh full compliance with systemic chemotherapy was about equal in both groups. Yeah. So um they found um that in their three year results um disease free survival with 78% in the induction arm and 77% in the consolidation arm. And this was not statistically significant difference between the two For a distant metastases free survival, 81% in the induction in 83% of the consolidation arm. Also not statistically significant. Um interestingly in regard to organ preservation. Um the induction armed demonstrated a 43% organ preservation rate and the consolidation are demonstrated a 58% organ preservation rate. So um what this study is suggesting is that upfront chemo radiation followed by consolidation chemotherapy resulted in a numerically higher watching late rate compared to induction chemotherapy followed by chemo radiation. So what often leads to mortality in patients with advanced rectal cancer is distant metastasis. Um And prior studies have found that preoperative chemo radiotherapy can help downstage tumors and lead to improve local regional control, but that the occurrence of distant metastases not necessarily decreased accordingly. So the aim of this study, the repeated trial looked at the addition of short course radiation therapy followed by chemotherapy and delayed surgery to reduce distant metastases without compromising the local regional control. Um This was a multi center open label randomized control phase three trial. They had 912 patients um with T. Four, the tumor with intravascular invasion. Lymph node involvement involved one of the selected fashion or in large ladder notes. Their primary endpoint, I was looking at three year disease related treatment failure. Um and they defined disease related treatment failure as first occurrence of local regional failure, distant metastases, new primary colorectal junior or treatment with related death. Um patients required a T two weighted MRI before and after preoperative treatment. In the experimental group. Um they had, they received a short course radiotherapy, which was a five grade five days but could be over a massive eight days, followed by six cycles of Cape Fox or whole Fox followed by TME. Uh The control group received the standard of care as we previously described. Um So, uh in both groups, the clinical target volume for radiotherapy did include the entire news direct, um with the primary tumor and regional influence. Um The median follow up was 4.6 years. A standardized, minimal follow up schedule on included interval clinical assessments, what CIA and colonoscopy in the first year and imaging for surveillance. And um at three years after randomization, the disease related treatment failure was 23.7% in group one versus 30% in group to which was statistically significant. And the pathologic complete response in group one was 28% versus 14% in group two. Um There were fewer disease related treatment failure events in the experimental group as we can see on graph A um and distant metastases um uh graph be that caused more disease related treatment failures. And at three years, the cumulative probability of distant metastasis was 20% in the experimental group versus 26.8% in the standard peer group. Um the cumulative probability of local regional failure at three years was 8.3% in the experimental group, compared with 6% in the standard of care, which was not statistically significant. So um in patients who were treated, what they found in patients who were treated with radiation therapy followed by 18 weeks of systemic chemotherapy before surgery, have a statistically significant uh lower probability of disease of related treatment failure at three years than patients undergoing standard of care in the experimental arm. The pathologic complete response was doubled in that of the standard of care group and the experimental treatment arm does offer the potential opportunity for patients who are seeking the organ preservation. Are watching late. Um The observed decrease related treatment failure in the experimental group they believe is most likely related to the increased efficacy of preoperative chemotherapy as opposed to adjuvant chemotherapy. And that short course radiation um With upfront preoperative chemotherapy can be considered as a new standard for high risk vocal advanced rectal cancer. So the importance of these studies is that they are changing the way that we view and treat rectal cancer. The clinical practice guidelines and the american Society of culinary rectal surgeons for the management of rectal cancer have mentioned the option of the watch and wait approach that can be considered or highly selective patients in a protocol is studying and additionally um thanks to the time trial and the preliminary findings of the Oprah study, the MCC guidelines were recently updated to include a total new management therapy as an option for stage two stage three rectal cancer. Um So it is pretty clear that the advancements in the treatment correction cancer will continue to develop and expand as more studies become a cool. Um And this is very exciting for all of us, especially as it relates to being able to provide more options for patients who are in need. Um So I will now transition to DR Williams as sends more information on the emerging research of the gut microbiome as it relates to colorectal cancer treatment Dr Martinez. Before you transition, we had a question. What are your thoughts about short course versus long course radiation. Yes. Um so I believe that the treatment should be individualized up to each of the patients needs, but there are reasons to consider a short course for a specific patient situations. Um For example, if there is a patient that you would like to expedite surgery on um short course radiation is an option because these patients can option just received the five days of the short course radiation and then have surgery within the next week. Um It's also an option for patients who are partially obstructed or having significant symptoms from there um tumors just leading our pain. Um And it is also an option for patients who have a very large primary tumor that has metastasized. Um and who you don't want to delay chemo by during surgery first. Um So um another option is that it's also a consideration for patients who don't necessarily have access to um going to a center to receive chemo radiation because of either socio economic factors were just distance from a tertiary care center. Um This is an option where they can receive all their therapy in just five days. Great, thank you. Mhm. A great job. That was really informative. Thanks dr Martinez. Um So I'd like to just talk to everybody a little bit about the gut microbiome and how it may relate to rectal cancer. So what is the microbiome and incorporates the genes and genomes of the microbiota uh and the products of that microbiota in particular environment um In this case the human body and specifically the record of the colon. Now the microbiota itself is a community of commencing and symbiotic pathogens. This includes bacteria, fungi, viruses and other things that may live in the gut. Um And they're usually identified by culture or by taxonomic identification using PcR to identify what's called 16 S. Are RNA sequences. And our R. N. A. Is important because it is an example or it is produced by replicating bacteria. So it shows that there's a live bacteria in the area. Uh This is a result of a market analysis done by the Polaris group. And in their analysis they estimated a 23.8% compounded annual growth rate in microbiota uh Industry. What that means is by 2027 the estimation is that this will be a $1.57 billion dollar industry. Oh, so the question is how does this relate to colorectal cancer? So in 2013 study was done by on at all. And they looked at 47 colorectal cancer subjects and compared these 2 94 controls. They did 16 s. are RNA sequencing on the fecal bacteria and the um and the DNA was then evaluated. Overall, they found almost 800,000 genes that they sequenced and analyzed. And the results found them. I found that they had a decrease overall microbial diversity in patients who had colorectal cancer. Uh Specifically they found increased incidents of fuse a bacterium and poor pheromones. So fuse a bacterium showed an odds ratio of Approximately just over four, which is quite an increase. Um and then pour pheromones was five now for pheromones ultimately ends up being associated with oral and Lauren geo type cancers. But further study was done on this beautiful bacterium. Um So the question was how could the microbiome then affect colon cancer or colon cancer growth? And one of the things you look at is the metabolism and that's the metabolism of the byproducts of the microbiome. And one of these products is beauty rate. So those of us that study the colon recognize that beauty rate is the primary fuel for Kalani sites or colon healthy colon cells. Um, whereas cancer cells preferentially utilize glucose as their carbon source vehicle psychologist. So a lot of people who have been diagnosed with cancer will tell you or will ask you, hey, I've heard that sugar is bad. Is that true? Should I avoid sugar? And this is where that comes from and how beautiful it works is. It will actually starve the cancer cells and it will compete uh in that it will it will essentially um kind of like weeds versus grasses. It will fertilize the grass so that the weeds can't grow. Okay, so what about futsal bacterium? Nuclear autumn. So this is the bacteria you mentioned before. There's a couple of different things that is involved with and that it enhances the epithelial proliferation. This allows cells to grow and then invade through that basement membrane. Uh and it does this through an engagement of adhesion molecule molecule fat A. And its association with the cat hearing. So by neutralizing fed a there's a prevention of the promotion of cancer in these mouse models and there's a possible activation of this toll like receptor for which we've seen other bacteria, Excuse me. And other cancers as well. And here is kind of a schematic of what we're talking about. So you can see the green uh oblong shaped spiky little thing is supposed to represent the fuse of bacteria and its involvement of fatty. Um And then we see other things opposite of that on the diagram you see due to rate and it's deregulation of the cellular enter genetics. Here's a little bit more of a depiction and I want you to focus kind of on the right hand of the screen where we talk about fuel cell bacterium just in the interest of time. And you can see that the fatty molecules that interact with that cat hearing. There's an activation of this beta cat and signaling. And anybody familiar with cancer will recognize the term beta cat me uh increases inflammation and activation of the side archives but it also increases. These are key genes an expression of specifically Scenic in the cycling D. One which we're going to see here in a minute. And how that relates in the adenoma to carcinoma sequence. As we said here, is that what we refer to as the adenoma carcinoma carcinoma sequence. And this is how cells in the colon go from being normal where you have a normal colonoscopy to develop a cancer. Typically this is somewhere between about a 10 to 20 year period. Most of the time three you see perfectly normal and then it advances into a late adenoma or an early cancer. You can see early in the beginning there's a scenic activation that we talked about before. What that does is by activating Scenic that turns on the adenoma sequence so that cells will divide. They will not become uh invasive yet, but they're actively dividing to create those adenomas further down the line as we see at the end is where we see this peak had here and involvement and that once it had hearing is involved. Now the cells are no longer held in place and they have this opportunity to become invasive and that's where we might see this increase invasion of these cancer cells due to the microbiome involvement. So this is a systematic review and meta analysis that looked at 27 papers. Okay, it included 11,000 papers that were evaluated on pub med And they ended up reeling it down to just 27. So in looking at these, they found that f nuclear item was associated with a decreased survival and a higher tumor stage. And this had a hazard ratio of 1.6. So almost 1.6 times increase in the risk there. Um If we adjusted that for a higher level F. Nuclear Autumn found on these uh sequences. And compare that to lower or no f nuclear Autumn, the hazard ratio still remained elevated at 1.47 So there's something called messy. So in colorectal cancer we talk about micro satellite instability and that's what M. C. Stands for. It's related to a genetic mutation in what's called the mismatch repair protein and mismatch repair essentially goes through. And if there's a single isolated change in the genome, it'll identify that and repair it. Well if the molecule that repairs it is broken and can't identify it now, you have what we refer to as an M. S. I. High uh cancer. What's interesting about this is even though it's a genetic variant and it sounds like it would be bad, it actually portends a better prognosis. However, there's a decreased response that are traditional chemotherapeutic agents like five F. You. Now there are drugs like keytruda or which is uh embolism um have been approved for mono therapy. What's further interesting is what we find in MSC heist uh tumors that have this lymphocytic reaction, meaning that when they look at them under the microscope, they not only see the cancer, they see an influx of lymphocytes and that lymphocytic positive tumors may have a higher five year disease free survival than those that are negative. Now why is that? And why might that occur? Well, there was a study that looked at if nuclear autumn in colorectal cancer and how it relates this immune response. And they looked at 1000 samples that came from this nurse's health study and the professionals follow up study 135 of these samples were positive for ethnically autumn. They took these and they did the pcr to to ensure that they had the f nuclear Autumn positivity. And then they also did a his so pathology looked at them under a microscope and determined if they had uh M. S. I. High uh diagnosis. And also if there was these T cell infiltrates of lymphocytes. What they found here is that patients that had messy high tumors that had a positive lymphocytic infiltrate and are positive for ethnically Autumn Actually portended better with an odds ratio of only 24/7 versus those that didn't have a head or worse outcome. So why why might this uh interaction occur? Well what we see is that f nuclear Autumn may have an adaptive immune response and these messy high tumors that then causes an inflammatory reaction, bringing in these T cell infiltrates. Thus, once you remove the the tumor, you have the stability for the T cells to fight off with what may be remaining. Okay, so what about radiation? Any effect that we might see on radiation? And this will become important later on in the talk? Um And there's this thing called the ab sculptural effect. And the abs couple effect is when you give radiation to a targeted local primary tumor, you actually may see regression in the distant metastatic disease, even though you didn't treat that with that specific radiation. Uh Where that becomes important is there was another study and we didn't include this in the interest of time where they actually biopsied some of these liver mets of a colon primary. And they found that they could identify ethnically autumn within these liver metastatic lesions. And so by giving radiation the primary, there may be a reaction that occurs with that f nuclear automated distance site. So what about research that we're doing here? T. G. H. And threw us f, well. One of the projects we decided to look into based on what Dr Martinez presented with this Oprah study and how we get these complete pathologic responders. Uh and also how we might determine who who becomes one of those responders is we kind of had this idea that perhaps microbiome might play a role. So our hypothesis is that the human gut microbiome plays a role in rectal adenocarcinoma development as well as its response to treatment and it can be implicated in those who have complete clinical response to me a watchman treatment. We had a couple of different aims of the study. The first aimless to determine if there actually was an association between rectal cancer and the bacterial microbiome specifically at the mucosal level, not just evaluating the stool samples. But then we wanted to further I classify that um and see if it was specific to just the sight of the tumor and not elsewhere. A second aim is to determine if there was a specific rectal microbiota associated with those that we have a clinical and pathologic, complete response following the neo adjuvant therapy. The primary outcome was to identify complete clinical responders and then describe their microbiota at the tissue level as well as that prior to the site and then determine the change that may occur in that microbiota during their treatment process. And finally, our 13 was determined if there is an association between the microbiome and early recurrence of rectal adenocarcinoma. So we would do this by looking at four different time points and we would biopsy the tumor as well as the micro as well as the mucosa, five centimeters away from the tumor proximal or upstream to it. We would determine the uh microbiome prior to treatment after radiation or induction chemo. And then after the total neo adjuvant treatment when they went into a non operative management phase or at the time of surgery. And then finally at one year post treatment or if they developed a recurrence sooner. And this is uh kind of a schema or schematic of what we had to do by biopsy and putting in the RNA later fixative all the way down to sequencing our preparations. And we had to evaluate these 630 base pairs. So that's 630 base pairs is where the bacteria would show up. And what you can see here on this side is sure enough with our first set of five patients looking at two different time points. And those two different samples for the majority of our patients, we were able to identify that there is indeed bacteria present on our back our biopsy samples. So we have significant data and this is only one year into our studies. So this is still pretty early. And our next phase here is to actually sequence these libraries and identify the specific bacteria that occurs at those sites. So we're getting good data through this. Now a secondary objective here uh is some is another study that we're looking at. And this involves the utilization of uh program that can induce bubbles and changes in cancer cells. So there is this product okay that we're looking at um developed by a company out of University of michigan that they found that giving pulse it'll sound waves cause the small gases within cells to start to expand rapidly and create these micro bubbles in creating these micro bubbles. It causes mechanical reaction that sells that LISZT the cells. These were done in animal models. And they found that they could isolate them specifically to uh tumor sites and to our sites that may have blood vessels coming through them and it didn't induce heat and didn't introduce damage to any of the surrounding tissue. So we've been involved now in this hope for liver trial. And the hope for liver trial is looking to see if we can utilize this product for metastatic or primary liver tumors. Uh The trial opened this year in 2021 Tampa General Hospital in U. S. F. We were lucky enough to be the very first sight to enroll a patient and successfully treat their metastatic liver disease with the use of this product. So this is just another study that were uh conducting here at T. G. H. And U. S. F. What's important about this in a relationship with the microbiome is how we may see if this has an interaction with the bacteria that is associated with these cancers as well. And does it play a role in those that are have positive treatment responses to this product and those that may have a complete response and not recurrence? So eligibility for this is anybody that has a primary liver or metastatic liver tumor. His intolerant of all first line therapy. Uh And that is including refusal. Uh They're not a surgical candidate and their life expectancy is better than six months. They will be ineligible at the target tumor. Have prior local regional therapy um that they are intolerant of withholding their systemic chemo for more than 30 days or have underlying comb or conditions or our transplant eligible eligible patients. So any of you that have patients out there with liver disease? This is a great option for them as well. So with that I will also take any questions. Great. Yes we had one come through um meteorite starve cancer cells. Do you see any role in the future for using this as treatment for colon cancer? Uh So there is utilization of beauty rate uh and short chain fatty acids and other problem um disease processes like um um prostatitis uh for example diversion prostatitis when we give someone a diverting colostomy. Uh And they have that we will often give this as of yet. It has not been uh indicated for treatment. But there is a possibility that we would see that along with things like probiotics or pre biotics in the treatment of rectal cancer and colon cancer in the future. Specifically those that may be um positive for f nuclear autumn or other specific bacteria that we might identify? Excellent. Another one came through. Are there any studies looking at microbiome changes as the cause of increasing incidents of C. R. C. In the 20 to 49 age group? This is a great question. Um And there are not at this time and that is one of the things that we're hoping to find as we enroll further patients um Obviously that while that age group is expanding it's still a pretty small number of the patients that develop rectal cancer. But hopefully if we can get that specific group into our study we might find that becomes the case. Um and that it may be implicated. Uh There is a likely association with not necessarily just genetics but something within the Food that we may consume or lifestyle that has changed over the past 30 years, that may be implicated in that process. Thank you. I have one more question in the queue. So audience, If you have anything else you'd like to add or other questions, please use this time to type them into the chat box. So next question um I think this one is for dr Martinez. Do you have a cut off in the younger patient population? Like when to take for a colonoscopy for bleeding? Um So there is no specific cut off in younger patients on when you would take them for a colonoscopy. Uh The current recommendations are for initial screening colonoscopy to start at age 45. Um if patients have a high risk profile, such as a family history of colon cancer, rectal cancer, we do recommend screening to begin 10 years before the age of the individual who was diagnosed or at the age of 45 whichever is earliest. But there really isn't a cut off. Even for hereditary colon cancers, patients can start screening even at the age of 10 if they have that kind of family history. Um So anyone who is developing symptoms such as bleeding, um change in bowel habits. Um These patients should speak with their primary care provider and consult with the gastroenterologist for colorectal surgeon um to have their screening colonoscopy done at an earlier time. And I would just like to add to that. I think the one thing to take home for those that may be primary care physicians or others out there is um if your patients 20 years or older uh and you think that the bleeding is just from hemorrhoids. That's one of the biggest things that we may see is a delay and that they get treated for hemorrhoids without proper work up or having a colonoscopy evaluation for cancer. And I think that that's One of the things that I've changed in my practice over the past 10 years is um now taking those patients for a colonoscopy. Uh interestingly enough, about five years ago, my cut off was 30. Now it's 20. Is that group gets younger and younger? Excellent. Thank you. That looks to be about it. Unless we have some other questions come through. I just want to send a reminder to everyone that um I'll email you all within the next couple of days for directions on how to plan your credits. Um And if that's it I want to say thank you for joining us and thank you to dr Williams and Dr Martinez for your time this evening. And thank you from everyone at T. G. H. And USFl have a good rest of your night. Published June 11, 2021 Created by
