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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parameters that predict tumor aggressiveness or response to therapy are potentially useful in selecting the most appropriate treatment. In theory, the biologic aggressiveness of an untreated bone tumor may be reflected in bone scan parameters. The purpose of this study was to assess the usefulness of bone scintigraphy as a predictive indicator of subsequent metastasis in 25 dogs with primary osteosarcoma. Dogs received radiotherapy and/or intra-arterial cisplatin prior to limb-sparing surgery. Quantitative bone scintigraphy of the tumor was performed prior to treatment (25 dogs) and following treatment but prior to limb-sparing surgery (22 dogs). All dogs developed metastasis at a median time of 202 days (range, 41-444 days) after initiation of treatment. A statistically significant relationship was identified between time to metastasis and: (1) the radiographic tumor area, (2) the pretreatment ratio of mean counts per pixel in tumor-to-adjacent nontumor bone (T/NTT), and (3) the pre:post-treatment T/NTT. Larger tumor area and high pretreatment tumor activity were associated with earlier metastasis. Tumors characterized by greater decreases in scintigraphic uptake after treatment were associated with earlier metastasis. These data suggest that osteosarcomas with high pretreatment mean counts per pixel signify aggressive tumors subject to early metastasis.
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PMID:Relationship between quantitative tumor scintigraphy and time to metastasis in dogs with osteosarcoma. 163 48

The prognostic influence on the DNA content was investigated in 189 patients (esophagus carcinoma n = 45, gastric cancer n = 103, pancreatic cancer n = 41) who underwent a curative resection. In a multivariate analysis the DNA content had a strong as well as an independent influence on the prognosis in esophagus cancer and in pancreatic carcinoma. In gastric cancer, the DNA content had no influence on the prognosis. These results show that the DNA content of the tumor cells, as a measurement of the numerous chromosomal aberrations, well reflects the aggressiveness of the tumor growth in esophagus- and pancreatic cancer. In these tumors it represents the decisive criteria for the prognostic judgement.
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PMID:[Image analysis of DNA cytometry in tumors of the upper gastrointestinal tract]. 163 18

Advances in understanding of the variables that adversely affect the prognosis of patients with superficial bladder cancer allow more accurate predictions of the aggressive biologic potential of tumors. Intravesical therapy appears to be an effective and essential adjuvant in those patients with high-risk tumor variables. Multiple risk factors related to the tumor, individual patient characteristics, and treatment modality must be evaluated. Assignment of the relative importance of these risk factors will differ from patient to patient. Factors useful for predicting tumor aggressiveness in order to decide the appropriateness of adjuvant intravesical therapy include tumor size, configuration, and grade; ploidy status; Tis and T1 categories; multifocality; postoperative cytologic analysis; the failure of prior intravesical therapy; and prostatic urethral involvement. The integration of this information with formulation of a treatment plan represents both the art and the science of urologic oncologic practice. Research efforts need to be directed at the development of better tumor markers for superficial bladder cancer.
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PMID:Recurrent or aggressive bladder cancer. Indications for adjuvant intravesical therapy. 163 33

One hundred and thirty-five cases of basal cell carcinoma (BCC) were investigated, focusing upon factors determining a postoperative prognosis. Out of the 135, nine tumors on the face recurred. All of these nine tumors were insufficiently extirpated at the initial operation, and showed micronodular or infiltrative patterns with stromal fibrosis. Dividing the degree of dermal invasion into four levels, all tumors with recurrence reached levels 3 and 4, the two deeper groups. The immunohistochemical study using anti-laminin and anti-type IV collagen antibodies showed various changes of staining pattern around tumor cell nests, such as attenuation, disruption, and thickening of basement membrane, in contrast with the normal thinly continuous staining around nontumorous control epidermis. The disruption of basement membranes was remarkable around the tumor cells showing a micronodular growth pattern, although the discontinuity of basement membrane was observed in all types of BCCs to a greater or lesser degree. Ultrastructural thickening, multiplication, or discontinuity of basement membranes were found in all 19 cases examined with a greater or lesser degree, although they were most frequently observed around the cell nests showing micronodular growth patterns. It was concluded that deep dermal and marginal invasions were the most ominous signs of recurrence of BCCs. Although the disruption of basement membranes might participate in the local aggressiveness of BCCs, especially in the tumor cells showing micronodular infiltrative growth, other factors may concern the recurrence of BCCs.
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PMID:Clinicopathological and immunohistochemical study of basal cell carcinoma with reference to the features of basement membrane. 164 22

Secreted metalloproteinases (MPs) and their specific inhibitors (TIMPs, tissue inhibitors of MPs) are important mediators of extracellular matrix metabolism. Previous studies have linked either excessive MP release or reduced TIMP-1 production to the invasive and metastatic phenotypes of cancer cells. In the present study we investigated the relationship between the expression of TIMP-1 and the clinical behavior of 28 non-Hodgkin's lymphomas. Northern blot analysis showed that levels of TIMP-1 mRNAs correlated directly with clinical aggressiveness: tumors in the high-grade category contained the highest levels of TIMP-1 transcripts approaching those found in maximally growth factor-stimulated fibroblasts in vitro. In situ hybridization localized the TIMP-1 expression to stromal cells of endothelial and fibroblastic origin. In contrast, transcripts hybridizing with metalloproteinase gene probes (interstitial collagenase and 72-Kd type IV collagenase) were expressed at very low levels in malignant lymphomas and their expression was not coordinately regulated with that of TIMP-1. The majority of tumors expressed either interstitial collagenase or 72-Kd type IV collagenase, and only a small number expressed both. Interstitial collagenase transcripts were only detected in high-grade tumors. The relative levels of TIMP-1 expression did not correlate with the degree of fibrosis of the tumors. Our data suggest the importance of tumor-stromal interactions in non-Hodgkin's lymphomas, and moreover, our results indicate a possible relationship between high-level, localized expression of TIMP-1 and the malignant phenotype of high-grade advanced-stage lymphomas.
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PMID:Tissue inhibitor of metalloproteinases-1 (TIMP-1) RNA is expressed at elevated levels in malignant non-Hodgkin's lymphomas. 164 4

An in vitro tissue culture was established using a giant cell bone tumor derived from a 66-year-old female. The tumor was clinically classified as stage 2, and grade 1 histologically. Morphological observations including, in vitro growth character, histochemical and immunohistochemical staining, and ultrastructural studies, support that the giant cell originated from the mononucleated stromal cell. They do not belong to the monocyte-macrophage system. In this aggressive case, we also tried to evaluate the significance of using DNA ploidy flow cytometry, and chromosomal study in predicting its clinical outcome. The DNA ploidies of both the primary and cultured tumor cells were diploid. The chromosomal analyses revealed its chromosome number ranging from 43 to 46 with three clonal structural changes; dic (19;20) (p13;q13), dic (19;22) (q13;q13) and dic (12;?) (p13;?). As previously compared and reported, cases with marker chromosomes usually had a more aggressive clinical course than those without marker chromosomes. Instability of the terminal portion of the F- and G- chromosome groups were reported in other studies and were also detected in our case. Possible association of clinical aggressiveness with the clonal structural changes, especially dic (19;20) (p;q) and dic (19;22) (q;q), needed further investigation.
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PMID:Tissue culture, DNA flow cytometric and cytogenetic studies of a giant cell tumor of bone. 166 79

The Ki-67 antigen is a cell cycle and tumor growth marker, which can be readily detected using immunocytochemistry methods. Ki-67 antigen is present only in the nuclei of cycling cells and is variably expressed as the cell goes through the various phases of the cycle: both the amount and the topographic distribution of Ki-67 antigen vary in a manner which is sufficiently specific to establish the precise cycle phase for each member of a cell population. From G1 through mitosis, the amount of Ki-67 antigen increases steadily: location of the antigen is nucleolar during G1 and both nucleolar and karyoplasmic during G2. The Ki-67 antigen is widely used to estimate the growth fraction of a tumor cell population; in many malignancies, the percentage of Ki-67-positive cells is correlated with parameters reflecting tumor aggressiveness or progression. These findings demonstrate the potential value of the Ki-67 antigen for the cytopathological or histopathological study of tumors, although neither its biochemical structure nor its function have been fully elucidated to date.
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PMID:[Ki-67 antigen, a cell cycle and tumor growth marker]. 166 69

P-glycoprotein mediates classic multidrug resistance by functioning as an efflux pump that excretes lipophilic chemotherapeutic drugs from cancer cells. We now report an association of P-glycoprotein in colon carcinomas with another tumor property, i.e., enhancement of local tumor aggressiveness. P-glycoprotein was detected with monoclonal antibody immunohistochemistry in 65 of 95 primary colon adenocarcinomas, which were stage B1 or greater. In all but 1 of the 95 cases, solitary invading carcinoma cells were present at the leading edge of the tumor. This subpopulation of invasive carcinoma cells expressed P-glycoprotein (P-Gp+) in 47 of the 95 surgically resected colon specimens. Cases were grouped on the basis of the presence (Group 1, 47 cases) or absence (Group 2, 48 cases) of P-Gp+ invasive carcinoma cells. There was a significantly greater incidence of vessel invasion (P less than 0.001) and lymph node metastases (P less than 0.01) in Group 1 cases. Groups 1 and 2 did not differ with respect to tumor size, depth of invasion of the bowel wall, histological grade, maximum tumor size, mitotic index, mucin production, or presence of perineural invasion (P greater than 0.1). Our findings indicate that P-Gp+ invasive colon cancer cells may have an increased potential for dissemination, suggesting that P-glycoprotein may influence cell behavior.
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PMID:Relationship of the expression of the multidrug resistance gene product (P-glycoprotein) in human colon carcinoma to local tumor aggressiveness and lymph node metastasis. 167 39

The relationship between interphase cytogenetics and tumor grade, stage, and proliferative activity was investigated in 27 transitional cell carcinomas of the urinary bladder. Using fluorescence in situ hybridization with chromosome-specific DNA probes, the copy number of pericentromeric sequences on chromosomes 7, 9, and 11 was detected within interphase nuclei in touch preparations from tumor biopsies. Monosomy of chromosome 9 was detected in 9 of 22 cases (41%), while tetrasomy for chromosomes 7 and 11 was detected in 10 of 26 (38%) and 6 of 23 (26%) cases, respectively. Copy number of chromosome 7 was the most highly correlated with increasing tumor grade (r2 = 0.616, P less than 0.001, Spearman rank correlation) or increasing pathological stage (r2 = 0.356, P less than 0.002). Copy number for chromosome 9 did not correlate with either grade or stage (P greater than 0.05). Tumor labeling index (LI) was determined after in vitro 5-bromodeoxyuridine incorporation, while proliferating cell nuclear antigen LI was determined immunohistochemically. Increasing LI by either method correlated with increasing copy number for all three chromosomes tested (r2 = 0.473, P less than 0.002 for 7; r2 = 0.384, P less than 0.01 for 11; and r2 = 0.316, P less than 0.05 for 9). Since high tumor grade, stage, and LI are all indicative of more aggressive tumor behavior and worse prognosis, these findings suggest that polysomy, especially for chromosome 7, may be highly predictive for bladder tumor aggressiveness.
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PMID:Centromeric copy number of chromosome 7 is strongly correlated with tumor grade and labeling index in human bladder cancer. 167 11

Clonal cell lines were derived from rat liver epithelial cells following their transformation with either v-raf or v-raf/v-myc. Cells transformed with v-raf alone showed reduced tumor incidence and tumor growth rates when implanted into nude mice, compared to cells also expressing the v-myc oncogene. A series of additional clones isolated from a tumor obtained following inoculation of an athymic nude mouse with the v-raf-transformed rat liver epithelial cells displayed an intermediate range of tumor aggressiveness. These findings indicate that unknown genotypic and/or phenotypic changes occur during tumor formation in vivo, which are required in addition to raf activation for complete expression of the malignant phenotype. This in vitro model of tumor progression was used to examine alterations in the expression of genes related to the growth control of liver epithelial cells, which may be involved in the malignant conversion of the preneoplastic cells. A close association was observed between the increased level of expression of the transforming growth factors alpha and beta 1, the decreased expression of extracellular matrix proteins fibronectin and collagen I, and the tumor aggressiveness (latency/growth rate), suggesting a causal role for these factors in the progression of v-raf-transformed rat liver epithelial cells to the fully malignant phenotype.
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PMID:Expression of growth-related genes during tumor progression in v-raf-transformed rat liver epithelial cells. 170 45


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