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)

The effect of growth hormone on tumor growth and metabolism in the tumor-bearing host is unknown. This study was done to determine the effect of recombinant growth hormone on primary tumor growth, tumor metastasis, and carcass weight in tumor-bearing animals. Twenty-seven female Lobund/Wistar rats with subcutaneous prostate tumor implants (PA-III) were randomized to receive a standard protein diet (22.0% protein; 4.27 kcal/g) or an isocaloric, protein-depleted diet (0.03% protein; 4.27 kcal/g) ad libitum orally. One half of the animals in each group were randomized to receive daily injections of either recombinant growth hormone (1000 mU/kg/day intramuscularly) or placebo (saline) for 14 days. A significant increase in body weight was observed in growth hormone-treated animals without acceleration of primary tumor growth. Spontaneous pulmonary metastasis was inhibited significantly in animals in both dietary groups treated with growth hormone. Thus, growth hormone selectively supports host growth and inhibits pulmonary metastasis in this tumor-bearing animal model. The potential metabolic effects and clinical consequences of treating cancer patients with growth hormone is discussed.
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PMID:Growth hormone inhibits tumor metastasis. 201 34

The case of a 52-year-old woman with acromegaly, diabetes insipidus, and visual impairment caused by a metastatic growth hormone-releasing hormone (GRH)-produced pancreatic tumor is reported. Serum growth hormone (GH) and somatomedin C levels were elevated to 14 ng/ml (normal < 5 ng/ml), and 3.20 U/ml (normal < 1.88 U/ml), respectively. Paradoxical increases were observed in GH levels after glucose tolerance and thyrotropin-releasing hormone-stimulation tests. Biopsy of a pituitary tumor observed on computerized tomography scans and magnetic resonance studies revealed a metastatic cancer. When circulating GRH levels were measured, a marked increase in plasma GRH (1145 pg/ml; normal < 4-1 pg/ml) was observed. The patient died of cachexia due to metastases. Postmortem examination revealed that a primary tumor, a malignant endocrine lesion, was present in the pancreas, with metastatic tumors in the pituitary, lung, liver, and adrenal glands. Synthesis and production of GRH by the tumor was demonstrated by Northern blotting and immunohistochemical analysis. The pituitary gland showed hyperplastic, but not adenomatous changes. The authors stress the importance of both exploration for an ectopic source of GRH and the search for a GH-producing pituitary adenoma when unusual signs and symptoms are seen in patients with acromegaly.
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PMID:Acromegaly, diabetes insipidus, and visual loss caused by metastatic growth hormone-releasing hormone-producing malignant pancreatic endocrine tumor in the pituitary gland. Case report. 767 23

Growth hormone has been shown to stimulate muscle protein synthesis, improve nitrogen balance and promote wound healing in a variety of catabolic states. Its role in the tumor-bearing host is controversial because of its potential to stimulate tumor growth. Twenty-seven Lobund/Wistar rats bearing a subcutaneous prostate tumor implant (PA-III), were randomized to receive growth hormone (1,000 mU/kg/day) or placebo (saline) in the protein-fed and protein-depleted states. Body weight, primary tumor growth and tumor metastasis were assessed to determine the effect of growth hormone and dietary protein intake on these parameters. Growth hormone significantly increased carcass weight in protein-fed animals and reduced carcass weight loss in protein-depleted animals. No stimulation of primary tumor growth occurred and tumor:body weight ratio was similar in all treatment groups. Inhibition of spontaneous pulmonary metastasis occurred following growth hormone therapy in protein-fed and protein-depleted animals. Thus, in this tumor model, growth hormone was found to support host growth selectively and inhibit pulmonary metastasis and may be used as an adjunct to treat cancer cachexia effectively in the future.
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PMID:Growth hormone and prostate cancer growth and metastasis in tumor-bearing animals. 837 96

Hypertrophic pulmonary osteoarthropathy (HPO) associated with non-small cell lung cancer in a 58-year-old man was accompanied by an elevated serum level of growth hormone (GH). HPO rapidly disappeared after resection of the primary tumor and the elevation of serum GH was resolved. Immunohistochemically the tumor contained growth hormone-releasing hormone (GHRH) but not GH. These findings suggest that the high serum GH level due to ectopic GHRH production in the tumor, was a contributing factor in HPO. This is the second reported case of non-small cell lung cancer which was immunohistochemically positive for GHRH associated with HPO.
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PMID:Hypertrophic pulmonary osteoarthropathy associated with non-small cell lung cancer demonstrated growth hormone-releasing hormone by immunohistochemical analysis. 1144 81

Pituitary carcinomas are defined by their metastatic growth. Most of them also invade into surrounding tissues. They should be classified by the site of their metastases (cerebrospinal, systemic, or combined) and by the presumable cell type of origin, respectively with the hormone being demonstrable by immunohistochemistry (adrenocorticotrophic hormone [ACTH], prolactin [PRL], growth hormone [GH], hormone-negative). Pituitary carcinomas develop from invasive adenomas. Nearly all tumors had been treated by surgery or X-ray before they metastasized. Since 1976, 37 cases demonstrated with modern methods were reported: 23 had metastasized into the brain or meninges, 10 showed extracerebral metastases, and 4 showed both types of metastases. In our collection of pituitary tumors, three carcinomas (0.13%) were identified: two with systemic metastases (one ACTH secreting and one PRL secreting) and one with meningeal dissemination and ACTH production. The diagnosis of pituitary carcinomas should be based on four criteria: a demonstrable metastasis, identification of the primary tumor as a pituitary tumor, similarity between the structure and immunohistological marker expression of metastasis and primary tumor, and exclusion of an alternative primary tumor.
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PMID:Pituitary Carcinomas. 1211 77

A mammary tumor cell line, designated MTCL, was successfully established from a mouse primary mammary tumor (MTP). The MTCL cells retain cytokeratin and both estrogen receptor (ER) and progesterone receptor (PR) in vitro. In vitro exposure of MTCL cells to progesterone causes a decrease in the cellular (3)H-thymidine uptake, indicating an inhibition by progesterone on MTCL cellular deoxyribonucleic acid synthesis, whereas exposure of the cells to a high dose of estrogen (15 pg/ml) for 48 h causes an increase of (3)H-thymidine uptake. We inoculated both MTP or MTCL tumor cells into normal cycling female C(3)HeB/FeJ mice and demonstrated that the post-resection metastatic recurrence of MTCL tumors, like the original MTP tumors, depends on the time of tumor resection within the mouse estrous-cycle stage. Both MTCL and MTP tumors have similar histological appearances with the exception of less extensive tumor necrosis and higher vascularity in MTCL tumors. Equivalent levels of sex hormone receptors (ER alpha, ER beta, and PR), epithelial growth hormone receptors (Her2/neu, EGFR1), tumor suppressors (BRCA1, P53), and cell apoptosis-relevant protein (bcl-xl) were found in these in vivo tumors by immunohistochemistry. Cyclin E protein, however, was significantly higher in MTP tumors compared with MTCL tumors. Our results indicate that MTCL cells retain many of the biologic features of the original MTP primary tumor cells, and to our knowledge, it is the first in vitro cell line that has been shown to maintain the estrous-cycle dependence of in vivo cancer metastasis.
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PMID:Creation of a stable mammary tumor cell line that maintains fertility-cycle tumor biology of the parent tumor. 1516 41

There have been concerns that growth hormone (GH) therapy may be associated with an increased risk of cancer. Although data are limited and conflicting, one recent report on cancer risk in individuals with no cancer history or risk factors for cancer who were treated with pituitary GH demonstrated a small increased risk of colon cancer and deaths from colon cancer and Hodgkin disease. The data from cancer survivors have consistently shown no increased risk of recurrence of the primary tumor in survivors of all tumor types who are treated with GH. One recent study did show a small increased risk of second solid tumors in survivors previously treated with GH. Limited data suggest that GH therapy is not associated with excess cancer risk in individuals with Langerhans cell histiocytosis and neurofibromatosis type 1. Overall, the clinical data are reassuring, but continued surveillance is mandatory.
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PMID:Growth hormone treatment: cancer risk. 1553 96

Hypertrophic osteoarthropathy is an important manifestation of lung carcinoma, particularly in a non-small cell tumor, and hampers quality of life. Although removal of the primary tumor usually resolves this syndrome, effective treatment in patients with advanced lung carcinoma has not been established. Recently, an orally active, selective epidermal growth factor receptor tyrosine kinase (EGFR) inhibitor ("Gefitinib") provided clinical anti-tumor activity. We describe a 71-year-old male smoker with cough, who presented with clubbed fingers. A transbronchial lung biopsy (stage T2N3M1-IV) on a cavity lesion in the left lower lobe showed the features of adenocarcinoma, while bone scintigram revealed bilaterally symmetrical abnormal uptakes in the lower extremities, suggesting secondary hypertrophic osteoarthropathy. The serum level of growth hormone was increased to 1.42 ng/ml. Chemotherapy (cisplatin, vinorelbine) was not effective. Gefitinib, as a second-line therapy, induced disappearance of the abnormal accumulation on bone scintigraphy and decrease of the cavity in the lung and of serum growth hormone. The presented case suggests that the EGFR inhibitor might be a promising option for the treatment of hypertrophic osteoarthropathy with advanced lung adenocarcinoma.
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PMID:Successful treatment of hypertrophic osteoarthropathy by gefitinib in a case with lung adenocarcinoma. 1608 Apr 71

Breast cancer is the most common cancer among women. It is estimated that 7% of women who have breast cancer will develop a subsequent second independent breast tumor within 10 years of the first. The status of estrogen (ER), progesterone (PR) and human growth hormone (HER2) receptors, individually and as phenotypic combinations, impacts the clinical course of breast cancer and may impact the course of subsequent primary tumors and patient survival. Our aims were to determine tumor marker phenotype concordance between first and second primary breast cancers (FPBC and SPBC), describe demographic and clinical characteristics, and examine first tumor treatments associated with phenotype concordance. A total of 76,209 cases of female invasive breast cancer were identified in the California Cancer Registry from 1999 to 2004. Of those, 1,407 women who had not undergone a prophylactic mastectomy, had information on the status of three tumor markers, and were diagnosed with an SPBC during the study period were selected. SPBCs were significantly smaller, diagnosed at a higher stage and were node positive. Patients whose FPBC was ER(+)/-/PR(+)/-/HER2- and triple negative (TN) (ER-/PR-/HER2-), often had concordant phenotypes for their SPBC. ER(+)/-/PR(+)/-/HER2+ and HER2-positive (ER-/PR-/HER2+) FPBCs, often had discordant phenotypes for their SPBC. ER(+)/-/PR(+)/-/HER2- SPBCs often lacked HER2 expression and were ER and/or PR positive. Tumor laterality and synchronicity significantly predicted concordance as did having a FPBC whose phenotypes were ER(+)/-/PR(+)/-/HER2+, HER2-positive and TN, while first primary tumor treatment with chemotherapy predicted discordance. The relationship between multiple primary breast cancer phenotype concordance and patient prognosis has yet to be determined. Our results indicate that SPBC surveillance strategies include consideration of FPBC phenotype. Although our results are provocative, they may have been influenced by current criteria used to determine tumor independence.
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PMID:Tumor marker phenotype concordance in second primary breast cancer, California, 1999-2004. 1962 80

We present the first reported case of a craniopharyngioma as a second primary tumor in a patient with acromegaly due to a growth hormone (GH)-secreting pituitary adenoma. The patient was lost for follow-up for 18 years after trans-sphenoidal pituitary surgery for a GH-secreting pituitary adenoma. She presented with headaches and decreased visual acuity, and showed unsuppressed GH in an oral glucose load test with high IGF-1 levels. Brain MRI showed a suprasellar cystic mass and the patient underwent surgery for cyst drainage resulting in postoperative improvement in her vision. Biopsy of the mass confirmed the diagnosis of a craniopharyngioma. We stress the need for close follow-up of patients with acromegaly with adequate control of GH and IGF-1 levels.
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PMID:Craniopharyngioma in a patient with acromegaly due to a pituitary macroadenoma. 2086 85


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