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

Seventy patients with transitional cell carcinoma of the kidney operated upon at Barnes Hospital during the last 25 years are reviewed. The relationship of the pathologic stage, grade, findings on excretory urography and survival is studied. The stage and survival rates were predicted fairly accurately on the basis of the excretory urogram alone. Survival of patients was determined occasionally by the status of the associated bladder tumors more than by the renal cancer. Because of tumor multiplicity we recommend total nephroureterectomy as the treatment of choice. The role of radiation therapy is considered.
 ...
PMID:Transitional cell carcinoma of the kidney 25-year experience. 66 Jul 26

The aim of the present study is to analyse the response in patients with cancer of the urogenital region to a primary antigen 2-4 dinitrochlorobenzene (DNCB). A total of 69 patients with neoplastic disease were studied (13 cases with kidney cancer, 34 cases with bladder cancer, 13 cases with prostatic cancer, 5 cases with testicular cancer, one case with penis cancer, and 3 cases with cancer of the cervix, comparatively with 13 patients with non-malignant urological diseases. Whereas in the control group, 78% of the patients gave a positive skin reaction to DNCB, 15% of the patients with kidney cancer, 56% of the patients with bladder cancer, 69% of the patients with prostatic cancer and 60% of the patients with testicular cancer gave a positive reaction. If we consider the stages of the disease, the reaction was positive, in 91% of bladder cancer at stage I and in 47% at stages II and III in 100% of prostatic cancer at stage I and in 62% at stages II and III, in 60% of testicular cancer at stage IV (but 100% of seminomas and 0% of dysembryomas have a positive reaction). It would therefore seem that a correlation exists between the degree of the extension of the disease and the skin reaction to DNCB.
 ...
PMID:Cutaneous response to dinitrochlorobenzene in patients with genito-urinary cancers. 85 14

Seventy-eight patients with advanced cancer received an adequate therapeutic trial with aniline mustard (NSC 18429). Significant anticancer activity with clinical benefit was demonstrated in five patients with cancer of the prostate and one patient with renal cancer. beta-glucuronidase levels in aspirate and imprint preparations of tumor cells were assessed by a timed cytochemical technique. A partial correlation appeared to exist between very intense glucuronidase staining and tumor regression in prostate and kidney lesions; however, these high levels were observed only rarely. Sequential observations in two patients demonstrated loss of enzymatic activity concomitant with development of clinical relapse.
 ...
PMID:Therapeutic trial of aniline mustard in patients with advanced cancer. Comparison of therapeutic response with cytochemical assessment of tumor cell beta-glucuronidase activity. 99 Nov 4

An unusual long-term survival of a patient with metastatic renal cancer is reported. Asthma developed after lung lesions were detected. After development of his allergy, new lesions have failed to appear and growth of old ones has slowed. The possibility that allergy can be a factor in the control of neoplasia is discussed.
 ...
PMID:Allergy and cancer. 114 26

1. The evaluation of renal masses has become an increasingly important topic because of the increasing incidence of kidney cancer, the improved cure rate of renal carcinoma with the proper preoperative diagnosis, and the proliferation in renal mass diagnostic methodology. 2. A variety of benign entities can produce an abnormal renal mass with attendant difficulties in being distinguished from malignant neoplasms. Among these benign lesions are: simple renal cysts, polycystic kidneys, congenital variations in renal size and shape, segmental renal hypertrophy, renal infarcts, intrarenal hematomas, renal hamartomas, renal leiomyomas, renal adenomas, renal angiomas, renal fibrolipomatosis, hydronephrosis of a duplicated collecting system, renal abscesses, and xanthogranulomatous pyelonephritis. 3. Nephrotomography, nephrosonography (ultrasound), adrenalin renal arteriography, selective magnification renal arteriography, renal venography and cavography, lymphangiography, renal scintillation scanning, abnormal levels of enzymes in blood and urine, immunologic studies (circulating antibodies and tumor-associated antigens), percutaneous needle aspirations, and retrograde renal brushing have all increased the diagnostic accuracy of determining the etiology of renal masses. None of these diagnostic procedures is infallible. A judicious combination of procedures gives the most reliable diagnostic results. 4. A search continues for (a) chemical agent(s) or a chemical profile in the blood or urine which is (are) specific for renal carcinoma, but as yet this is an investigational area and not a practical clinical reality.
 ...
PMID:Evaluation of renal masses including retrograde renal brushing. 125 Dec 98

The development of Wilms' tumor, a pediatric kidney cancer, has been linked to the inactivation of a tumor suppressor gene both by epidemiologic studies and by genetic analyses. Like retinoblastoma, Wilms' tumors can occur bilaterally in individuals with apparent genetic susceptibility to this disease. This led Knudson and Strong to propose in 1972 that two genetic events were rate limiting in tumor development and that predisposed individuals had already inherited one mutation in the germline. The observation of karyotype abnormalities in predisposed children and studies of the molecular genetics of Wilms' tumor specimens enabled the identification of chromosome band 11p13 as one genetic locus inactivated in Wilms' tumor. The recent isolation of the WT1 gene, which is the specific target within that locus, offers new insight into the etiology of Wilms' tumor. This gene has properties distinct from those of other known tumor suppressor genes. WT1 encodes a zinc finger transcription factor that is alternatively spliced and has high sequence homology to the early growth response genes (EGR). Unlike the retinoblastoma (RB1) and p53 genes that are expressed ubiquitously, WT1 is expressed in specific cells of the kidney and only during a short period in development. Thus, disruption of a gene that is active during a critical period in the development of a specific organ can lead to neoplastic growth in that organ. Future studies are aimed at exploring the link between the role of the WT1 gene in normal development and in tumorigenesis of the kidney.
 ...
PMID:WT1: a novel tumor suppressor gene inactivated in Wilms' tumor. 131 85

Wilms tumor is a pediatric kidney cancer that has been linked to the inactivation of a tumor-suppressor gene at chromosome locus 11p13. The WT1 gene, mapping to this locus, is developmentally regulated in the kidney and encodes a putative transcription factor that has been shown to be mutated in Wilms tumor specimens. We have suggested that one such altered product of the WT1 gene may be capable of trans-dominant suppression, since the mutated allele was found to be coexpressed with the wild-type allele in a sporadic Wilms tumor. We therefore tested the ability of this mutant WT1 allele, containing an in-frame deletion within the DNA-binding domain, to transform primary baby rat kidney cells. The mutant WT1 gene was found to cooperate with the adenoviral E1A gene in transforming baby rat kidney cells, as demonstrated by growth in soft agar and tumorigenicity in nude mice. The wild-type WT1 gene in all of its alternatively spliced forms neither suppressed E1A-induced focus formation nor cooperated with E1A. Our results indicate that impairment of DNA binding of the WT1 tumor-suppressor gene product can result in a dominant negative mutation.
 ...
PMID:A dominant mutation in the Wilms tumor gene WT1 cooperates with the viral oncogene E1A in transformation of primary kidney cells. 132 31

Gemcitabine (dFdC) and DMDC are new antimetabolites with good antitumor activities against various tumors which include human leukemic cell lines and a number of rodent and human solid tumors and human tumor. They are structurally related to cytarabine (Ara-C) which is known as one of the most effective drugs against adult acute leukemia, but many solid tumors are insensitive not been found to the drug. Gemcitabine acts as an inhibitor of ribonucleoside diphosphate reductase and inhibits DNA synthesis. Biochemically Gemcitabine is rapidly phosphorylated to dFdCTP which has a comparatively longer half-life than that of Ara-C, showing a therapeutic activity against tumors. In the phase I trials, the reported maximum-tolerated doses were 790 mg/m2 to 1370 mg/m2 at the schedule of 30 minutes i.v. infusion once a week for three weeks but higher dose levels (2,500 mg/m2 to 4,800 mg/m2) were reported in the schedule of prolongation of the infusion time. Reported toxicities were myelosuppression, fatigability, fever, appetite loss and skin rash. Toxicities were seemed to be mild. In USA, Europe and South Africa, phase II trials of Gemcitabine at the schedule of 30 minutes infusion once a week for three weeks followed by one week rest were performed against solid tumors (breast cancer, ovarian cancer, renal cancer, colorectal cancer, pancreas cancer, head and neck cancer, and lung cancer) and showed good responses to those tumors. DMDC was developed in Japan, and a phase I trial is currently on-going.
 ...
PMID:[New antitumor antimetabolites--gemcitabine and DMDC]. 133 22

The rapid pace of research in the genetics of human cancer will predictably render any review of the topic out of date by the time of its publication. Prospects for the near future will likely include the identification of a chromosome 3p gene(s) linked with the development of familial renal cancer and, perhaps, also lung cancer. In addition, the availability from the Human Genome Project of an increasing number of well-characterized markers will accelerate the search for additional human recessive oncogenes. Many questions still remain about the etiology of lung cancer and how to apply this information for patient care. For example, identification of the cell of origin for small cell and non-small cell lung cancers will facilitate our understanding of the development of these tumors and improve the possibilities for future preventive strategies. In addition, we now realize that these cancers arise from the sequential accumulation of multiple genetic mutations (Table 3; Fig. 1). Therefore, a central question is which of these targets are essential for the process of carcinogenesis, and whether there is a critical temporal order for this process with a defined premalignant phase in a discrete field of bronchial tissue. In addition, are there genetically inherited susceptibilities to the development of lung cancer (either directly or via variabilities in carcinogen metabolism) that could be accurately identified in the general population? Finally, is there a rate-limiting mutation and will the genetic correction of this defect suffice to restore growth regulation, or will the replacement of multiple gene products be required for tumor suppression? We are already witnessing the beginnings of the use of molecular diagnostic markers as a research tool for assigning prognostic information. The expression of neuroendocrine markers in non-small cell lung cancer has recently been applied as an indicator of the potential response to combination chemotherapy [15]. Similar methods are being applied to the expression of tumor suppressor genes or the presence of somatic mutations in dominant oncogenes such as the ras gene. However, the clinical benefit of this prognostic information with currently available treatment programs is still uncertain.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Oncogenes in human lung cancer. 136 67

The purpose of this study was to determine whether nm23 steady-state mRNA expression levels correlate with metastatic potential of mouse K-1735 melanoma cells, human KM12 colon cancer cells, and human SN12 renal cancer cells. Since neoplasms are heterogeneous and contain subpopulations of cells with different metastatic potentials, we analyzed multiple sets of nonmetastatic and metastatic clones isolated from each neoplasm. In addition, we also examined nine somatic cell hybrids produced by the fusion of nonmetastatic and metastatic K-1735 clones. In the mouse melanoma, we found heterogeneity in nm23-1 steady-state expression levels among the clones and hybrids that did not correlate with their metastatic phenotype. Clones isolated from human colon or renal carcinomas expressed similar levels of nm23-HI regardless of metastatic potential in nude mice. All of the human tumor cells were heterozygous for the nm23-HI-specific allelic DNA fragments, with no allelic deletions or gross alterations detected. Since the failure of tumor cells to produce metastasis can be due to multiple deficiencies, these data stress the importance of using independent clones with different metastatic potentials for the analysis of gene regulation of this process.
 ...
PMID:Expression level of the nm23 gene in clonal populations of metastatic murine and human neoplasms. 139 7


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>