Lastly is hormonal therapy, approximately one-third of patient’s with advanced or recurrent endometrial cancer will respond to progesterones, well differentiated tumors tend to have better response rate than undifferentiated tumors. Unfortunately, the tumors that tend to metastasize or become recurrent are the undifferentiated tumors and they have less of a response to progesterone, but it is recommended for patient’s who are not chemotherapy candidates who have received chemotherapy and are no longer chemotherapy candidates, about a third of them will respond to progestins and that includes patient’s that do not have hormonal receptors and they really don’t understand that mechanism. And lastly, they are looking at combining tamoxifen with progesterone, the reason for tamoxifen although it’s in the back of our mind that it causes endometrial cancer, but what tamoxifen does in recurrent or advanced endometrial cancer is produce progesterone receptors and so it is felt that it aids in the use of using Megace or progesterone agents in getting a hormonal response. There are some trials out there now looking at tamoxifen combined with progesterone therapy. Because endometrial cancer usually presents as stage I disease, it’s a very favorable cancer, usually surgery combined with postoperative radiation if needed, gets very long term survival and very good quality survival, our survival rates can be as high as 90% and well differentiated tumors and still even in stage II tumors which are advanced tumors, we are still getting five year 50% survival. So overall, it is a favorable tumor we can work with. Unfortunately, if you get a tumor that’s well advanced or recurrent, it is a very difficult tumor to irradiate because it’s not chemo sensitive and only a third will respond to progesterone agents.

For people who have advanced stage II endometrial cancer, which means there is involvement of the cervix, if the cervix is not grossly involved, meaning there is only endocervical involvement and you have picked this up on a fractional D&C, these patient’s can still undergo a total abdominal hysterectomy, bilateral salpingo-oophorectomy plus your pelvic and periaortic lymph node dissection, send it to pathology and decide if this patient needs postop treatment or not. Most likely she is going to need postoperative radiation therapy because she has at least endocervical involvement. Some GYN oncologists were proposed to a radical hysterectomy for endocervical involvement and therefore necessity for adjunctive radiation therapy. This can be tough in patient’s who have endometrial cancer because #1, these patient’s tend to be elderly and doing radical hysterectomies in the elderly, although it is a completely acceptable treatment for a stage II disease, you are going to leave them with bladder atony and difficulty with their bowels, so it’s a tough surgery to put these patient’s through, plus a lot of them are morbidly obese, and therefore not a surgical candidate to undergo a radical hysterectomy. If the cervix is grossly involved, meaning there is no way you can get out, it’s 4 or 5 cm, what we usually do is treat with external beam radiation followed by one inter cavitary implant followed by an extra fascial hysterectomy following the surgery, and then for huge, large unresectable tumors, anything goes, you use a combination of chemotherapy, plus radiation, plus some surgery to give the patient the optimal palliative result.
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For patient’s who have recurrent or advanced endometrial cancer, there is chemotherapy and progestins. The most active chemotherapeutic agent for endometrial cancer to date has been Adriamycin, it has been proposed to have a 35 to 40% response rate. Now response rate means that if you take patient’s who have a measurable lesion, and given them Adriamycin , it does not mean that 40% of them will have a complete response, that means there will be some shrinkage of tumor. The response rates for Adriamycin last anywhere from seven months. The most active regimen that has been deemed by the gynecologic oncology group looked at single agent Adriamycin versus Adriamycin plus cisplatinum and there was a slightly higher response rate with a combination of cisplatinum and Adriamycin, so that is felt to be the gold standard for endometrial cancer and all the other trials are looking at that.

As GYN oncologists we do not send the specimen to pathology, you are asking your pathologist to do an awful lot on a frozen section. Sometimes it’s difficult, sometimes they will upgrade your tumor on the final histology and sometimes they will have foci of deep myometrial invasion or middle third myometrial invasion which cannot be picked up on the gross frozen section, so it’s very difficult to get a frozen section that sometimes 50% of the time can be changed. So in patient’s who undergo hysterectomies for endometrial cancers, I tend to sample their nodes. If, however, the patient has a well differentiated cancer or atypical hyperplasia, and there is not a GYN oncologist or somebody who can sample the nodes, a complete hysterectomy and peritoneal washings, it’s completely appropriate. Further adjunctive therapy would be based on the final hysterectomy specimen and the staging would then go to the old clinical systems.

Survival based on your histiologic cell type, if you have one of the adenocarcinomas, your survival is very good, depending on the tumor differentiation, so if you have a well differentiated adenocarcinoma you are going to do very well, if you have a grade III adenocarcinoma you are going to do far better than if you have papillary serous or clear cell carcinoma. These are variants of endometrial cancer and really don’t follow the lymph node metastases and other problems that we see with advanced adenocarcinoma of the endometrium. They behave uniquely and they behave very similar to ovarian cancers. As I eluded to before, as the tumor loses differentiation, the survival rate directly goes down and there are several reasons for that. Here is a nice, well differentiated cancer, you can tell if you look at that, you would say it almost looks like normal endometrium, it’s a little crowded but it’s probably going to behave pretty much like a normal endometrium, it probably has estrogen and progesterone receptors and this is probably a cancer that you would ordinarily see in somebody who is morbidly obese, you’re uterine specimen is very small, has very superficial myometrial invasion., and this again is aggressive, ugly, it’s going to infiltrate, it’s going to have your uterus enlarge, it’s going to be infiltrating deeply into the myometrium and into the myometrium there are several lymphatics and once it’s in the lymphatics, it can spread to the pelvis, the periaorta and out toward the adnexa and into the peritoneal cavity.

So as the tumor loses differentiation, so does it gain access into the aortic lymph nodes, the higher the grade, the higher the incidence of lymph metastases and the reason for that is, if you have myometrial invasion, if it’s deep myometrial invasion that’s your highest risk for lymph node metastases because the lymphatics are in the myometrial wall, and if you have a tumor that’s deeply invasive into the myometrium, it’s going to gain access into your lymphatic system. If you have a tumor that is confined to the endometrium, your chance of having aortic and lymph node metastases is about zero, if you have deep myometrial invasion, this is going to be a tumor that most likely if you look hard enough and do a more thorough dissection, you are going to find metastases. The survival directly goes down with the amount of myometrial invasion.

So if we look at endometrial cancer again, the higher the stage, is usually associated with higher grade lesions. As a GYN oncologist, of course I see all spectrum and I see people who have well differentiated cancers who walk in the door with a stage III disease simply because they let their disease process go. I am briefly going to review the staging of endometrial cancer, this is something you will need to study on your own, briefly, stage I is confined to the fundus, stage II has cervical involvement, stage III has adnexal involvement or lymph node involvement and then stage IV is distal metastases. You will have to take some time to go over the one, two, three’s and the ABCs, but in general if you just keep it in mind, one fundus, two cervix, three, adnexal lymph nods, four distal. That will help you on your exam. The distribution of endometrial cancer as I said, 75% of the patient’s who walk in are postmenopausal, 75% are stage I, so it’s not very helpful in treating these people with adjunctive therapy unless you can divide up your stage I patient’s to decide who needs further treatment and who doesn’t. The higher the stage of the cancer, it’s rare to pick them up, also, their survival is not very good.
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The most important prognostic factor when dealing with endometrial cancer is the grade of the tumor, it’s also the histology of the tumor. If you read in your review courses, you are going to find five different histologies. What I would like to do is take about two minutes to break those down. Adenocarcinoma is the most common and is the garden variety cancer that we see, this is the lady who is obese, hypertension, diabetic, and she walks in the door and she has an adenocarcinoma, that makes up about 60%. Adenocanthoma is a benign variant of adenocarcinoma, it means there are squamous components that are not malignant, and you grade the tumor based on the adeno component, therefore you can say now that 80% of your patient’s walk in the door, have the garden variety adenocarcinoma. Adeno squamous back in the olden days was felt to have a worse prognosis than adenocarcinoma and adenocanthoma. However, and this is because the squamous component is invasive. If you just grade the adeno component and if you look at just the grade of the adeno, that is what makes the prognosis of an adeno squamous a poor prognosis, almost virtually all patient’s who have adeno squamous carcinoma of the endometrium also have a grade III tumor, so they behave as a grade III tumor.

Now looking at the symptomatic and symptomatic, the big to do about this paper is that they are trying to point out that asymptomatic patient’s, there was no incidence of atypical hyperplasia, if they were asymptomatic and there was no incidence of cancer, and only a very small percentage who had thickened endometrial stripes, actually had atypical hyperplasia, in this study, they felt that simple hyperplasia was not a precursor to cancer. So because 70 to 80% of patient’s who had thickened endometrial stripes had insufficient tissue or normal endometrium as the study went on, they resampled these patient’s in one year, and their philosophy was even on a fraction D&C, you only sample 20% of the tissue, so could it be that in these patient’s who have a thickened endometrial stripe, whether they are symptomatic or asymptomatic, are we really missing pathology? So these patient’s that were in the insufficient and normal group got resampled in one year and of the patient’s who got resampled, there was a small percentage of patient’s who had atypical hyperplasia, 10% and a small percentage that had cancer. Their conclusions where that people who were asymptomatic who had thickened endometrial stripes one endovaginal vaginal ultrasound, none of them had atypical hyperplasia which is considered a precursor to cancer or cancer, so without symptoms, just because you have a thickened endometrial stripe on ultrasound, you should follow the patient’s symptoms, and that is pretty much the philosophy of patient’s who are are on tamoxifen therapy.

The last diagnosis of endometrial cancer is occasionally picked up on an asymptomatic woman which again is very rare to have a patient who has endometrial cancer who is asymptomatic, but it does occur, to pick it up on a Pap smear. If you have 100 patient’s that have endometrial cancer and you took Pap smears from those patient’s, only 20 would have an abnormal Pap smear. Of the 20 that have an abnormal Pap smear, about 80% would be AGUS, meaning atypical glandular cells of undetermined significance, not ASCUS, atypical squamous cells of undetermined significance, if you ever have a patient in your practice that has atypical glandular cells, those patient’s really need to be worked up thoroughly with an endocervical curettage plus an endometrial curettage, but the Pap smear is not designed to pick up endometrial cancer, it designed to pick up precancerous lesions and does a very poor job for screening for endometrial cancer. The office biopsy is 90% accurate, meaning if you can gain access to the endometrial cavity and you have a patient that has endometrial cancer, 90% of the time it will give you the answer that you have a cancer, 10% of the patient’s who truly do have a cancer that you have done the office Pipel or Randall curette, whatever your choice, 10% of those patient’s will be missed. So therefore, it is imperative that patient’s who have abnormal uterine bleeding that you strongly suspect need to be worked up to rule out an endometrial cancer in your office, biopsy comes back negative. For those small percentage of patient’s, the 10%, they really should undergo a formal procedure, a D&C if that’s medically possible. There are other ways of diagnosing endometrial cancer, one of the new advances has been hysteroscopy which is used on conjunction with D&C and I think this is a very nice technique, it can pick up polyps which you can miss on your D&C, you can also look at the endocervical canal, occasionally you can be working somebody up for an endometrial cancer and find out that indeed they had adenocarcinoma of the endocervix and it not from the endometrium, so I think that hysteroscopy does add t the D&C, it’s not absolutely necessary for complete workup of endometrial cancer, it’s just a diagnostic tool. Hysteroscopy is very infrequently used, it’s used in conjunction with ultrasound. It’s a technique where they look with the ultrasound machine at the uterine strip, and they place saline in to see if this is a cancer. If you’re going to go to that extreme, at some point you are still going to have to sample the patient with either an office biopsy or fractional D&C so I’m not sure that the added expense of this test is always indicated.

If we look at late menopause again, this is a subjective symptom, sometimes you will have women who come in and say, well I have been bleeding and their 65 years old, well obviously they haven’t gotten with the program that they are having abnormal bleeding, they have gone through the change but they are having abnormal bleeding. Diabetes and hypertension is disease processes that are associated with the elderly and also associated with the obese. So it’s unclear whether diabetes and hypertension actually have a cause and effect relation with endometrial cancer, they tend to present with the patient package of an elderly patient who is overweight, who has adult onset diabetes and therefore has adult onset hypertension caused from her obesity. The number one risk factor for endometrial cancer is unopposed estrogen, and this is for the garden variety endometrial cancer, adenocarcinoma, it does not hold true for papillary or clear cell carcinomas, the run of the mill adenocarcinoma is associated with unopposed estrogen.
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In recent years, there has been a lot of use with tamoxifen therapy in breast cancer prevention and in patient’s who have breast cancer to prevent the other breast from receiving tamoxifen in order to be protective against receiving another breast cancer in the opposite breast. There has been a lot of controversy in the literature saying that if you are on tamoxifen, your risk of developing endometrial cancer is seven times that of normal, and indeed that is true. However, of all the patient’s if you take 1000 patient’s who are on tamoxifen therapy for breast cancer prevention, out of the thousand, only two will develop endometrial cancer, therefore, 998 patient’s who are on tamoxifen will not get endometrial cancer. The type of endometrial cancer that patient’s get while they are on tamoxifen is exactly identical to what they get if they are not on tamoxifen. The present with postmenopausal bleeding and therefore, have an early warning sign that allows you to sample them. Patient’s who are on tamoxifen who develop endometrial cancer frequently will present with postmenopausal spotting and when you work them up, they will have a well differentiated tumor and a very early cancer that is very treatable with hysterectomy or radiation, whatever the case may be. Therefore, it is felt that the benefits of tamoxifen therapy far outweigh the risks and therefore, though there is a seven time increased risk of developing endometrial cancer on tamoxifen, the overall risk for patient’s on tamoxifen is actually quite low.