SEARCH · PubMed Health

Results for “Metastatic patterns”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 883 records · Page 49Linked to original sources

PubMedDate not supplied

Patterns of pancreatic metastasis from lung cancer.

BACKGROUND: Metastatic involvement of the pancrease is not an uncommon autopsy finding, however, pancreatic metastasis is an infrequent clinical condition and the pattern of the metastases have not been studied. We conducted a retrospective study in order to evaluate the pattern of the metastasis from lung cancer. PATIENTS: From 1976 to 1997, 26 patients with pancreatic metastasis were identified by searching the medical records of 850 patients with lung cancer. RESULTS: The usual pattern of pancreatic metastasis involved a solitary nodule in 19 patients (73.1%); multiple nodules in 3(11.5%), and diffuse swelling in 4(15.4%). Nineteen(73.1%) and 18(69.2%) of 26 patients had liver and adrenal gland metastases, respectively. CONCLUSIONS: Pancreatic metastasis represents a common site of extrathoracic spread of disease for the small number of patients with advanced lung cancer, especially in small cell lung cancer. The usual pattern of the metastasis is a solitary nodule. In order to diagnose exactly, abdominal CT scan would be helpful in such metastasis.

Adult↗

PubMed1988

Gastric carcinoma metastatic to the breast diagnosed by mucosubstance histochemistry and electron microscopy.

Bilateral breast tumors with a histologically scirrhous pattern were conclusively diagnosed as gastric carcinoma metastatic to the breast using mucosubstance histochemistry and electron microscopy. The majority of the carcinoma cells gave histochemically positive reactions for galactose oxidase-Schiff, stable class III con A, and high-iron diamine-alcian blue (HID-AB). Also electron microscopically, numerous HID-positive mucus droplets (sulfomucin) were seen in the carcinoma cells. These findings invalidated the possibility that the carcinomas were primary breast cancer. The practical applications of distinctive patterns of mucus secretion are discussed.

Adenocarcinoma, Scirrhous↗

PubMed1996

The lectin-binding sites for peanut agglutinin in invasive breast ductal carcinomas and their role as a prognostic factor.

The present study was designed to analyze the expression of lectin-binding sites for peanut agglutinin (PNA) in paraffin sections of primary invasive ductal carcinoma not otherwise specified and to consider PNA lectin histochemistry as a further aid in the prognostic evaluation of breast cancer. The expression of lectin-binding sites was studied using the avidin-biotin complex/ immunoperoxidase technique, and analyzed in relation to the different clinical, pathological, and biological parameters of the primary disease, i.e. the presence or absence of nodal metastases, pre- or post-menopausal age, size of the tumor, mitotic activity index, morphometric prognostic index, DNA content, S-phase fraction, and steroid receptor status. The results show significant differences in PNA binding patterns among malignant epithelial breast cells. There was no expression of PNA-binding sites in 14 out of 157 tumors, while 64 showed mostly apical (membrane) staining and 124 non-apical (membrane and/or cytoplasmic) staining. Apical staining was mostly observed in patients without lymph node metastasis, with positive steroid receptor status, and those who were postmenopausal diagnosis; non-apical staining was mostly observed in lymph-node-positive premenopausal patients negative for steroid receptors and with aneuploid tumor cells. Our results indicate that, in malignant breast cells, there is an alteration of cell-surface glycoconjugates, shown by heterogeneity within a histopathologically defined group, which is related to different properties of tumor cells. The apical PNA binding pattern indicates a better differentiation of tumor cells while non-apical PNA binding suggests a higher metastatic potential. Specific PNA lectin binding patterns should be considered as a further reliable prognostic factor in breast cancer.

Breast Neoplasms↗

PubMed1986

Non-glial specificities of immunocytochemistry for the glial fibrillary acidic protein (GFAP). Triple expression of GFAP, vimentin and cytokeratins in papillary meningioma and metastasizing renal carcinoma.

In an extensive immunocytochemistry study for glial fibrillary acidic protein (GFAP) of human neuropathological biopsy or autopsy tissue specimens examined for diagnostic or research purposes, rare non-glial specificities of the GFAP immunostain were observed: Schwann cells of some small nerves in salivary gland, renal capsule, and in epidural fat adjacent to a metastatic carcinoma, Schwann and satellite cells in a spinal ganglion invaded by tumor, chondrocytes of epiglottic cartilage, few cells of a malignant pleomorphic adenoma of salivary gland, most cells of a recurrent papillary meningioma with areas similar to the hemangiopericytic variant, and many cells of a renal carcinoma metastatic to brain; the primary renal tumor had been operated 4 years earlier and focally contained some GFAP-positive cells. To ascertain the specificity of such unexpected immunoreactivities for GFAP and to exclude possible crossreactivities with other intermediate filament (IF) proteins, a panel of different antibodies was used for immunocytochemistry with the peroxidase-antiperoxidase (polyclonal antisera) or labeled biotin-avidin (monoclonal antibodies) techniques: two monoclonal and four polyclonal anti-GFAP, three monoclonal and one polyclonal anti-cytokeratins (CK), and two monoclonal anti-vimentin (VIM) antibodies. Triple expression of GFAP, VIM and CK was found in the papillary meningioma (in patterns suggesting frequent co-localization), in the metastatic carcinoma (in patterns suggesting little co-localization), and in the pleomorphic adenoma (only few GFAP-positive cells). Co-expression of GFAP and VIM was seen in epiglottic chondrocytes and reactive astroglia; another metastatic carcinoma was labeled only for CKs. In the light of previous reports on non-glial specificities of the GFAP immunostain, and of the consistency of our immunostaining results obtained by all monospecific anti-GFAP antibodies as well as the lack of immunocytochemically evident crossreactivity with other IF proteins, authentic GFAP production by some rare non-glial tissues and tumors is suggested.

Aged↗

PubMedDate not supplied

Hepatocellular carcinoma versus carcinoma metastatic to the liver. Value of stains for carcinoembryonic antigen and naphthylamidase in fine needle aspiration biopsy material.

Staining for amino acid naphthylamidase and carcinoembryonic antigen (CEA) was examined as an ancillary technique to improve the accuracy of differentiating hepatocellular carcinoma from metastatic carcinoma to the liver in fine needle aspiration (FNA) biopsy specimens. Twenty-four cases of FNA specimens from the liver, in which air-dried smears and/or cell blocks were available, were examined. Naphthylamidase-positive bile canalicular structures were present in 2 cases of hepatocellular carcinoma and absent in 8 cases of metastatic carcinoma studied. Ninety percent of the hepatocellular carcinomas were immunoreactive with the antibody to CEA, showing a predominantly bile canalicular pattern. Ninety percent of the cases of metastatic carcinoma were positive with the antibody to CEA, showing a diffuse cytoplasmic pattern. These findings indicate that both staining techniques may be useful in differentiating hepatocellular carcinoma from metastatic carcinoma. Since the naphthylamidase stain requires air-dried smears, which may not be available, whereas immunocytochemistry can be done on fixed material, the latter technique is more practical.

Adenocarcinoma↗

PubMed2006

OCT4 is superior to CD30 in the diagnosis of metastatic embryonal carcinomas after chemotherapy.

Correctly diagnosing a metastatic germ cell tumor after chemotherapy may be challenging because of the diverse morphological manifestations of postchemotherapy tumors. Both OCT4 and CD30 are sensitive markers for the identification of primary embryonal carcinomas; however, loss of expression of CD30 (65%) has been reported in metastatic embryonal carcinomas after chemotherapy. The present study was conducted to evaluate the expression patterns of OCT4 and CD30 in postchemotherapy metastatic embryonal carcinomas and to compare their utility as diagnostic tools. Twenty-five cases of metastatic embryonal carcinoma after chemotherapy were immunohistochemically analyzed for CD30, OCT4, and cytokeratin AE1/AE3 expression. The staining intensities and the percentages of positively staining tumor cells were recorded. Nineteen (76%) of 25 cases revealed diffuse, moderate to strong nuclear OCT4 staining in postchemotherapy embryonal carcinomas. Among these 19 OCT4-positive cases, 8 also revealed diffuse and moderate to strong membranous CD30 staining. Seven of these OCT4-positive cases retained focal and weak CD30 expression. The remaining 4 OCT4-positive cases demonstrated a complete loss of CD30 expression. The 19 OCT4-positive cases showed a positive but variable cytokeratin AE1/AE3 expression pattern. Six (24%) of 25 cases were negative for both CD30 and OCT4 but demonstrated diffuse and strong cytokeratin AE1/AE3 staining. OCT4 is a useful diagnostic marker to identify metastatic embryonal carcinomas after chemotherapy, with a better sensitivity than CD30.

Adult↗

PubMed1983

Nonrandom distribution of metastases in neuroblastic tumors.

Metastatic behavior of neuroblastic tumors was analyzed to determine whether the secondary distribution of tumor was random, or whether the pattern of metastases was predictable and related to tumor type. The authors reviewed the 64 patients subjected to complete autopsy who had metastases from a neuroblastoma, retinoblastoma, medulloblastoma, or pinealoblastoma. The organ and tissue distribution of metastases was recorded in relation to location of primary tumor, type of therapy, survival, and presence of central nervous system metastases. Data were analyzed using chi-square contingency tables, correlation coefficients, and cluster analysis. The results indicate that: (1) the development of central nervous system metastases from neuroblastoma correlates with the pattern of extracentral nervous system metastases; (2) the pattern of tumor metastases is altered by chemotherapy and/or radiation; and (3) regardless of the site of origin, neuroblastic tumors behave in a uniform manner with a nonrandom metastatic distribution in particular tissues within the central nervous system. Cluster analysis demonstrated patterns of neuroblastoma tumor metastases which were consistent with both Hutchison and Pepper syndromes. The findings suggest that a random distribution, as might be secondary to blood flow, does not account for metastatic patterns, but rather that there are preferential patterns of growth, possibly reflecting trophic tendencies in neoplasms.

Adolescent↗

PubMed1999

Vascular channel formation by human melanoma cells in vivo and in vitro: vasculogenic mimicry.

Tissue sections from aggressive human intraocular (uveal) and metastatic cutaneous melanomas generally lack evidence of significant necrosis and contain patterned networks of interconnected loops of extracellular matrix. The matrix that forms these loops or networks may be solid or hollow. Red blood cells have been detected within the hollow channel components of this patterned matrix histologically, and these vascular channel networks have been detected in human tumors angiographically. Endothelial cells were not identified within these matrix-embedded channels by light microscopy, by transmission electron microscopy, or by using an immunohistochemical panel of endothelial cell markers (Factor VIII-related antigen, Ulex, CD31, CD34, and KDR[Flk-1]). Highly invasive primary and metastatic human melanoma cells formed patterned solid and hollow matrix channels (seen in tissue sections of aggressive primary and metastatic human melanomas) in three-dimensional cultures containing Matrigel or dilute Type I collagen, without endothelial cells or fibroblasts. These tumor cell-generated patterned channels conducted dye, highlighting looping patterns visualized angiographically in human tumors. Neither normal melanocytes nor poorly invasive melanoma cells generated these patterned channels in vitro under identical culture conditions, even after the addition of conditioned medium from metastatic pattern-forming melanoma cells, soluble growth factors, or regimes of hypoxia. Highly invasive and metastatic human melanoma cells, but not poorly invasive melanoma cells, contracted and remodeled floating hydrated gels, providing a biomechanical explanation for the generation of microvessels in vitro. cDNA microarray analysis of highly invasive versus poorly invasive melanoma tumor cells confirmed a genetic reversion to a pluripotent embryonic-like genotype in the highly aggressive melanoma cells. These observations strongly suggest that aggressive melanoma cells may generate vascular channels that facilitate tumor perfusion independent of tumor angiogenesis.

Biomarkers, Tumor↗

PubMed1992

The use of molecular genetic markers to demonstrate the effect of organ environment on clonal dominance in a human renal-cell carcinoma grown in nude mice.

Transduction of the SN12C human renal-cell carcinoma line with the neoR gene produces a genetically "tagged" cell population within which individual clones can be identified if they dominate the tumor during its growth in vivo. We used this technique to determine whether the clones that dominate the primary local tumor and its metastases are the same or different when the tumor is growing in different organ sites in nude mice. The results show that clonal dominance is influenced by the organ environment in which the primary tumor grows, i.e., distinct clones dominated in the kidney, colon and subcutaneous sites. In addition, tumors grown in the orthotopic site (kidney) were all populated by the same dominant clones, and each distant visceral metastasis retained the same clonality. SN12C neoR-cells grown in an epithelial, ectopic site (colon) produced tumors with uniquely different dominant clones, and their visceral metastases retained the dominant pattern expressed by the parent tumor from which they were derived. In contrast, SN12C tumors growing subcutaneously showed a random pattern of clonal dominance in both their primary and metastatic sites. Parallel cytogenetic analyses could not demonstrate these patterns. We conclude that the organ environment significantly influences clonal dominance of human renal carcinoma and that tumor injection into orthotopic sites may produce a more reproducible selection of dominant clones.

Animals↗

PubMed1989

[Blood coagulation and metastasis].

To elucidate the correlation of platelet aggregating activity of tumor cells and their metastatic potentials, we established a highly and a low metastatic clone with a different platelet aggregating activity from murine fibrosarcoma (Meth A). The parental Meth A cell and its low metastatic clone (ML-01) showed a typical platelet aggregation pattern with a certain lag time, while a highly metastatic clone (MH-02) showed a biphasic aggregation with no lag time in which the first reversible aggregation was caused by ADP released from MH-02, since it was eliminated by apyrase treatment. The highly metastatic potential, however, was not solely due to the platelet aggregating activity because the administration of PGI2-analogue TEI-8153A did not completely inhibit their pulmonary metastasis. In fact, MH-02 attached more preferentially to type IV collagen or endothelial cell than ML-01 in vitro. These results suggest that MH-02 exerts its high metastatic property through the mechanisms involving multiple factors such as the increased platelet aggregating potential or enhanced adhesiveness.

Animals↗

PubMed1998

High homogeneity of MAGE, BAGE, GAGE, tyrosinase and Melan-A/MART-1 gene expression in clusters of multiple simultaneous metastases of human melanoma: implications for protocol design of therapeutic antigen-specific vaccination strategies.

Human melanoma cells express several antigens which are recognized by autologous and specific CTL clones in association with HLA-class-I molecules. Many of these antigens represent suitable targets for tumor immunotherapy, since their expression in human melanoma cells is common and highly specific. In order to achieve real clinical success with therapeutic vaccination strategies, one important requirement is the expression of the target antigen by all the tumor lesions of a patient. We have studied this issue by assessing, through an RT-PCR approach, the expression of MAGE-1, MAGE-2, MAGE-3, BAGE, GAGE-1/2, Tyrosinase and Melan-A/MART-1 genes in 17 clusters of simultaneous in-transit or regional lymph-node metastases collected from 15 stage-III and 1 stage-IV (AJCC/UICC pTNM system) melanoma patients. In 14 out of 17 clusters of simultaneous metastatic lesions (82%), the homogeneity in the pattern of gene expression within the cluster was complete. Heterogeneity within the same cluster was observed in only 3 out of 17 clusters (18%) and represented only minor features. Our data reveal that, in AJCC-stage-III melanoma patients, different but simultaneous metastatic lesions express the same pattern of antigen-coding genes. These observations have 2 main clinical implications: (i) the antigenic characterization of one single and easily accessible lesion allows identification of optimal targets for an active antigen-specific immunotherapy treatment; (ii) almost all the metastatic lesions are expected to be hit by the immune response eventually induced against the tumor antigen. Moreover, these data suggest that active specific immunotherapy directed against MAGE-1, MAGE-3, BAGE, GAGE-1/2, Melan-A/MART-1 and Tyrosinase antigens could be exploited as an adjuvant treatment to surgery in high-risk AJCC-stage-III-melanoma patients.

Antigens, Neoplasm↗

PubMed2004

Hypermethylation of CpG islands in primary and metastatic human prostate cancer.

Aberrant DNA methylation patterns may be the earliest somatic genome changes in prostate cancer. Using real-time methylation-specific PCR, we assessed the extent of hypermethylation at 16 CpG islands in DNA from seven prostate cancer cell lines (LNCaP, PC-3, DU-145, LAPC-4, CWR22Rv1, VCaP, and C42B), normal prostate epithelial cells, normal prostate stromal cells, 73 primary prostate cancers, 91 metastatic prostate cancers, and 25 noncancerous prostate tissues. We found that CpG islands at GSTP1, APC, RASSF1a, PTGS2, and MDR1 were hypermethylated in >85% of prostate cancers and cancer cell lines but not in normal prostate cells and tissues; CpG islands at EDNRB, ESR1, CDKN2a, and hMLH1 exhibited low to moderate rates of hypermethylation in prostate cancer tissues and cancer cell lines but were entirely unmethylated in normal tissues; and CpG islands at DAPK1, TIMP3, MGMT, CDKN2b, p14/ARF, and CDH1 were not abnormally hypermethylated in prostate cancers. Receiver operator characteristic curve analyses suggested that CpG island hypermethylation changes at GSTP1, APC, RASSF1a, PTGS2, and MDR1 in various combinations can distinguish primary prostate cancer from benign prostate tissues with sensitivities of 97.3-100% and specificities of 92-100%. Hypermethylation of the CpG island at EDNRB was correlated with the grade and stage of the primary prostate cancers. PTGS2 CpG island hypermethylation portended an increased risk of recurrence. Furthermore, CpG island hypermethylation patterns in prostate cancer metastases were very similar to the primary prostate cancers and tended to show greater differences between cases than between anatomical sites of metastasis.

Adult↗

PubMed1992

Evaluation of metastatic human tumor burden and response to therapy in a nude mouse xenograft model using a molecular probe for repetitive human DNA sequences.

A sensitive DNA dot-blot assay for repetitive human DNA sequences was developed and applied to the quantitative determination of spontaneous metastases of a human melanoma in various tissues of nude mice. The assay was useful for defining the time course and pattern of tissue distribution of metastatic cells as well as for assessing response to therapy. The methodology is relatively simple, can be performed using nonradioactive DNA probes, and should be broadly applicable to studies of metastasis of human tumors in nude mice.

Animals↗

PubMed2005

Pictorial review: sonographic patterns of diffuse and focal fatty infiltration of the liver: differential diagnosis to metastatic liver disease.

Many important articles about fat distribution disorders within the liver have been published in the 1980s and 1990s. However, the diagnostic dilemma of distinguishing diffuse or focal fat distribution disorders especially from malignant neoplasmas persists and is still of clinical relevance. Rare and more common sonographic patterns can be subdivided according to their echogenicity, location, quantity, shape and boundaries by B-mode sonography. The knowledge of the characteristic sonographic patterns of diffuse and focal fat distribution disorders within the liver avoids in most cases costly and more invasive diagnostic procedures. Depending on clinical background in individual cases confirmation of diagnosis of focal fatty liver disease is necessary.

Diagnosis, Differential↗

PubMed1995

Modulation of heparan-sulphate/chondroitin-sulphate ratio by glycosaminoglycan biosynthesis inhibitors affects liver metastatic potential of tumor cells.

Previous data have indicated that the proteoglycan (PG) pattern is different on tumor cells with different liver metastatic potential. We selected "conventional" glycosaminoglycan (GAG) biosynthesis inhibitors, beta-D-xyloside (BX), 2-deoxy-D-glucose (2-DG), ethane-l-hydroxy-l,l-diphosphonate (ETDP) and the newly discovered 5-hexyl-2-deoxyuridine (HUdR), to modulate PGs on highly metastatic/liver-specific 3LL-HH murine carcinoma and HT168 human melanoma cells and to influence their liver colonization potential. These compounds all induced remarkable changes in GAG biosynthesis, but to varying degrees: glucosamine labelling was affected mainly by 2-DG, and HUdR and sulphation by BX and HUdR. Furthermore, the ratio of heparan sulphate/chondroitin sulphate (HS/CS) of PGs was increased by ETDP and decreased after treatment by HUdR. In addition to changes in PG metabolism, tumor-cell proliferation and adhesion to fibronectin were affected; BX and 2-DG stimulated cell proliferation and adhesion, while HUdR inhibited both proliferation and adhesion. Most interestingly, HUdR, the most effective inhibitor of HS/HSPG, depressed the formation of liver colonies, while ETDP, the most effective inhibitor of CS/CSPG, stimulated the appearance of liver colonies. These observations indicated that, at least in these experimental systems, tumor cells with a high HS/CS ratio are more likely to form liver metastases; consequently, anti-HS agents could also be anti-metastatic.

Animals↗

PubMed2004

Two-color immunostaining of liver fine needle aspiration biopsies with CD34 and carcinoembryonic antigen. Potential utilization in the diagnosis of primary hepatocellular carcinoma vs. metastatic tumor.

OBJECTIVE: To examine immunohistochemical staining of cell block material with antibodies against vascular marker CD34 and polyclonal carcinoembryonic antigen (pCEA) for their clinical utility as part of a 2-color staining protocol in fine needle aspiration (FNA) biopsy of liver masses to distinguish metastases from primary hepatocellular carcinoma (HCC). STUDY DESIGN: The authors obtained cell block material from 96 liver FNAs and performed simultaneous (i.e., "dual-color") immunohistochemical staining utilizing antibodies against vascular marker CD34 and pCEA. Cases were blinded and evaluated by the authors for staining pattern and intensity. A consensus was obtained, the results were unblinded, and the diagnoses were correlated. RESULTS: After staining, 89 cases had sufficient tissue for evaluation. Of the 19 HCC cases, 16 (84%) showed peripheral staining with CD34, and 13 (68%) showed a canalicular or mixed canalicular-cytoplasmic staining pattern for pCEA. Thirteen cases (68%) showed staining for both antigens. All HCC exhibited immunostaining for at least 1 antibody in an appropriate staining pattern. Of the 67 cases of metastatic malignancy, 5 (7%) showed a predominantly transgressing pattern of CD34 staining, 43 (64%) showed a predominantly cytoplasmic or mixed cytoplasmic-canalicular pattern of pCEA staining, and 2 cases (3%) showed staining for both antigens in a transgressing CD34 pattern and cytoplasmic pCEA pattern. None of the 3 normal liver tissue blocks showed staining with either antigen. CONCLUSION: Two-color immunohistochemical staining of liver cell block material obtained by FNA with antibodies to CD34 and pCEA can be helpful in differentiating metastatic tumors vs. primary HCC.

Antigens, CD34↗

PubMed2004

Association of E-cadherin and beta-catenin with metastasis in nasopharyngeal carcinoma.

BACKGROUND: This study was designed to detect methylation of E-cadherin gene promoter and gene mutation of beta-catenin in exon 3 and their expression of protein and mRNA in primary tumor and lymph node metastatic tumor of nasopharyngeal carcinoma (NPC), and investigate the mechanism of invasion and metastasis of neoplastic cells in NPC. METHODS: Fourty-two fresh biopsy samples were taken from untreated NPC patients at the Affiliated Hospital of Sun Yat-sen Medical College, Sun Yat-sen University, Guangzhou, China during the period of 1999-2002. Among them 21 were taken from primary tumors and the other 21 from lymph node metastatic tumors. The gene promoter methylation of E-cadherin was detected by methylation-specific PCR (MSP). The mutation in exon 3 of beta-catenin was detected by direct sequencing analysis. RT-PCR, Western blot and immunohistochemical staining were used to detect the mRNA and protein expression patterns in both primary and metastatic tumors of NPC. RESULTS: Down-regulated expression of E-cadherin in metastatic tumor was compared with that in primary tumor. Reduced expression of E-cadherin was found to be correlated with lymph node metastatic tumor of NPC (P = 0.004); but there was no obvious correlation between primary and metastatic tumors in the expression of beta-catenin (P = 0.698). The mRNA expression level of E-cadherin in metastatic tumors decreased significantly compared with that in primary tumors. However, little change was observed in the mRNA level of beta-catenin in different tumor tissues. Only 4 samples (19.1%) displayed gene promoter methylation of E-cadherin in primary tumor and 10 samples (47.6%) showed methylated form of E-cadherin. The gene promoter methylation of E-cadherin was more common in metastatic tumor than in primary tumor of NPC (P = 0.024). Only 2 (4.76%) of the 42 samples showed mutations in exon 3 of beta-catenin at 41 (T41A, ACC-->GCC) and codon 47 (S47T, AGT-->ACT). The cytoplasmic and nuclear expression of beta-catenin in tumor was not found in any samples of NPC. CONCLUSIONS: The results suggest that the downregulation of E-cadherin results from the gene promoter aberrant methylation of E-cadherin and that the methylation of E-cadherin plays an important role in invasion and metastasis of tumor cells in NPC. However, beta-catenin mutation is an infrequent event in NPC, and beta-catenin is not a critical factor influencing the invasion and metastasis of tumor cells in NPC.

Adult↗

PubMed2000

Flow cytometric analysis of primary tumors and their corresponding metastatic nodes in breast cancer.

Human breast carcinoma is biologically heterogeneous, and its clinical course may vary from one which is indolent to one which rapidly progresses. Although it is the metastasis rather than the primary tumor that ultimately overwhelms the patients, studies concerning the DNA pattern have focused on the primary tumors. This study was undertaken to identify heterogeneities between primary tumors and metastases, and to evaluate the prognostic significance of the ploidy pattern and the S-phase fraction (SPF) of metastatic nodes in axillary node positive patients. Seventy-four frozen specimens of the primary and corresponding metastatic nodes from 37 patients have been analyzed by flow cytometry and the SPF calculated. The results of ploidy pattern analysis in primaries revealed 25 diploidy (67.6%) and 12 aneuploidy (32.4%), while those in metastasis showed 17 diploidy (46.0%) and 20 aneuploidy (54.0%). The aneuploidy group in metastatic nodes had the poorer histological grade (85.0% vs. 15.0%, p = 0.02), and more mean metastatic nodes (5.75 +/- 2.10 vs. 3.05 +/- 1.56, p = 0.018), and more frequent lymphatic vessel invasion (65.0% vs. 11.8%, p = 0.031) than its counterpart. Decreased expression of ER (70.6% vs. 25.0% p = 0.006) and increased expression of c-erbB2 (65.0% vs. 23.5%, p = 0.012) were observed in the aneuploidy of metastatic nodes. The group with higher SPF in metastatic nodes had more metastatic nodes (5.47 +/- 2.31 vs. 4.00 +/- 1.78, p = 0.042), and the higher incidence of lymphatic vessel invasion (57.9% vs. 22.2%, p = 0.027), and poor histological grade (71.4% vs. 37.5%, p = 0.039). In conclusion, the cell populations in metastatic nodes revealed DNA pattern which differed from that of primary tumors. The ploidy pattern and SPF in metastatic nodes might be considered as discriminate measure for risk factors in breast cancer patients with positive axillary node.

Adult↗