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.
Pancreatic cancer is the second most common GI cancer in the U.S. Almost 30,000 cases a year. Virtually 100% fatal. Primarily a disease of the developed countries. Here are the statistics; down at the bottom worldwide, but it’s number two in the U.S. and because of rounding to two decimal places, the incidence rate and the death rate are the same. This is virtually the same geographical distribution as for colorectal cancer. Risk factors in pancreatic cancer: cigarette smoking is important. There has been demonstrated roughly a twofold risk ratio for cigarette smokers, and this has been shown to be dose related. There was a Japanese study that looked at people who smoked more than two packs a day with a risk ratio up around 3 or 4. Dietary carcinogens are certainly important, but there are few good studies to define them, other than the general kind of study that you do by plotting protein intake or calorie intake on one axis and rate of cancer on the other. But the same risk factors that apply to the other GI cancers, in terms of diet, are probably important in pancreatic cancer.
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Chronic pancreatitis, acquired or the usual pancreatitis that you see in the alcoholic is a minor risk factor. It is a risk factor, it has been shown to be, but familial relapsing pancreatitis, hereditary pancreatitis is a major risk factor. Probably not important are alcohol consumption, coffee consumption and diabetes. There have been lots of studies that link diabetes to pancreatic cancer but in general the studies that have looked prospectively have failed to see an increase in the rate of pancreatic cancer in patients who have had long-standing diabetes. So it is assumed that they are either common risks or that some of the diabetes that is associated with pancreatic cancer is a result of the cancer itself.
The fallopian tube is the least common site of gynecologic cancer in females, accounting for fewer than 1,000 new cases each year. Histologically, these tumors resemble papillary serous carcinoma of the ovary in more than 90% of cases. Diagnostic criteria for primary fallopian tube carcinoma include the following:
• The main tumor is in the tube and arises from the endosalpinx.
• The pattern histologically reproduces the epithelium of the mucosa and usually shows a papillary pattern.
• If the wall is involved, the transition between benign and malignant tubal epithelium should be demonstrable.
• The ovaries and endometrium are either normal or contain less tumor than the tubes.
The major concern is to distinguish these cancers from primary ovarian cancers. The staging system used for fallopian tube cancer is modified from the staging system for ovarian cancer because there is no FIGO-established official staging system for fallopian tube cancer.
Fallopian tube cancer and ovarian cancer spread in a similar manner. The classic triad of colicky pain, abnormal bleeding, and leukorrhea is rarely seen in its entirety; the most common symptom is abnormal vaginal bleeding. Pain, however, is reported frequently as an early symptom.
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The therapy of fallopian tube cancer is similar to the therapy of ovarian cancer; the most important initial therapy is effective cytoreductive surgery. As in ovarian cancer, residual disease is a good predictor of survival rates. The adjuvant therapy of choice is chemotherapy with platinum-based multidrug therapy, followed by a second-look laparotomy and second-line therapy as necessary. There are no reports of the use of paclitaxel in fallopian tube cancer, but one would surmise that this drug will have a significant role in the therapy of the disease.
Sex cord-stromal or sex cord-mesenchymal tumors include tumors of the female type (granulosa cell tumors and granulosa-theca cell tumors), the male type (Sertoli-Leydig tumors), and very rare types such as lipid cell tumors and gynandroblastoma. The majority of these rare tumors will never be seen by the practicing gynecologist.
Ovarian cancer
The granulosa cell tumor is the most common malignant tumor of this group of neoplasms. As shown in Figure 4, these tumors occur throughout a woman’s lifetime but are more common in the first four decades. They are bilateral in only about 5% of cases. All granulosa cell tumors should be considered potentially malignant, and late recurrences are common. There are two major histologic types: the adult variety and the juvenile form. The juvenile form is much more likely to result in a malignancy.
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The therapy of granulosa cell tumors is surgical removal; there is no proven benefit for adjunctive therapy. In younger patients who desire to retain their childbearing capability, unilateral salpingo-oophorectomy and full surgical staging are the treatment of choice. Patients with residual or recurrent disease should receive chemotherapy. The usual choice of chemotherapy is bleomycin, etoposide, and platinum, as it is in germ cell tumors. There are too few reported series of granulosa cell tumors treated with chemotherapy to provide accurate figures on response rates to chemotherapy.
Cancer treatment
Young patients with granulosa cell tumors may show precocious puberty because these tumors may produce estrogen. In older women, menstrual irregularity or post-menopausal bleeding due to estrogen production may be the presenting symptom.
Sertoli-Leydig tumors occur less frequently than granulosa cell tumors and are rarely bilateral. These tumors may produce androgens and can present clinically with defeminization or masculinization. The malignant potential of these tumors is directly related to the degree of differentiation, and they are usually classified as well differentiated, moderately differentiated, or poorly differentiated. A fourth classification is Sertoli-Leydig tumors with heterologous elements.
The treatment for these tumors is surgical removal, and unilateral salpingo-oophorectomy is indicated for patients with properly staged disease and tumors confined to one ovary. Little is known about the responsiveness of these tumors to chemotherapy, but most authors recommend bleomycin, etoposide, and platinum chemotherapy for persistent or recurrent disease.
Other stromal tumors are very rare. In general, the therapy is total abdominal hysterectomy and bilateral salpingo-oophorectomy, with full surgical staging for patients who do not desire further childbearing. For younger patients, unilateral salpingo-oophorectomy and full surgical staging are indicated.