Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evaluation of the patient with metastasis of unknown origin should be structured to quickly identify treatable tumors or the need for palliation while avoiding prolonged hospital stays and testing that will result in neither improved treatment nor better prognosis. The evaluation should be symptom-directed and pathologically oriented. It is the responsibility of the family physician in caring for a patient with MUO to ensure that communication is facilitated between surgeon, oncologist, pathologist, and patient. The physical examination should include thyroid, breasts, pelvic, and rectal examinations. General lab analyses should include fecal occult blood testing, complete blood count, urinalysis, serum calcium, and liver function studies. Men should have assays for prostate-specific antigen and serum prostatic acid phosphatase. Women should undergo mammography and pelvic ultrasound. Undifferentiated carcinoma is likely to originate from either small cell bronchogenic, lymphoma, or germ cell, and thus, serum should be assayed for HCG and AFP. Further radiologic studies, in the absence of specific symptoms, should be limited to chest radiographs and abdominal CT. Contrast studies should be included only if there is organ dysfunction. Biopsy of the malignant tissue should be done early, and studies should include histochemistry, immunohistology, and electron microscopy. Tissues from female patients should be studied for estrogen and progesterone receptors. When a biopsy is planned, advance communication between the family physician or surgeon and the pathologist greatly increases the chance of identifying a primary site. It is important that the surgeon obtain sufficient material to enable study, not only by standard histologic techniques, but also by electron microscopy, special stains, estrogen receptor activity, hormonal markers, and tumor markers. Treatment of patients for whom a primary tumor remains undiscovered must include toxic therapies only for those with good functional status who are likely to respond. Therapy must be pursued for palliation of symptoms when they develop. As physicians, we must control the urge to do something at those times when doing nothing is more appropriate. We must provide continuous support for both the patient and family, protecting to the best of our ability their quality of life. A physician should never convey the impression that it is "not cost-effective" to look for the source of a patient's malignancy. It can be emphasized that further search for a primary tumor carries both medical risk and expense, yet is unlikely to locate the primary tumor or improve the response to therapy or the quality of life.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Metastasis of unknown origin. 146 85

Noninvasive methods for the diagnosis of prostatic cancer, its staging and evaluation of response to therapy are often not sufficiently sensitive or specific. Prostate-specific antigen (PSA) was identified in 1979 and has been evaluated since then as a marker, both at the serum and the tissue level. A review is presented in this article. PSA is an organ-specific glycoprotein presented in most prostatic carcinomas, but also in normal prostatic tissue and in benign prostatic hypertrophy (BPH). The monitoring of serum PSA concentrations by serial measurement can be used for the detection of residual or recurrent tumor after primary treatment and for the evaluation of response to systemic treatment of advanced disease. At the tissue level immunohistochemical detection of PSA may help to identify metastatic tumor of unknown origin. PSA serum assays have not been sufficiently sensitive and specific for staging of the primary tumor or for screening purposes. PSA is an equally specific, but more sensitive marker of prostatic carcinoma compared to prostatic acid phosphatase.
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PMID:Prostate-specific antigen (PSA). A tissue-specific and sensitive tumor marker. 168 77

Prostate cancer, the most prevalent cancer affecting men, frequently metastasizes to the axial skeleton where it produces osteoblastic lesions with growth rates often exceeding that of the primary tumor. To evaluate the role of tumor cell-host stromal interaction and stromal specific growth factors (GFs) in prostate cancer growth and progression, we coinoculated athymic mice with human prostate cancer cells (LNCaP) and various nontumorigenic fibroblasts s.c. LNCaP tumor formation was most consistently induced by human bone (MS) fibroblasts (62%), followed by embryonic rat urogenital sinus mesenchymal (rUGM) cells (31%) and Noble rat prostatic fibroblasts (17%), but not by NIH-3T3, normal rat kidney, or human lung CCD16 fibroblasts. Carcinomas formed preferentially in male hosts, demonstrating in vivo androgen sensitivity. The human prostate component of these tumors was confirmed with immunohistochemical staining for prostate-specific antigen (PSA), Northern analysis for PSA expression, and Southern analysis for human repetitive Alu sequences. Elevations in serum PSA paralleled the histomorphological and biochemical findings. LNCaP and fibroblast cell-conditioned media (CM) was used to determine whether autocrine and paracrine mitogenic pathways exist between LNCaP and fibroblast cells in vitro, and various defined GFs were tested to identify possible active factors. Mitogenic assays revealed a 200-300% bidirectional stimulation between LNCaP and bone or prostate fibroblast-derived CM. Lung, normal rat kidney, and 3T3 fibroblast CM were not mitogenic for LNCaP cells. Among the purified GFs tested basic fibroblast growth factor (bFGF) was the most potent mitogen, stimulating LNCaP growth 180% in a concentration-dependent manner. Transforming growth factor alpha and epidermal growth factor were both minimally mitogenic. Coinoculation of LNCaP cells with a slowly absorbed matrix (Gelfoam) absorbed with bFGF or dialyzed and concentrated rUGM or MS CM was also capable of inducing LNCaP tumor formation in vivo. These observations illustrate that fibroblasts differentially modulate prostate cancer growth through the release of paracrine-mediated GFs, possibly including bFGF, and that tumor-stromal cell interactions play an important role in prostate cancer growth and progression.
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PMID:Acceleration of human prostate cancer growth in vivo by factors produced by prostate and bone fibroblasts. 171 49

Twenty-eight pretreatment and posttreatment biopsies from 11 cases of prostatic adenocarcinoma were stained for prostate-specific acid phosphatase (PAP), prostate-specific antigen (PSA), and keratin to determine the effect of hormonal (diethylstilbestrol) therapy on these immunological markers. Treatment intervals ranged from 2 to 63 months. All pretreatment tumors were strongly positive for PAP, and nine were strongly positive for PSA. Two were weakly positive for PSA, and all were negative for keratin. In five of the 11 posttreatment group cases, staining with both PAP and PSA was reduced. In three posttreatment cases, the malignant epithelium showed a squamoid appearance, and in these areas the keratin gave a positive reaction. These findings indicate that immunohistochemical staining with PAP and PSA may change in response to hormonal therapy. These alterations may lead to false-negative results when using these techniques to identify the primary tumor source of metastatic deposits of prostatic carcinoma.
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PMID:Changes in immunohistochemical staining in prostatic adenocarcinoma following diethylstilbestrol therapy. 241 32

The efficacy of immunocytochemical staining for prostate-specific antigen (PSA) and prostate-specific acid phosphatase (PSAP) was studied in aspiration biopsy specimens from 19 patients. Eighteen patients had prostatic carcinoma and one had hyperplasia of prostate. Specimens were obtained from both the primary tumors and metastatic sites. Immunoperoxidase staining was performed on alcohol-fixed cytology smears (some prepared up to 9 years previously) using appropriate antisera followed by an avidin-biotinylated horseradish peroxidase complex. Results were scored according to the percentage and intensity of positively stained malignant cells. Corresponding histologic specimens were stained and scored in a similar fashion. Correlations were made between the staining characteristics of the tumor markers and grade of tumor, using the University of Texas M.D. Anderson Hospital classification of prostate carcinoma. Overall there was good correlation between cytologic and histologic specimens for the presence of PSA and PSAP, although metastases tended to show fewer positively stained cells than the primary tumor. There was no relationship between tumor grade and percentage of positively stained cells. Ninety-three percent of aspirated primary and secondary prostatic tumors stained positively for PSAP compared with 81% for PSA. In one of 3 patients, negative staining of neoplastic cells by both PSAP and PSA was helpful in confirming the existence of a second primary tumor.
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PMID:Role of immunocytochemistry in diagnosis of prostatic neoplasia by fine needle aspiration biopsy. 242 83

Prostate-specific antigen (PSA) was assayed retrospectively in 131 prostate cancer patients. Pretreatment levels at primary tumor diagnosis were above 5 ng/ml in 13/16 (81%) of stage B and C patients and in 28/28 (100%) of stage D (D1 and D2) patients. At the discovery of metastasis in treated patients, they were above this value in 12/17 (71%) of patients. To determine the value of PSA assays when physical exams were negative, 52 patients were reevaluated at a maximum interval of 12 months as a function of their initial PSA concentration. When the initial PSA was negative, there was no clinical evolution during the next 6 months; when PSA was positive, patients had a 55% risk of progression in the next 4 months. All PSA assays were coupled with prostatic acid phosphatase (PAP) measurements. No PAP values were positive when PSA was negative.
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PMID:Evaluation of prostate-specific antigen in prostate cancer. 246 78

We report a case of secondary penile carcinoma with primary tumor in the pancreas. Immunoperoxidase tissue staining of carbohydrate antigen 19-9, carcinoembryonic antigen and prostate-specific antigen was useful for diagnosis of original tumor.
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PMID:Case report: secondary penile carcinoma. 266 65

A metastatic tumor involving the mandibular condyle presented symptoms of temporomandibular joint (TMJ) dysfunction. Positive identification of the primary malignant lesion as prostatic adenocarcinoma was accomplished through the use of immunohistochemical stains for prostate-specific antigen and subsequent prostate biopsy. A review of the literature revealed fifteen additional cases of metastatic lesions of the mandibular condyle, seven of which also demonstrated TMJ-related symptoms as the initial manifestation of malignant disease. Such cases represent a diagnostic challenge, both clinically and microscopically. Symptoms of TMJ dysfunction coupled with radiographic evidence of a destructive lesion or pathologic fracture should suggest a possible malignant process indicating the need for biopsy. Subsequent examination of routine sections in combination with the use of selected stains, including immunohistochemistry may be helpful in identification of the primary tumor site.
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PMID:Metastatic tumors of the mandibular condyle. Review of the literature and report of a case. 386 14

The clinical and pathologic staging of prostate cancer involves determination of the anatomic extent and burden of tumor based on the best available data. Two major classification schemes are currently used: the modified American system and the TNM system [primary tumor (T), regional lymph node (N), and metastases (M)]. Both systems stratify patients according to the method of tumor detection, separating nonpalpable "incidental" prostate cancers detected during transurethral resection for clinically benign prostatic hyperplasia (BPH) and palpable cancers detected by digital rectal examination. These staging systems also recognize nonpalpable tumors detected by an elevated serum prostate-specific antigen (PSA) level or an abnormal transrectal ultrasound image. Current staging is limited by a significant level of clinical understaging (up to 59%, in our experience) and overstaging (up to 5%) according to comparison with pathologic examination of resected specimens. Proposed improvements in staging include preoperative systematic sextant biopsies to assess tumor volume, volume-based prognostic index, and a multiple prognostic index. In this report, we evaluate the current aspects of clinical and pathologic staging of prostate cancer with emphasis on the early stages in which there is the greatest chance of cure.
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PMID:Staging of prostate cancer. 750 5

To date androgen receptor (AR) expression and structure in human prostatic cancer have been studied in primary tumor specimens and in cell lines. Investigation of alterations in the androgen-signalling transduction cascade in prostatic carcinoma metastases is important to improve our understanding of tumor progression towards androgen insensitivity. In the present study we have collected data comparing AR expression in both the primary tumors and the respective pelvic lymph node metastases. Formalin-fixed and paraffin-embedded tissues derived from the primary tumors and positive lymph nodes of 12 patients undergoing radical prostatectomy were immunostained for the AR and prostate-specific antigen (PSA). AR expression was evaluated with the polyclonal antibody PG-21, which is directed against amino acid 1-21 in the N-terminal region of the AR. All primary tumors stained for the AR. In 8 of the 12 lymph nodes examined more than 50% of the tumor cells were AR positive and displayed a uniform staining pattern; in one lymph node metastasis remarkable heterogeneity in AR expression was observed. In two cases less than 10% of the tumor cells stained for the AR. In one case the lymph node metastasis was immunohistochemically negative for the AR, whereas the primary tumor obtained from the same patient displayed intense staining for the AR. PSA was expressed in all metastases and primary tumors. Our data demonstrate that loss of the AR in lymph node metastases from prostatic carcinoma is a rare event.
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PMID:Androgen receptor status of lymph node metastases from prostate cancer. 860 94


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