Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is no longer reasonable to divide cancers into those that are genetic in origin and those that are environmental in origin. With rare exception, carcinogenesis involves environmental factors that directly or indirectly exert a change in the cell's genome. Virtually all causes of cancer are multifactorial, sometimes involving an inherited predisposition to the carcinogenic effects of environmental factors, which include chemicals, ionizing radiation, and oncogenic virus. Carcinogenesis is a multistep process including induction, promotion, and progression. Initiation requires an irreversible change in the cellular genome, whereas promotion is commonly associated with prolonged and reversible exposure. Tumor progression results in genotypic and phenotypic changes associated with tumor growth, invasion, and metastasis. Most information on human cancer risk is based on epidemiologic studies involving both exposed and unexposed individuals. The quality of such studies depends on their ability to assess the strength of any association of exposure and disease and careful attention to any potential bias. Few cancers are inherited in a Mendelian fashion. Several preneoplastic conditions, however, are clearly inherited and several malignancies demonstrate weak familial patterns. Environmental factors may exert their effect on DNA in a random fashion, but certain consistent changes, including specific translocations of genetic information, are often found. Currently, there is great interest in the close proximity of certain oncogenes governing growth control to the consistent chromosomal changes observed. Such changes may represent a final common pathway of action for environmental carcinogens. Sufficient laboratory and epidemiologic evidence exists to establish a causal association of several chemical agents with cancer. The most important carcinogenic chemicals are associated with life-style factors, whereas agents related to other environmental, occupational, or medical exposure are numerically less important. Most chemical agents exert their carcinogenic effects as electrophilic reactants covalently binding to DNA. Certain agents such as asbestos are carcinogenic by virtue of their physical properties. Several short-term tests have been used to screen for chemical carcinogens. Whole-animal studies remain the standard for predicting carcinogen risk in humans, although major limitations in such studies exist. Ionizing radiation also exerts its carcinogenic effect through damage to cellular macromolecules including DNA. Excess cancer risk appears after a latent period of several years following exposure. Risk increases in approximately a linear fashion in proportion to the radiation energy, cumulative dose, and a variety of host biologic factors. The greatest source of average radiation exposure to the US population is from the uranium decay product radon.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Risk factors for cancer. 141 59

Soft tissue sarcomas (STS) represent a heterogenous group of malignant tumors arising in mesenchymal tissue and in the autonomal and peripheral nervous systems. Only 1% of all malignancies in adults are STS. Most of them are localized at the extremities, but they also occur in the abdomen and the thorax as well as at the abdominal and chest wall. They are usually surrounded by a pseudocapsule which contains tumor cells and they can exhibit a discontinuous growth pattern. Macroscopically undetectable branches might grow along given anatomical structures. Thus the whole sarcoma-related anatomic compartment should be judged as tumor-contaminated. The high rate of local failure is often caused by insufficiently extended primary resections. Lymph node metastases are rare. The main prognostic factors are histological grading, tumor size and surgical radicality. Diagnosis of STS is often made at a rather late state of tumor progression often too late for curative therapy. Early histological diagnosis is thus of great importance. The operation aims at the removal of the whole tumor bearing anatomic compartment. Even wide excisions of the sarcoma surrounded by 3 cm of tumor free tissue will lead to at least 60% local recurrencies. Excisions along the pseudocapsule (enucleation) will most likely leave parts of the tumor behind. Insufficient surgical radicality cannot be compensated for by adjuvant therapies. The resection should be carried out without compromises.
 ...
PMID:[Soft tissue sarcoma in adulthood]. 141 47

In a previously studied family with inherited renal cell carcinoma (RCC), RCC was shown to segregate with a constitutional balanced t(3;8)(p14.2;q24.1). In addition, we recently showed that in a RCC tumor from this family the constitutional translocation became unbalanced, suggesting a genetic mechanism that may be associated with the primary genetic events of tumorigenesis. We now report that the RCC tumor cells from this case showed additional cytogenetic alterations, possibly related to tumor progression, which include an additional tumor-specific translocation involving band 14 of chromosome 13. Because this band contains the retinoblastoma (RB) gene, we examined the tumor for aberrations in the RB gene using DNA sequence polymorphism analysis and pulsed-field gel electrophoresis (PFGE), but did not detect alterations in the RB gene.
Cancer Genet Cytogenet 1992 Oct 01
PMID:Cytogenetic and molecular studies of a familial renal cell carcinoma. 142 22

A volume of data that has accumulated for over a century has suggested that fibrin may facilitate the persistence and progression of malignancy. Techniques that have been developed recently have shown that fibrin is indeed a component of the connective tissue stroma in human malignancy but in only a few tumor types. However, therapeutic intervention studies with drugs that limit thrombin activity or enhance fibrinolysis have shown favorable clinical effects in at least one such tumor type. These favorable findings affirm the concept that cause-and-effect relationships do, in fact, exist between thrombin generation with fibrin formation and tumor progression, and suggest that a rational basis exists for the design of future drug intervention trials that target reactions relevant to specific tumor types. These findings also provide a basis for the design of experiments capable of defining further the role of fibrin in the integrity of these tumor types. Because fibrinogen is found much more commonly than fibrin in the connective tissue of a variety of human malignancies, attention might reassumably be directed to determining the possible contribution of this molecule as well as of fibrin to tumor progression.
Cancer Metastasis Rev 1992 Nov
PMID:The role of fibrin in tumor metastasis. 142 19

Prostaglandins and other eicosanoids have been studied extensively in their physical, biochemical, biophysical and pharmacological aspects. However, studies on their role in tumor progression, especially metastases are relatively recent. Following a brief overview of the history of discovery and metabolism of eicosanoids and other fatty acids, we discuss the functions of these fatty acids (with emphasis on prostacyclin, thromboxane A2, 12-hydroxyeicosatetraenoic acid and 13-hydroxyoctadecadienoic acid) in cell transformation, tumor promotion and particularly in tumor cell metastasis. The relation between these monohydroxy fatty acids and tumor cell metastasis is discussed from three different perspectives, i.e., their effects on tumor cells, on platelets and on endothelial cells. The mechanism of these effects are then addressed at cell adhesion molecule, motility, protease, cell cytoskeleton, protein kinase and eicosanoid receptor levels. Finally, regulation of three key enzymes which generate eicosanoids (phospholipase, prostaglandin endoperoxide synthase and lipoxygenase) is explored.
Cancer Metastasis Rev 1992 Nov
PMID:Fatty acid modulation of tumor cell-platelet-vessel wall interaction. 142 24

Patients with ulcerative colitis carry an increased colorectal cancer risk. The cumulative cancer risk for patients with pancolitis is 0.5-0.7% per patient year. Dysplasia as a histologic marker of a neoplastic transformation is used to identify patients with an increased cancer risk during colonoscopic surveillance. Because the classification of dysplasia is subject to inter- and intraobserver variation new methods for the detection of risk patients have been investigated. DNA analysis by flow cytometry seems to be of value for the detection of DNA aneuploidy and the identification of patients who are at risk for neoplastic progression. The significance of DNA aneuploidy is being evaluated in prospective studies. Surveillance guidelines depend on duration and anatomical extent of the colitis as well as on the detection of dysplasia.
 ...
PMID:[Risk of colorectal cancer in ulcerative colitis--monitoring strategies and identification of risk patients]. 144 7

DNA stemlines of hepatocellular carcinoma (HCC) model of adult Wistar rats established by diethylnitrosamine were quantitatively measured by flow cytometry. The cancer-inducing course was divided into four stages, eg, precirrhosis stage, cirrhosis stage, early cancer stage and cancer progression stage. The advantageous DNA stemline of hepatocytes of normal adult Wistar rats was tetraploid (4C). It was from the cirrhosis stage that atavistic proliferation of hepatocytes with diploid (2C) DNA stemline started and replaced 4C hepatocytes, resulting in a new advantageous population. The features of early cancer stage were formation of HCC with 2C DNA stemline, whereas during the cancer progression stage, HCC cells with aneuploid (AN) DNA stemline presented the advantageous growth. The study clearly shows the change pattern of DNA stemline during the course of hepatocarcinogenesis from 4C-2C-AN, which is believed to be the biokinetic mechanism of the development and progression of HCC.
 ...
PMID:Characteristic changes of DNA stemlines during hepatocarcinogenesis in rats. 145 56

We found that the human colon cancer cell line SW480 consists of two distinct subpopulations which we have designated E-type (epithelial) and R-type (round). Pure cultures of each type were obtained by subcloning, and both have maintained their characteristic phenotypes for at least 1 year (40 passages). E-type cells are the major (> 98%) type in the parental SW480 cell line. They form flat epithelial-like colonies. In contrast, R-type cells, which constitute a minor fraction (< 2%) of the parental cell line, have a rounded shape and grow in clusters of piled-up cells. Compared to E-type cells or the parental SW480 cells, isolated R-type cells display decreased doubling time, loss of contact inhibition, less adhesiveness to culture plates, higher anchorage-independent growth in soft agar, and a much more aneuploid karyotype. When injected s.c. into nude mice, R-type cells produce much larger tumors within the same period of time than E-type cells, and the tumors are less differentiated than those produced by the E-type cells. Cell fusion experiments between R-type and E-type cells revealed that the R-type phenotype is dominant, and the results suggest that this is due to one or a few genetic changes. Taken together, these findings suggest that the R-type cells represent a more malignant variant of the E-type cells. They may be useful, therefore, for studying mechanisms involved in tumor progression.
Cancer Res 1992 Dec 15
PMID:Isolation and characterization of a highly malignant variant of the SW480 human colon cancer cell line. 145 72

Sixty-day bioassays of iodinated glycerol, trichlorfon, and acetaminophen were conducted using a leukemia transplant model in 6- to 8-week-old F344 rats to investigate the potential of these chemicals to affect tumor progression. The chemicals were administered in the drinking water at doses that approximated those used in previously conducted 2-year carcinogenesis studies. Simultaneous with dose administration, half of a group of young, healthy, syngeneic rats were given subcutaneous transplants of mononuclear cells derived from spleens of leukemic donors. Variables used to quantitate tumor progression included body weight, spleen weight, white blood cell (WBC) and red blood cell (RBC) counts, packed cell volume, hemoglobin concentration, and platelet counts. Iodinated glycerol at 1.25 or 2.5 mg/ml caused a greater increase in leukocytosis in dosed transplant recipients in comparison to that experienced by undosed recipients: trichlorfon at 2.5 or 5.0 mg/ml enhanced splenomegaly and induced greater reductions in RBC parameters in dosed recipients in comparison to that experienced by undosed recipients. Acetaminophen at 3.0 and 6.0 mg/ml resulted in insignificant but dose-related increases in spleen weight and leukocytosis only in the female rat transplant recipients, as was observed in 2-year studies. Based on results from the short-term leukemia transplant model, data from 2-year carcinogenicity studies, and structure-activity considerations, exposure to iodinated glycerol and trichlorfon was more strongly associated with the expression of leukemia than exposure to acetaminophen. The potential carcinogenicity of each of these chemicals should be taken into consideration when calculating estimates of risk and decisions for their use.
Cancer Detect Prev 1992
PMID:The effects of iodinated glycerol, trichlorfon, and acetaminophen on tumor progression in a Fischer rat leukemia transplant model. 145 7

For transitional cell carcinoma of the bladder, clinical data indicate that invasive, metastatic tumors can arise through at least two different progression pathways. The majority of invasive, metastatic bladder neoplasms clinically present de novo, i.e., the patients have no history of malignant bladder disease. This implies that the highly malignant tumor cells either arise de novo or have undergone a rapid progression. Alternatively, a considerable fraction of patients with superficial bladder cancer process to invasive disease after a history of relatively benign superficial TCC. The molecular and cell biological basis of tumor progression is only poorly understood. Clearly, a better understanding of this progress could have profound clinical implications, since patients with superficial TCC with a high risk for progression would have to be treated more aggressively. We discuss the problems that are associated with tumor biological studies on early steps in the progression of TCC, especially from a "model system point of view."
 ...
PMID:Critical review of the models to study the biologic progression of bladder cancer. 146 97


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