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At least 19 recordsLinked to original sources
PubMed1983

[Increase in tumor microvascular pressure by angiotensin-induced hypertension: implication for pharmacokinetic analysis of drug delivery into tumor tissue].

Tumor microvascular pressure was measured by using a newly developed transparent chamber of rat. The pressure of tumor vessels, 20-100 microns in diameter, increased from 9.2 +/- 2.6 cm H2O to 15.4 +/- 3.2 cm H2O when the mean arterial pressure was elevated from 103.3 +/- 8.6 mmHg to 159.2 +/- 7.9 mmHg with continuous infusion of angiotensin II. It was frequently observed that the blood began to flow into the vessels in tumor tissue, where the statis of flow had been seen, when the pressure was elevated from normotension to hypertension by angiotensin II. Based on the results obtained, the mechanism of drug delivery into tumor tissue was discussed in correlation with the enhancement of chemotherapeutic effects in both animal experiments and cancer patients by induced hypertension chemotherapy.

Angiotensin II↗
PubMed1997

Telomerase activity and metastasis: expansion of cells having higher telomerase activity within culture lines and tumor tissues.

Tumor cells with metastatic potential may have a high telomerase activity that augments telomeric DNA repeats, allowing the cells to escape from the inhibition of cell proliferation due to shortened telomeres. We examined the expression level of telomerase activity using the telomeric repeat amplification protocol among a series of cell lines obtained by repeated transplantation of a mouse fibrosarcoma. The lines could be grouped into three; one has no metastatic potential, and the other two show metastatic abilities after intravenous or subcutaneous injection. Comparison of their telomerase activity indicated that more malignant lines had higher activity. A similar relation was seen in metastatic nodules formed through clonal expansion from the heterogeneous population of inoculated cells; clonality was monitored in terms of variable patterns of subtelomeric repeats. The results suggest that a high level of telomerase activity may not be requisite for metastasis, but may confer a propensity to dominate in a tumor tissue.

Animals↗
PubMed1999

Lamotrigine concentrations in human serum, brain tissue, and tumor tissue.

PURPOSE: Although lamotrigine (LTG) has been used for years as an antiepilepic drug (AED), there are no data on penetration into the brain with the exception of a single case report. It was our aim to determine the LTG content in the brain and the tumor tissue and to bring the same into relation to the serum concentration and protein binding in neurosurgically operated patients. METHODS: Neurosurgical intervention was performed on 11 patients with brain tumors. Tumor tissue was removed, and LTG kinetics was carried out for 12 h. LTG was determined by means of (HPLC) and the protein binding by means of ultrafiltration. RESULTS: At the time of the section of the tumor, the LTG concentrations in the serum were an average of 3.7 microg/ml (range, 1.1-9.8); in the brain, an average of 6.8 microg/g (range, 1.0-14.9); and in the tumor, an average of 4.4 microg/g (range, 2.0-8.3). Brain/serum and tumor/serum ratios of 2.8 and 1.9, respectively, result from these data. The protein binding was on average 68% (range, 46-96). CONCLUSIONS: LTG is a lipophile AED with a moderate protein binding that penetrates brain tissue well and can be proven even in the tumor tissue.

Adult↗
PubMed1992

Increased inosine-5'-phosphate dehydrogenase gene expression in solid tumor tissues and tumor cell lines.

Inosine-5'-phosphate (IMP) dehydrogenase, a regulatory enzyme of guanine nucleotide biosynthesis, may play a role in cell proliferation and malignancy. To assess this role we examined IMP dehydrogenase expression in a series of human solid tumor tissues and tumor cell lines in comparison with their normal counterparts. Increased IMP dehydrogenase gene expression was observed in brain tumors relative to normal brain tissue and in sarcoma cells relative to normal fibroblasts. Similarly, in several B- and T-lymphoid leukemia cell lines, elevated levels of IMP dehydrogenase mRNA and cellular enzyme were observed in comparison with the levels in peripheral blood lymphocytes. These results are consistent with an association between increased IMP dehydrogenase expression and either enhanced cell proliferation or malignant transformation.

Animals↗
PubMed2004

[From cytogenetics to cytogenomics of adipose tissue tumors: 2. Malignant adipose tissue tumors].

Malignant adipose tissue tumors, also called liposarcomas, are the most common sarcoma of adult life. They may be hard to distinguish from benign adipose tissue tumors as well as from other types of sarcomas. Well-differentiated liposarcomas and myxoid liposarcomas are the two histological subtypes that have been best characterized at the genetic level. The defining genetic features of well-differentiated liposarcoma cells are supernumerary circular ("ring") and giant linear rod chromosomes. These rings and giant chromosomes contain amplification of the 12q14-15 region, including the MDM2 gene, associated with coamplification of various other chromosomal regions. In addition, they most often lack alpha-satellite centromeric sequences. The detection of MDM2 amplification is a valuable tool for the differential diagnosis between well-differentiated liposarcomas and lipomas. Dedifferentiated liposarcomas usually present with patterns of MDM2 amplification similar to those observed in well-differentiated liposarcomas. In addition, recent CGH-array studies suggest that co-amplification of MDM2 with the 6q23-25 region might be a specific feature. Myxoid and round-cell liposarcomas are characterized by a translocation t(12;16)(q13;p11) that fuses the DDIT3 and FUS genes. A rare variant translocation t(12;22) that fuses DDIT3 with EWS has also been described. The genetics of pleomorphic liposarcoma is still obscure. Pleomorphic liposarcomas show complex karyotypes with many numerical and structural chromosomal aberrations. To date, no specific molecular abnormality has been identified.

Chromosomes, Human, Pair 12↗
PubMed2005

Expression of albumin, IGF-1, IGFBP-3 in tumor tissues and adjacent non-tumor tissues of hepatocellular carcinoma patients with cirrhosis.

AIM: To explore the expression of albumin (ALB), insulin-like growth factor (IGF)-1, and insulin-like growth factor binding protein (IGFBP)-3 in tumor tissues and adjacent non-tumor tissues of hepatocellular carcinoma (HCC) patients with cirrhosis. METHODS: Twenty-four HCC patients with cirrhosis who underwent hepatectomy were studied. ALB mRNA, IGF-1 mRNA, and IGFBP-3 mRNA in liver tissues (including tumor tissues and adjacent non-tumor tissues) were detected by reverse transcriptase-polymerase chain reaction (RT-PCR). Liver Ki67 immunohistochemistry staining was studied. At the same time, 12 patients with cholelithiasis or liver angioma who underwent operation were segregated as normal control. RESULTS: In HCC patients with cirrhosis, hepatic ALB mRNA, IGF-1 mRNA, and IGFBP-3 mRNA of tumor tissues or adjacent non-tumor tissues were lower than the normal liver tissues, while in tumor tissues, hepatic ALB mRNA and IGFBP-3 mRNA were lower, hepatic IGF-1 mRNA was higher than in adjacent non-tumor tissues. Liver Ki67 labeling index (Ki67 LI) in tumor tissues or adjacent non-tumor tissues were higher than that in the normal liver tissues, while in tumor tissues it was higher than that in adjacent non-tumor tissues. CONCLUSION: Imbalance of IGF-1 and IGFBP-3 may play a role in hepatocarcinogenesis and tumor development of liver cirrhosis patients.

Albumins↗
PubMed2003

Analysis of CUL-5 expression in breast epithelial cells, breast cancer cell lines, normal tissues and tumor tissues.

BACKGROUND: The chromosomal location of CUL-5 (11q 22-23) is associated with LOH in breast cancer, suggesting that CUL-5 may be a tumor suppressor. The purpose of this research was to determine if there is differential expression of CUL-5 in breast epithelial cells versus breast cancer cell lines, and normal human tissues versus human tumors. The expression of CUL-5 in breast epithelial cells (HMEC, MCF-10A), and breast cancer cells (MCF-7, MDA-MB-231) was examined using RT-PCR, Northern blot analysis, and Western blot analysis. The expression of mRNA for other CUL family members (CUL-1, -2, -3, -4A, and -4B) in these cells was evaluated by RT-PCR. A normal human tissue expression array and a cancer profiling array were used to examine CUL-5 expression in normal human tissues and matched normal tissues versus tumor tissues, respectively. RESULTS: CUL-5 is expressed at the mRNA and protein levels by breast epithelial cells (HMEC, MCF-10A) and breast cancer cells (MCF-7, MDA-MB-231). These cells also express mRNA for other CUL family members. The normal human tissue expression array revealed that CUL-5 is widely expressed. The cancer profiling array revealed that 82% (41/50) of the breast cancers demonstrated a decrease in CUL-5 expression versus the matched normal tissue. For the 50 cases of matched breast tissue there was a statistically significant approximately 2.2 fold decreased expression of CUL-5 in tumor tissue versus normal tissue (P < 0.0001). CONCLUSIONS: The data demonstrate no apparent decrease in CUL-5 expression in the breast cancer cell lines (MCF-7, MDA-MB-231) versus the breast epithelial cells (HMEC, MCF-10A). The decrease in CUL-5 expression in breast tumor tissue versus matched normal tissue supports the hypothesis that decreased expression of CUL-5 may play a role in breast tumorigenesis.

Breast↗
PubMed1981

Retention of tumor markers in F1 progeny plants from in vitro induced octopine and nopaline tumor tissues.

Tumorous tobacco shoots have been derived from callus tissues produced by Agrobacterium tumefaciens--induced transformation of tobacco protoplasts and by fusion of normal protoplasts with those from crown gall tumors. The continued presence of T-DNA sequences in shoots is directly demonstrated by Southern blotting and is also revealed by the presence of the tumor markers octopine and nopaline. When grafted onto normal tobacco plants, both octopine- and nopaline-type shoots (including those from somatic hybrids) produced flowers and set seed. Germination of these seeds gave F1 progeny that showed retention of morphological markers of their parental shoots, and one seedling retained the ability to synthesize nopaline. The data demonstrate that T-DNA markers can be retained during meiosis and are expressed in F1 plants.

Arginine↗
PubMed1991

[Lymphocytic subsets of tumor tissue, non tumorous kidney, and the peripheral blood in primary renal cell carcinoma].

Lymphocyte subsets were examined in renal cell carcinoma (TILs), adjacent non-tumor renal tissue and peripheral blood (PBLs) by flow cytometry and histochemistry in eighteen patients with renal cell carcinoma. CD5-positive cells were predominant in the TILs in 14 patients. In the renal cell carcinoma tissue, CD8-positive cells were predominant over CD4-positive cells, resulting in a less than unity ratio of CD4/CF8-positive cells. The lymphocyte number was significantly in adjacent normal renal tissue than in renal cell carcinoma. However, lymphocyte subsets ratios were not significantly different between these two tissues. PBLs showed the same proportions (CD4/CD8 mean 1.9 +/- 0.8) as the previously published healthy controlled data. The proportions of CD8-positive cells were significantly increased (p less than 0.05) and those of CD4-positive cells were also significantly decreased (p less than 0.01) in the TILs. The infiltrating pattern of TILs in 17 patients was divided histochemically into cluster (N = 7), single (N = 4), and mixed types (N = 6). The cluster and mixed types were significantly more common in grade 1 tumors and the single type was more common in the grade 2 tumors (p less than 0.05). The pT3 tumors showed the single type of TIL infiltration pattern, but showed no significant difference. In the cluster pattern of TILs, CD8-positive cells were surrounded by CD4-positive cells. Non-tumorous kidneys showed no infiltration of lymphocytes, except in 2 patients of pyelonephritis. These results suggest that cytotoxic T-cells stained as CD8 play an immunoreactive role against renal cell carcinoma.

CD4-CD8 Ratio↗
PubMed1998

Interstitial fluid pressure, fraction of necrotic tumor tissue, and tumor cell density in human melanoma xenografts.

Interstitial fluid pressure (IFP) has been shown to differ substantially between individual tumors, but the tumor properties governing the intertumor heterogeneity in IFP have not been identified conclusively. The purpose of the work reported here was to investigate whether the fraction of necrotic tissue and the density of tumor cells are major determinants of the intertumor heterogeneity in IFP. The study was based on the hypothesis that the resistance against fluid flow in the tumor interstitium is influenced significantly by these parameters. Xenografted tumors of four human melanoma lines (A-07, D-12, R-18, U-25) were included in the study. Tumors showing large variation in necrotic fraction but similar cell densities (D-12, U-25) were used to study the influence of necrosis on IFP, whereas tumors showing no or insignificant necrosis but large variation in cell density (A-07, R-18) were used to search for correlations between IFP and cell density. IFP was recorded using the wick-in-needle technique. Necrotic fraction and cell density were measured by stereological analysis of histological sections using an image processing system. Significant correlations between IFP and necrotic fraction were not found, implying that the IFP of tumors is not influenced significantly by the development of necrosis. The R-18 tumors, which had a high cell density, showed a significantly higher IFP than the A-07 tumors, which had a low cell density. Significant correlations between IFP and cell density were not found when individual tumors of the same line were considered. These two observations suggest that the IFP of tumors depends on the cell density, but the cell density is probably not a major determinant of the IFP.

Animals↗
PubMed1977

[Study of distribution of 169Yb, 69Ga and 111In in tumor tissues by macroautoradiography; comparison between viable and necrotic tumor tissues].

The localization of 169Yb, 67Ga and 111In in tumor tissues was determined macroautoradiographically. 169Yb-citrate and 111In-citrate were injected intravenously to the rats subcutaneously transplanted Yoshida sarcoma and were injected intraperitoneally to the mice subcutaneously transplanted Ehrlich tumor. These animals were sacrificed 3, 24 and 48 hours after injection. These tumor tissues were frozen in n-hexane (-70 degrees C) cooled with dry ice-acetone. After this, these frozen tumor tissues were cut into serial thin sections (10 micron) in the cryostat (-20 degrees C). One of the slice of these sections was then placed on X-ray film and this film was developed after exposure of several days. On the other hand, next slice of these sections were then stained using the hematoxylin and eosin. From the observations of these autoradiogram and H-E stained slice, the following results were obtained. Concentration of 169Yb, 67Ga and 111In was predominant in viable tumor tissue rather than in necrotic tumor tissue, regardless of time after the administration. 67Ga and 111In were distributed uniformly in viable tumor tissue, but deposition of 169Yb was observed more avidly in viabl tumor tissue neighboring to necrotic tumor.

Animals↗
PubMed1987

Analysis of false multiple primary cancers: Hiroshima Tumor Tissue Registry's experience. Hiroshima Tumor Tissue Registry, Acting Committee.

During the period 1978-84 a total of 34,422 cases with malignant tumors were accessed by the Hiroshima Tumor Tissue Registry. Of these, 3,136 (9.1%) were classified as having multiple primary cancers (MPC). A detailed review was conducted on 1,148 cases selected from the latter group, and 330 (29%) were found to have been falsely registered as having MPC. "False" MPC cases were classified into six major categories according to the type of error: Category I--invasions or metastases occurring at the same or adjacent site within three months of the primary tumor, misclassified as separate primaries; Category II--invasions or metastases occurring at the same or adjacent site more than three months of the primary tumor, misclassified as separate primaries; Category III--metastases to distant sites, misclassified as separate primaries; Category IV--tumors lacking a clear description of location, resulting in registrations as "false" MPC; Category V--tumors with revisions or corrections in their pathological diagnoses resulting in false MPC; Category VI--tumors with errors in coding and other operational procedures resulting in false MPC. The cases in Categories I, II and III together comprised 52% of all false MPC cases (18%, 23% and 11%, respectively). In many of these cases, it was difficult to reject the possibility of one tumor being a metastasis of the other. This suggests that specific criteria may help reduce the number of false MPC cases of these types. Cases in Categories IV, V and VI represented 24%, 14% and 9%, respectively, of all false MPC cases. Errors encountered in these cases may be prevented by the concentrated efforts of clinicians and hospital pathologists as well as by an improvement in the operation of the registry.

Diagnostic Errors↗
PubMed1999

Stress protein/peptide complexes derived from autologous tumor tissue as tumor vaccines.

Vaccination of inbred mice with tumor-derived stress proteins hsp70, hsp90, and gp96/grp94 elicits a protective immunity to the tumor from which the vaccine was purified. There is now comprehensive experimental evidence that the antigenicity of tumor-derived hsp70, hsp90, and gp96 preparations results from diverse arrays of endogenous peptide antigens complexed with these stress proteins. Vaccination with tumor-derived stress protein/peptide complexes leads to their uptake and processing by professional antigen-presenting cells and to presentation of associated tumor peptide antigens to cytotoxic T cells. This induces a tumor-specific cytotoxic T cell response. The attractiveness of the concept of using tumor-derived stress proteins as vaccines is derived from two observations: (i) tumor stress protein vaccines mirror the individual antigenicity of a tumor, which results from random mutations due to genetic instability; and (ii) stress proteins represent powerful adjuvants for the peptide antigens complexed to them.

Animals↗