New Treatments for 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.