Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with Klinefelter's syndrome is described who also had transitional cell carcinoma of the bladder. His mother and maternal grandfather died of neoplasms. It is suggested that neoplasm and aneuploidy in the same family could have been caused by an inherited chromosomal instability rather than coincidence.
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PMID:Klinefelter's syndrome and bladder cancer. 100 71

Immunological studies are presented on a patient with a long clinical history suggesting the existence of a tumor-specific immune response. His tumor, first considered benign, progressed to a highly malignant osteosarcoma. Cell-mediated immune reactivity against biopsy cells and against tumor extract was detected in vitro by the autologous tumor stimulation test (ATS) and in vivo by the skin test. In one ATS-test with tumor extract, blastogenesis of T-cells was demonstrated. The amount of Ig(s) in consecutive biopsies increased. Biopsies taken in the later period of the disease stimulated only after trypsin treatment. This stimulation was inhibited by autologous serum or acid eluate of the biopsy. The inhibitory factor in the serum was not intact immunoglobin. Blood lymphocytes did not show a discriminatory or disease-related cytotoxicity, either directly or after co-cultivation with the tumor material. Lymphocytes isolated from one biopsy were non-reactive in both the ATS and the cytotoxicity test.
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PMID:Search for anti-tumor response in a bone tumor patient with a long clinical history. 106 20

An association of the histidine auxotroph of Salmonella typhimurium (strain TA1538) within the gastrointestinal tract of otherwise germfree Sprague-Dawley rats is maintained during periods of observation lasting as long as 7 months. The bacteria are found at levels exceeding 10(7) per g in the forestomach and at levels greater than 10(8) per g in the lower bowel and in the feces. Only approximately 10(4) bacteria per g are found in the posterior stomach and in the upper small intestine. The association of the salmonella mutants is maintained when the bacterial association is increased by the addition of other bacteria characteristic of the gastrointestinal flora. Carcinogenic amines, which cause strain TA1538 to revert to histidine independence in Ames' in vitro assays, increase the number of revertants in the feces when fed to the salmonella-associated rats. In contrast, the number of revertants in the feces does not increase when the rats are fed structurally related compounds which are not mutagenic to the bacteria in vitro and for which no evidence of carcinogenicity exists. Sacrifice of rats after feeding the carcinogen 2-nitrofluorene indicates that the number of revertants is increased in the cecum and colon as well as in the feces. The apparent proximity of the bacterial mutagenic response to the location of the tumor response in the colon suggests that the rat associated with the histidine auxotroph may provide a useful model for further investigation of the possible association between bacterial mutagenesis and carcinogenesis within the gastrointestinal tract. In addition, with this model it may be possible to evaluate selectively the effects of various constituents of the flora on the activation of compounds provoking the revertant response.
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PMID:Association of salmonella mutants with germfree rats: site specific model to detect carcinogens as mutagens. 110 85

Curve-fitting procedures indicated that exo-2-amino-bicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH) modified V and Km for one of two systems serving for histidine transport into the S37 ascites tumor cells. When this system was obliterated by leucine in the medium, BCH had no effect on histidine transport. Curve-fitting procedures similarly suggest N-methyl-alpha-aminoisobutyric acid affected the Km and V values for the other histidine-transporting system and that carboxymethylhistidine (His(Cm)) inhibited both transport systems. His(Cm) further inhibited histidine uptake into leucine-inhibited cells. Km and V values were altered simultaneously in the presence of several inhibitory analogs. Alanine methyl ester markedly inhibited high-concentration histidine uptake, whereas leucine methyl ester markedly inhibited low-concentration histidine uptake. The present results confirm earlier suggestions that our high c system is Christensen's A system and our low c system his L system. We also confirm a very high degree of specificity of N-methyl-alpha-aminoisobutyric acid for the A or high c system, and of BCH for the L or low c system. We suggest the utility of combining two approaches to the study of transport system properties; use of specific analogs and modification of biphasic plots. We demonstrate that the carboxyl group is not a prerequisite molecular feature for inhibitory interaction with the A or L system.
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PMID:Biphasic kinetic plots and specific analogs distinguishing and describing amino acid transport sites in S37 ascites tumor cells. 113 29

The potent skin tumor promoter (12-O-tetradecanoyl phorbol-13-acetate (TPA) stimulates epidermal macromolecular synthesis as well as proliferation, but little is known of specific functional aberrations produced by TPA. This report presents results of a study on the effects of TPA on epidermal histidase (L-histidine ammonia lyase), an enzyme found in normal epidermis but not in dermis or in mouse squamous cell carcinomas. Histidase activity was assayed on postmitochondrial supernatants obtained from hairless mouse epidermis after removal by keratotome. Topical TPA treatment at doses active in tumor promotion (1.7 to 17.0 nmoles/application) produced dose-dependent decreases in epidermal histidase specific activity at 19 hr posttreatment. The onset of the decrease occurred at 12 hr with recovery to control level specific activity by 5 days, showing kinetics similar to those obtained for stimulation of DNA synthesis. This decrease in histidase could not be attributed to a general inhibition of soluble protein synthesis or to the appearance of an inhibitor of histidase activity. The strong promoter TPA produced a greater histidase decrease than did the moderate promoter and mitogen 12,13-didecanoyl phorbol at equimolar dose, while phorbol, a nonpromoter and nonmitogen, produced no effects on histidase. The relationship of this histidase depression to tumor promotion and not initiation is further indicated by the finding that (a) Tween 60, a structurally unrelated tumor promotor, also produced a decrease in histidase; and (b) the tumor initiator urethan and an initiating dose of 9,10-dimethybenz(a)anthracene showed no effects on histadase activity.
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PMID:Decrease of epidermal histidase activity by tumor-promoting phorbol esters. 118 5

Verified breast cancer was present in a father, his mother, and his daughter. His sone had a brain tumor (by history) and his grandson, (ehs sone of the affected daughter), had a histologically verified rhabdomyosarcoma. This familial aggregation of cancers (except for leukemia, which is absent) is consistent with a newly described familial breast cancer syndrome. A single pleiotropic, dominantly transmitted gene, possibly interacting with carcinogenic factors, such as an oncogenic virus, may be the cause. A cancer-control potential exists for tumor associations such as those exhibited in this kindred, as well as for other cancer genetic syndromes where careful consideration is given to all histologic varieties of cancer.
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PMID:Breast cancer genetics and cancer control. Tumor association. 119 Oct 14

A 60-year-old man was admitted with anosmia, memory disturbance and disorientation in 1971. He was diagnosed the left olfactory groove meningioma and received the removal of the tumor after ligation of the left external carotid artery. Over the following two years he was admitted again with progressive memory disturbance and mental disorder in Aug. '73. Physical examination disclosed no abnormalities except for slight hypertention. His CSF pressure was 120 mm H2O and pneumoencephalograms showed marked dilatation of the lateral ventricles. Right carotid angiography revealed the right olfactory groove meningioma which was receiving a rich circulation from the branches of right ophthalmic artery. And right selective external arteriography showed an arteriovenous communication between the occipital artery and the transverse sinus. Contrast medium flowed to the left transverse sinus. Left internal carotid arteriography showed an anomalous arteriovenous communication between the tentorial branch (Bernasconi-Cassinari artery) of the internal carotid artery and sigmoid sinus. Further left vertebral arteriography revealed another arteriovenous communication between the left occipital artery anastomosed with vertebral artery and the transverse sinus. An operation for the right olfactory groove meningioma was made in Sep. '73. Some considerations on the pathogenesis of developement of these arteriovenous communications were discussed.
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PMID:[A case of arteriovenous communication between external and internal carotid arteries and the sinus after removal of the meningioma (author's transl)]. 123 33

A man with bronchogenic carcinoma lost the ability to elevate his left eye voluntarily. His eyes were level in the primary position and the Bell phenomenon was normal, indicating that the ophthalmoplegia was caused by a supranuclear lesion. Other clinical and radiologic evedence indicated that there was a lesion in the rostral midbrain. A metastatic tumor, found in the right pretectum at autopsy, probably produced the ophthalmoplegia by interrupting axons destined for the superior rectus portion of the homolateral oculomotor nucleus and the interior oblique portion of the contralateral oculomotor nucleus.
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PMID:Supranuclear paralysis of monocular elevation. 123 56

Histologic study of the conduction system of the heart of a 16-year-old girl who died suddenly demonstrated a benign mesothelioma of the AV node, with almost complete replacement of the structure by the tumor. Teh past history was unremarkable, except for few syncopal episodes at 9 and 11 years of age and during pregnancy. Immediately postpartum, she developed a 2:1 AV block and intermittent complete AV block. Six weeks later, during diagnostic work-up in the cardiac catheterization laboratory, she died suddenly. Electrophysiological studies during this work-up disclosed complete AV dissociation, with normal QRS complexes. The block was proximal to the His-bundle recording site, with a normal H-V interval. Occasional syncopal attacks in young adults should alert the physician to the possibility of this diagnosis and lead to pacemaker insertion.
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PMID:Sudden death caused by benign tumor of the atrioventricular node. 124 54

We report a case of granulocyte colony-stimulating factor (G-CSF) producing lung large cell carcinoma with sarcomatous transformation. A 57-year-old man was admitted for evaluation of an abnormal shadow near the right pulmonary hilus on chest X-ray film. Brush cytology specimen from right B6 disclosed large cell carcinoma. His clinical stage was already IIIB (T3N3M0) on admission, so we immediately administered chemotherapy and radiation therapy. However, the patient's condition gradually deteriorated and he died of respiratory failure. Although there was no evidence of infection throughout his clinical course, his peripheral white blood cell count gradually increased and reached 47,000/mm3 (neutrophils 96%) before death. Histological study of the autopsy specimen revealed that the primary tumor was composed of two different elements (large cell carcinoma and spindle cell sarcomatoid element). The spindle cell sarcomatoid element appeared to have arisen from sarcomatous transformation of carcinoma cells, because the transition margin of the carcinoma to the sarcomatoid element was smooth, and special and immunohistochemical staining of both elements showed the same properties. Moreover, immunohistochemical study with monoclonal antibody to human G-CSF, 4A6 clearly demonstrated granular staining of G-CSF in the cytoplasm of tumor cells.
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PMID:[Granulocyte colony-stimulating factor producing lung large cell carcinoma with sarcomatous transformation]. 127 57


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