Archive for the Pancreatic Cancer category.
Palliative treatment: the two symptoms to palliate are pain and the best modality is a celiac plexus block. For the jaundice, surgical bypass for patients who have good performance status and look like they have reasonable survival. It’s almost worthwhile to invest in long term palliation. Stents can be inserted either endoscopically or percutaneously. Celiac plexus block can either be done at the time of surgery by the surgeon or can be done. They last for months. Commonly they cause some orthostatic hypotension which usually is self-limiting. A couple of years ago I would have said, “No chemotherapy offers a survival advantage in pancreatic cancer.” These are some large trials. And then we go to Memorial Sloan-Kettering’s just baseline data of how their patients did when they presented with non-resectable pancreatic cancer. And we are starting to see some influence on survival. This is the Burrus trial of gemcitabine versus weekly bolus 5FU. Consider the weekly gemcitabine did have a statistically significant survival advantage. I’ll let you decide for yourself whether it’s a clinically significant survival advantage. We are not there yet. This is another comparison. This is not a prospectively randomized trial but it’s almost as good. This is two trials that were done to test in Europe in which they randomized patients between octreotide and best supportive care. The other was done in the United States in which they randomized patients between octreotide or best supportive care. Laid exactly on top of each other, and in the United States protracted 5FU with or without octreotide laid exactly on top of each other. There is some survival advantage there. This is a trial done by Glomelius published in the Annals of Oncology. It’s not quite a randomized objective between any chemo, selected by the patient’s oncologist, and best supportive care. And there was a difference there also. To my thinking, in advanced pancreatic cancer, quality of life is the only end point at this point. They don’t have much of a life expectancy and it’s not going to be influenced very much by chemotherapy. So anything that improves the quality of life.
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We have for low stage lesion surgery … somehow I didn’t get in the GITSG adjuvant chemo-radiotherapy. Adjuvant chemo-radiotherapy and resected pancreatic carcinoma. One of them was a prospective study that took over a decade to accrue. Basically best supportive care followed by – these are all patients who had Whipple resections and no evidence of disease – and half of them got chemo-radiotherapy and a rather poor schedule of 5FU. But nevertheless, there is statistically significant benefit for the chemo-radiotherapy. Not a prospective study but was published from Hopkins and used a better schedule of 5FU and full dose that chemo-radiotherapy is effective. There has been a European trial that did not produce a positive result but had a lot of problems. For locally advanced disease, chemo-radiotherapy is the standard, the usual treatment at some centers with aggressive surgeons. It’s a tossup between chemotherapy and supportive care.
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Markers for pancreatic cancer: CEA is frequently elevated in pancreatic cancer, but the marker which is most useful negative will not make CA19-9, but without exception CA19-9 usually reaches very high levels, in the thousands false positives and biliary disease. Patients with infectious cholangitis have very high levels, sometimes in cirrhosis and if you. Before going to chemotherapy for pancreatic cancer, I want to insert a couple of caveats. And these are that you have to be very careful when you interpret. In the old trials, the response rate in pancreatic cancer to chemotherapy is almost invariably grossly overstated. And the reason is because of non-uniform response criteria. The benefits that patients feel from chemotherapy in pancreatic cancer is much more frequent. There is a lot of wishful thinking. Those are largely the trials in which single agents were evaluated. They are what we have, but there are a lot of scar tissue in them and they are very slow to resolve. Even if the chemotherapy is working. So there is a negative bias in looking at objective response rate. Overall the objective response rate is low and is slow to occur. Palliative responses are more common and any trial in pancreatic cancer nowadays should have some and to know what you are dealing with. Because these numbers are much bigger than these numbers and you have to compare one with the same parameter. There are basically two that are well documented: infusional 5FU and gemcitabine and then there are all the rest, some of which may be promising but don’t have much data yet. Here are the data for 5FU. Probably the response rate for bolus schedules of 5FU is less than 10%. With leucovorin involving the GI tumor study group schedule, the Mayo schedule and yet another. You put them all together and only 3% responses. It’s only when you get into the infusional schedules that response rates. Protracted infusion or the 24 hour weekly high dose schedule with leucovorin, popularized by Arnold high dose infusion.
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Here are the single agent data for gemcitabine. Objective response rates ranging between 5-10%. Clinical benefit response rates ranging between 20-30%. Survival quite uniform even though the clinical benefit response was good. This is the phase III trial, Burrus et all, that resulted in gemcitabine being approved. It was a randomized trial between gemcitabine in their right mind would use that schedule. It was a stroke of genius to get the FDA to accept it as a control arm. There were no objective responders in the 5FU arm, and only 5% clinical benefit responses. This is a excellent objective responders in the gemcitabine trial and 24% CBR’s. There’s also a small difference in survival, which was statistically significant. Other drugs, various other drugs. Most of these older single agent numbers are quite suspect. They are purported to be objective response rates, but in the old days FAM or SMF were used widely for pancreatic cancer because of some promise. Both ended up in cooperative group trials and large cooperative group trials, and they’ve largely been abandoned when it was seen that out of five arms involving these trials. On the other hand, regimens based on protracted infusional 5FU do have reproducible objective response rates, running up in the response rates in the 40-50% range. Even protracted 5FU by itself is not bad. There are two trials with protracted 5FU plus gemcitabine which was published this year in JCO by Hildago and group. That’s the regimen that we are currently using off protocol.
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Now for those patients that can’t be resected, surgery still can give good palliation. The main problems that these patients have is jaundice, pain and sometimes gastric outlet obstruction. So palliative surgery would consist of a biliary decompression. Most surgeons will do an intraoperative celiac access block with absolute alcohol. The subject of gastric outlet bypass is controversial. Some surgeons will do this as a preventative measure but it carries its own morbidity. I think most surgeons would not do it unless gastric outlet obstruction was really threatened.
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Non-surgical decompression for the jaundice: there are two ways to do it. One is to insert a stent by ERCP. These are generally maintained longer, less subject to infection, but it is highly skill-dependent. You have to have a good endoscopist who has done a lot of ERCP’s to get a reliable result. Percutaneously at PTC you can pass a stent. It can usually be advanced through the lesion. This is complementary to ERCP because it sometimes can be done when ERCP fails, and vice-versa. Complication rate is higher with percutaneous stenting, mainly infections. There have been two studies now looking at the question of patients who present with severe jaundice but are thought to be operative candidates and are felt to be debilitated because of their jaundice. Would it be advantageous to stent them first before surgery, allow them to metabolically recover, and then do the surgery a week or two later? Both of those studies were negative. This is one series: complication rate of percutaneous stents over the life-span of the patient. About half of them were subject to some form of blockage or dysfunction. About one-third of the patients became septic, and about 5% required surgery for some complication of the stent.
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Radiotherapy is an effective modality for pain control in pancreatic cancer. Radiotherapy is the modality that is usually used for locally unresectability of the great vessels, is the most common reason, but still not metastasized distantly. It can even be used for pain control in someone with metastatic disease. Usually a patient with metastatic disease doesn’t have too much time to wait for their relief. There’s a small survival advantage for radiotherapy. That survival advantage is significantly improved by the dose, so you give a different dose for palliative purposes than you would for somebody who appears to be in good performance status. Three series in which chemo-radiotherapy was compared with radiotherapy for locally advanced pancreatic cancer. These patients all received full therapeutic doses of radiotherapy. Around 60 studies, prospective comparisons. And they show almost a 2:1 prolongation of survival with the addition of chemotherapy. At Jefferson, this is a comparison, basically drawing on the same patient population and it shows basically the same result. This is a study from Fox-Chase showing about what can be expected with full dose therapeutic radiotherapy and concurrent infusional chemotherapy to the tail, although these patients will probably eventually all die. But developing out around 15% at almost three years __(tape skipping). This is the randomized GITSG trial that was on the previous chart, in which they were looking at the question of whether chemotherapy added, randomized into three groups. One received what was considered to be the standard treatment, which was roughly 60 gray. The other group received the same 60 gray plus 5FU and did just about as well. And the 60 gray alone was definitely inferior.
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Staging: T1 and T2, which are resectable in anybody’s book, are tumors limited to the pancreas. Limited extension to the duodenum or to the ductus, T3, that’s still resectable in many hands. T4, to the stomach, spleen, colon, or the one that usually bars resection is the great vessels, which are the closest. And there is just zero or 1 depending on whether the regional nodes are involved. If further nodes are involved, it’s M1. The group staging: stage I, is T1 or T2. Stage II is T3, still N0. Stage III are node-positive lesions. Stage IV is divided between the metastatic lesions, which are obviously unresectable, and stage IVa which is T4 disease but without distant spread and, depending upon the extent of vascular invasion, might be resected by aggressive surgeons at some centers.
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Surgery for pancreatic cancer is the radical pancreatoduodenectomy, the Whipple procedure. You take out a lot of tissue. Here it’s all listed for you. Less than 25% of presenting pancreatic cancers will be resectable by the usual standards; which means, major vessel involvement bars resection. Historically the operative mortality of this procedure was very high. In some series, even higher than 30%. It’s gotten a lot better in recent years. We’ll see some of those series in just a second. Median survival historically has been 6-24 months, usually less than 20% long term survival. Here is just a schematic representation of what is resected at the Whipple procedure, and then the gastric outflow tract is reconstructed, the pancreatic outflow tract is reconstructed, and the bile duct is also anastomosed to a loop of small bowel.
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Applicability of surgery: most surgeons will operate stage I and stage II. They usually don’t know if it’s stage III and they usually will operate stage III. Many will operate stage III. That’s often not determined until the surgical path is back. It takes an aggressive surgeon to go after stage IVa. More of them will resect the SMV portal complex than will resect arterial. Harry Wonabeau at Brown even resects SMA’s. This is a Memorial series as was presented by Brennan and his chapter in an earlier edition of Da Vita. Out of 818 patients they resected less than 20%. Of those that were resected with follow-up, 16% were alive at five years, 12% were alive without disease at five years. So the overall disease free survival at five years was 2% in that series. Here it is as a pie graph. Here’s all their patients. All the patients as they presented, about a quarter of them had such obvious distant disease that they weren’t even considered candidates for surgery. Of the three-quarters that were explored, two-thirds of them – 54% of the total patients – were bypassed but not resected, and less than 20% were resected. Here’s the same pie looking at the resected patients. Here’s the ones that were surviving at five years. It’s not a good disease. In case you think Memorial doesn’t do very well, you can look at the series from Yale New Haven as well; 200 patients over ten years. They explored about the same percentage of them, a little over half. They resected 8%. So of those 196 patients all together, there were 27 survivors at one year. There’s only one survivor at five years. By the way, that five year survivor was one of the non-resected patients. Makes you think that there might have been a pathologic error in the diagnosis, and emphasizes the point of recognizing islet cell tumors.
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Here’s more recent surgical results, and they are getting better. I think the one I would point to, because it is a large one and it’s very good, this is the Hopkins series. Cameron and Yo and that group. Less than 1% operative mortality in the last ten years, 21% five year survival, which is very good. This improved five year survival reflects partly improved surgical technique, reduced mortality, but also it reflects – I think, in part – in the last ten years or so there has been increasing use of adjuvant chemo-radiotherapy, which is effective.
Presenting symptoms: early symptoms are non-specific. Weight loss, anorexia, abdominal discomfort or pain. Jaundice can be an early or late presentation. A small subset of these patients with carcinomas of the head of the pancreas, the tumor will be located so that even at a small size it obstructs the common bile duct, and these are patients who present early with jaundice and are the most likely candidates for a surgical cure. The late symptoms: wasting and severe pain, perineoplasty, which we’ll get into. The severe pain of pancreatic cancer is sensed as abdominal pain radiating to the back. And it’s really a very major problem and it is almost universal in patients who develop advanced disease. More than once I’ve recognized in the waiting room a patient with pancreatic cancer because they are sitting there in their chair and they are leaning forward. The pain, the back pain of pancreatic cancer, is due to invasion of nerve structures behind the pancreas and it is somewhat relieved by leaning forward. It is susceptible to control by ablation, as we’ll come to later, by alcohol injection.
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Signs at presentation: commonly, none. Patient will come in and say, “I’ve lost appetite, I’ve lost 10 pounds, I’ve got this vague abdominal pain.” You examine them and find nothing. Jaundice, abdominal mass, tenderness, hepatomegaly, ascites are all possible. A non-tender palpable gall bladder, Courvoisier’s sign, is sometimes seen. That’s not a very common finding but it’s striking when it’s there. Trousseau’s syndrome is the perineoplastic syndrome that we associate most with pancreatic cancer. Trousseau was a French physician. He described this syndrome in the French literature and died shortly thereafter, because he described it in himself. This is associated with mucinous adenocarcinomas. It’s not specific for pancreatic carcinoma. I see more of it in adenocarcinoma of the lung than I see in pancreatic cancer but it’s important to remember that this is procoagulant-induced. Mucins and certain species of mucins, are strong procoagulants, therefore cutting back on the factors by administering Coumadin is not going to be a very effective way to deal with this painful thrombophlebitis, and you really need heparin to manage it.
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Diagnosis: CT scan is the preferred study. This is supplemented by sonograms, ERCP and angiography in some selected cases helps the surgeon to make decisions. But it is difficult to diagnose because small lesions of the pancreas are sometimes hard to recognize. Here’s one that’s not hard to recognize. Here’s a carcinoma of the head of the pancreas. The major reason that these tumors are not resectable – although some surgeons will do vascular resections as well – but the main reason these are not resectable at many centers is involvement of one of the major vessels. So what the CT scan, a good spiral CT scan, can usually – even without angiography – let you recognize whether the major vessels are involved. Here you see the portal SMV complex free of the tumor, and the SMA. These are the two that are the main ones to worry about. Here’s another carcinoma of the head of the pancreas, involving the portal SMV complex and the SMA and not resectable. More and more centers are willing to do vascular interpositions and resect if the SMV portal complex is involved, or is involved nominally as it is here, and the SMA is clear. Dr. Evans at M.D. Anderson, to whom I am indebted for this particular slide – he uses it as an example of a lesion that he would resect – has done a fairly large series of these and has compared survival and the extent of other involvement, nodal involvement and other indicators of how advanced the disease is, and really there is not – if the surgeon is willing to be aggressive and to resect the portal complex and replace it with a graft – then the outcome is not terribly different than if that complex had not been involved. Here’s a mass in the tail of the pancreas. Most lesions in the tail of pancreas are in minority but most of them become advanced to the point of not being resectable by the time they present. ERCP is also used for diagnosis and supplements the CAT scan. This is the classic ERCP finding in pancreatic cancer, the double duct sign, where you see an occlusion of both the common bile duct and the duct of Wirsung. This almost never occurs except with an expanding mass in the head of the pancreas, which is almost invariably pancreatic cancer.
Genetics: K-ras activation is almost universal in pancreatic cancer. Interesting work has been done looking for K-ras mutations in the pancreatic juice by ERCP. There was a French study not too long ago in which they screened patients who had pancreatic disease, suspected of pancreatic cancer, and in every case except two in which they detected K-ras mutations in a large fraction, a significant fraction of those patients, and in every one except two of the patients who had K-ras mutations they were able to confirm pancreatic cancer. So they thought they had a very high predictive value, but it turned out that those two negatives – one of them developed pancreatic cancer a year later and the other developed it four years later – so this may turn out to be a very useful modality, although it does require an invasive procedure. Other mutations are common, the same ones we see in other GI cancers. Virtually all pancreatic cancers have karyotypic abnormalities, lots of them. All of the abnormalities that have been identified so far, with almost no exceptions, are somatic mutations.
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Basically pancreatic cancer is mostly exocrine, and that’s all I’m going to talk about. Of the exocrines, the vast majority are adenocarcinoma, mainly ductal. And the significance of the ductal is the great degree of desmoplasia you see in these. The neuroendocrine carcinomas are important to distinguish because they behave differently. They are sensitive to different drugs, they are more indolent, more responsive and you should remember that morphology is not always adequate to distinguish them. The well-differentiated islet cell carcinoma stands out and speaks for itself, but there are some poorly differentiated ones that even a good pathologist can confuse with a poorly differentiated adenocarcinoma. Desmoplasia is a almost universal feature of ductal carcinomas and pancreatic carcinomas in particular. It’s important for several reasons. To begin with, if you are looking at a metastatic carcinoma of undetermined primary and you see a very desmoplastic tumor, your pathologist will tell you, “I suspect this is a ductal carcinoma” and sometimes they’ll even go so far as to say, “We think this is a pancreatic.” But, the scar component of these tumors takes a long time to resolve, even if you successfully treat the tumor with chemotherapy. So it modifies the response to chemotherapy. As we will see, this is the main reason for the big difference between objective response rates and clinical benefit response in pancreatic cancer. Imaging modalities can’t resolve the difference between tumor and scar, so the mass that you visualize on a CAT scan may resolve very slowly. Even if you are going to get a good response, you may not see it for some time.
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This is a pancreatic cancer. You see these nests of very terrible looking, poorly differentiated cells. But it’s immersed in this huge sea of scar tissue, desmoplasia.