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 847 records · Page 47Linked to original sources

PubMed1994

Cytodiagnosis of neoplastic metastases to the liver. Immunocytochemical studies.

Differential diagnosis of neoplastic metastases to the liver encounters difficulties associated with the presence mainly of metastasized adenocarcinomas characterized by a similar cytological pattern. Determination of a metastatic site of origin only from routinely stained cytological smears is frequently impossible. Therefore it was attempted to employ immunocytochemical studies in differentiation of metastatic neoplasms using monoclonal antibodies against cytokeratin 7 and 20 and against colon specific antigen and pancreatic specific antigen. The results of the present study show that in a group of anaplastic small-cell carcinomas, squamous cell carcinomas and hepatocellular carcinomas immunocytochemistry does not add significant information on their diagnosis. In contrast, with respect to adenocarcinomas the method is fundamental in limiting the range of search for the metastatic site of origin and thus shortens the diagnostic procedure.

Adenocarcinoma↗

PubMed1993

p53 Protein expression in nevi and melanomas.

p53 Protein immunohistochemical expression is a wide-spread feature of the malignant phenotype; most melanomas are reported as p53 positive, while nevi are reported as p53 negative. We investigate a series of 75 benign nevi and 47 melanomas (40 primary and seven metastatic) to evaluate their pattern of p53 immunoreactivity with a panel of specific antibodies (PAb1801, PAb240, DO7, and CM1) in view of a possible diagnostic role of p53 immunostaining. Our results demonstrate that 15% of nevi show p53 immunoreactive nuclei (usually in less than 1% of the cells) and that 30% of melanomas show p53 immunoreactive nuclei (one case with 20% immunoreactive cells, six cases with 1% to 5% positive cells, and four cases with less than 1% positive nuclei). p53 Positivity was seen also in basal and suprabasal keratinocytes. p53 Positivity in nevi is at variance with literature data supporting that nevi are p53 negative. p53 Positivity in nevi and in epidermis may be related to mechanisms of DNA repair, apoptosis, or to a specific phase of the cell cycle. In our series, p53 expression in melanomas is not as frequent as reported in the literature. Population-based differences or differences in case selection and sample handling may account for the above discrepancies. The demonstration of p53 positivity in benign skin lesions greatly hinders the possibility of a diagnostic use of p53 immunostaining in dermatopathology.

Adolescent↗

PubMed1998

Elevated expression of caveolin is associated with prostate and breast cancer.

To identify genes associated with prostate cancer progression, we developed a strategy involving the use of differential display-PCR with a panel of genetically matched primary tumor- and metastasis-derived mouse prostate cancer cell lines. We isolated a cDNA fragment with homology to the mouse caveolin-1 gene. Northern blotting with this fragment revealed increased caveolin expression in metastasis-derived cell lines relative to primary tumor-derived cell lines. Western blotting with a polyclonal caveolin antibody confirmed increased caveolin protein in metastasis-derived mouse cell lines and expression in three of four human prostate cancer cell lines. Immunohistochemical analysis of a human prostate cancer cell line demonstrated a prominent granular pattern of caveolin accumulation. Subsequent analysis of mouse and human prostate specimens revealed minimal caveolin expression in normal epithelium with abundant staining of smooth muscle and endothelium. The frequency of caveolin-positive cells was increased in prostate cancer with markedly increased accumulation of caveolin and a granular staining pattern in lymph node metastatic deposits. In human breast cancer specimens, increased caveolin staining was detected in intraductal and infiltrating ductal carcinoma as well as nodal disease. Caveolin therefore appears to be associated with human prostate cancer progression and is also present in primary and metastatic human breast cancer.

Animals↗

PubMed2026

Tumor evolution shapes metastatic competence in colorectal cancer.

In this issue of Cancer Cell, Manca et al. investigate the genomic evolution and metastatic tropism of over 7,000 colorectal cancers. Integrating primary tumor location, genomic alterations, and clinical variables, they reveal how distinct patterns of tumor evolution shape metastatic competence and impact organ tropism, offering a framework to refine surveillance.

Humans↗

PubMed1993

Clinical manifestations of lung cancer.

The initial clinical manifestations of lung cancer are diverse and may occur with or without symptoms. Manifestations of pulmonary malignant lesions are produced by local growth or invasion, metastatic disease, or paraneoplastic processes. Patterns of local invasion such as Pancoast's syndrome or the superior vena cava syndrome are relatively uncommon but well recognized. Metastatic lung cancer can involve almost any anatomic area by hematogenous, lymphatic, or, occasionally, interalveolar dissemination. Complications related to malnutrition, infection, electrolyte disturbances, and coexisting diseases influence the initial manifestations. Although individual tumor cell types are associated with characteristic features, no constellation of findings is pathognomonic for a specific histologic variant. Because successful treatment of pulmonary carcinoma depends on early detection, awareness of the typical clinical manifestations is important.

Humans↗

PubMed1983

Complex cytokeratin polypeptide patterns observed in certain human carcinomas.

Human epithelial cells contain, intermediate-sized filaments formed by polypeptides related to epidermal alpha-keratin ("cytokeratins") which are expressed in different combinations in different epithelia. Using cytoskeletal proteins from human biopsies and autopsies we have examined, by two-dimensional gel electrophoresis and immunoblotting experiments, the cytokeratin polypeptide patterns of diverse primary and metastatic carcinomas and have compared them with those of corresponding normal epithelial tissues and cultured cells. Five groups of carcinoma cytokeratin patterns can be discriminated. (1) Cytokeratins typical of simple epithelia (polypeptides Nos. 7, 8, 18, 19) are expressed, in various combinations, by many adenocarcinomas, for example those of gastrointestinal tract. (2) Cytokeratins typical of stratified epithelia (Nos. 1, 5, 6, 10, 11, 14-17) are found, in various combinations, in squamous cell carcinomas of skin and tongue. (3) Complex patterns showing polypeptides Nos. 7, 8, 18, 19, and one basic component (No. 5 or 6) are detected in certain carcinomas of the respiratory tract and the breast. (4) Complex patterns containing cytokeratins widespread in stratified epithelia (Nos. 4-6, 14-17) as well as components Nos. 8 and 19 occur in diverse squamous cell carcinomas derived from non-cornified stratified epithelia, with or without additional small amounts of cytokeratin No. 18. (5) Patterns of unusually high complexity can be found in some rare tumors as is shown for a cloacogenic carcinoma. No significant qualitative changes of expression of cytokeratins were found when primary tumors and metastases were compared. When compared with cytokeratin patterns of normal epithelia, carcinomas of the first type usually display a high degree of relatedness to the tissue of origin. Other carcinomas do not express some of the cytokeratins present in the tissue of their origin and, vice versa, certain components which are minor or apparently absent in normal tissue are major cytokeratins in the corresponding tumor. These differences may be explained by cell type selection during carcinogenesis, but changes of expression during tumor development cannot be categorically excluded. The possibility of cell type heterogeneity within a given tumor is also discussed. Similarly complex patterns of cytokeratin polypeptides have been noted in certain cultured human carcinoma cell lines (e.g., A-431, RPMI 2650, Detroit 562, A-549) and can also be observed in cell clones. The possible value of analyses of cytokeratin patterns, by gel electrophoresis or specific monoclonal antibodies, in distinguishing different carcinomas by non-morphologic criteria is discussed.

Breast Neoplasms↗

PubMed2005

Neurological deficit from metastatic low grade liposarcoma.

Myxoid liposarcoma is a malignant soft tissue tumor with a relatively indolent natural history. It commonly occurs in the extremities with extrapulmonary metastatic potential. Round cell liposarcoma, recently, is widely agreed to be the aggressive counterpart of the myxoid liposarcoma, mostly arising in adverse, local recurrence, and metastatic lesions. Metastatic liposarcoma with pure myxoid element is unusual. The authors report an extremely rare case of a 47-year-old Thai male patient having a metastatic pure myxoid liposarcoma to the thoracic vertebrae, one year after primary tumor documented on the left thigh. Histology of the primary and metastatic sites shows only myxoid pattern. Round cell feature was not documented. To the best of the authors' knowledge, this is the second case report of metastatic myxoid liposarcoma without round cell morphology.

Humans↗

PubMed2003

Loss of heterozygosity in the MXI1 gene is a frequent occurrence in melanoma.

Melanoma development and progression is thought to be the result of a multi-step accumulation of genetic damage, with loss of heterozygosity in chromosome 9p (MTS1) frequently described. In addition, chromosome 10q allelic loss has been reported, implicating the tumor suppressor gene PTEN/MMAC1 on 10q23.3. The MXI1 gene at 10q24-25 is another candidate tumor suppressor that has only rarely been studied in melanomas, with conflicting results. We used microdissection-based genotyping to investigate 29 melanomas from 20 patients for loss of heterozygosity in intragenic and flanking microsatellite markers for this latter gene. Concurrently, the MTS1 gene was similarly studied using two flanking microsatellites. Fifty-four percent (15 of 28) of the informative cases showed loss of heterozygosity for one or both MXI1 markers, as compared with 67% (16 of 24) of the informative cases for MTS1. MXI1 allelic loss was seen more frequently in recurrent/metastatic tumors (59%), as compared with in primary (33%) lesions. Eighty percent of the primary tumors showed loss of heterozygosity for MTS1, as well as 63% of recurrent/metastatic ones. We studied more than one tumor in eight patients, with those from three patients showing discordant genetic patterns. One patient showed a metastatic tumor with allelic loss for MXI1 that was not identified in the primary melanoma or a local recurrence. The other two patients showed clonal heterogeneity in MXI1 at synchronous and metachronous metastatic foci. These findings support MXI1 as a putative tumor suppressor gene involved in conventional melanoma progression. Genetic heterogeneity seen in different metastases from the same primary suggests a nonlinear pattern of chromosomal damage, with the development of multiple clones within the primary tumor, each acquiring its own metastatic potential.

Adult↗

PubMed2006

Clonal origin of metastatic testicular teratomas.

PURPOSE: Testicular teratomas in adult patients are histologically diverse tumors that frequently coexist with other germ cell tumor (GCT) components. These mixed GCTs often metastasize to retroperitoneal lymph nodes where multiple GCT elements are frequently present in the same metastatic lesion. Neither the genetic relationships among the different components in metastatic lesions nor the relationships between primary and metastatic GCT components have been elucidated. EXPERIMENTAL DESIGN: We examined metastases from 31 patients who underwent primary retroperitoneal lymph node dissection for metastatic testicular GCT. All patients had metastatic mature teratoma with one or more other GCT components. This study included a total of 72 metastatic GCT components and 16 primary GCT components from 31 patients. Genomic DNA samples from each component were prepared from formalin-fixed, paraffin-embedded tissue sections using laser-assisted microdissection. Loss of heterozygosity (LOH) assays for seven microsatellite polymorphic markers on chromosomes 1p36 (D1S1646), 9p21 (D9S171 and IFNA), 9q21 (D9S303), 13q22-q31 (D13S317), 18q22 (D18S543), and 18q21 (D18S60) were done to assess clonality. RESULTS: Twenty-nine of 31 (94%) cases showed allelic loss in one or more components of the metastatic GCTs. Twenty-nine of 31 mature teratomas showed allelic loss in at least one of seven microsatellite polymorphic markers analyzed. The frequency of allelic loss in informative cases of metastatic mature teratoma was 27% (8 of 30) with D1S1646, 34% (10 of 29) with D9S171, 37% (10 of 27) with IFNA, 27% (8 of 30) with D9S303, 46% (13 of 28) with D13S317, 26% (7 of 27) with D18S543, and 36% (10 of 28) with D18S60. Completely concordant allelic loss patterns between the mature teratoma and all of the other metastatic GCT components were seen in 26 of 29 cases in which the mature teratoma component showed LOH. Nearly identical allelic loss patterns were seen in the three remaining cases. In six cases analyzed, LOH patterns of each metastatic component were compared with each GCT component of the primary testicular tumor. In all six cases, each primary and metastatic component showed an identical pattern of allelic loss. CONCLUSION: Our data support the common clonal origin of metastatic mature teratomas with other components of metastatic testicular GCTs and with each component of the primary tumor.

Adolescent↗

PubMed2005

Pattern of drainage in sentinel lymph nodes after intra-arterial chemotherapy for oral and oropharyngeal cancer.

PURPOSE: Prerequisite for lymphoscintigraphy-guided sentinel lymph node (SLN) biopsy in head and neck cancer patients has been a previously untreated primary tumor to avoid disturbance of the lymphatic flow. We evaluated the feasibility in a multimodality treatment approach to oral and oropharyngeal cancer comprising presurgical intra-arterial chemotherapy of the primary tumor. PATIENTS AND METHODS: In a prospective study of 35 consecutive patients with primary oral and anterior oropharyngeal cancer T1-4N0 treated with superselective intra-arterial chemotherapy with high-dose cisplatin, SLN scintigraphy was performed on the day of surgery, including gamma camera imaging before and hand-held gamma probe identification of the SLN during surgery. SLN biopsy was performed in 50 neck sides, followed by radical resection of the primary in the same session. Elective neck dissection was not carried out. The pattern of lymphatic drainage was recorded and compared with the literature on well-known patterns found in lymphographic studies and metastatic disease in neck dissection specimens of patients without presurgical treatment. RESULTS: Drainage patterns of SLN related to different primary locations mapped the mentioned comparison patterns. SLN drainage patterns gave strong evidence that there are SLN in levels 3 and 4 with direct drainage from the primary. After a median observation time of 24 months, no patients had a neck relapse. CONCLUSIONS: The results suggest that intra-arterial chemotherapy of the primary tumor does not significantly alter lymphatic drainage and that SLN biopsy following intra-arterial chemotherapy is feasible and offers valid results comparable to those obtained from patients without presurgical treatment.

Antineoplastic Agents↗

PubMed1991

Tumor cell heterogeneity and subpopulations with metastatic ability in differentiated adenocarcinoma of the lung. Histologic and cytofluorometric DNA analyses.

To investigate tumor cell heterogeneity and subpopulations with metastatic ability in differentiated adenocarcinoma of the lung, the primary and metastatic lesions in 20 cases of differentiated adenocarcinoma were examined by histologic and cytofluorometric DNA analyses. The primary tumor was divided histologically into three compartments: tumor area of type 1, papillary adenocarcinoma with thin stroma; tumor area of type 2, papillary adenocarcinoma with thickened fibrovascular stroma: tumor area of type 3; solid carcinoma with scant gland formation. The nuclear DNA content (NDC) was higher in type 2 than in type 1 tumor in terms of mean NDC and DNA histogram pattern (p less than 0.01). Metastatic tumors in distant organs often resembled the type 2 of primary tumors histologically and also in their DNA histogram patterns, and their mean NDC values were significantly correlated with each other (p less than 0.01). Metastatic tumors in regional lymph nodes had a significantly lower mean NDC than those in distant organs (p less than 0.01). These results suggest that (1) type 2 tumors originate from type 1 tumors by malignant progression and metastasize hematogenously, and (2) hematogenous metastases are composed of tumor subclones different from those of lymphatic metastases.

Adenocarcinoma↗

PubMed1992

[An autopsied case of papillary thyroid carcinoma showing DNA heterogeneity-comparison of DNA content between primary focus and metastatic focus].

A 56-year-old female case of papillary thyroid carcinoma is reported. Nuclear DNA analysis using flow cytometry and immuno-histological staining with thyroglobulin, CA19-9 and CA125 of the primary and metastatic foci from the autopsy specimens were performed. Correlation between ploidy patterns and immuno-histological staining was not found. Although two histogram patterns namely DNA diploid (DP) and aneuploid (AP) with DNA index of 1.3 were seen in primary, sternal and lung metastatic foci, only DP pattern was seen in the lymph node metastatic foci.

Antigens, Tumor-Associated, Carbohydrate↗

PubMed2001

Identification of extracapsular invasion of the metastatic lymph nodes as a useful prognostic sign in patients with resectable colorectal cancer.

PURPOSE: The present study was undertaken to evaluate whether the microscopic patterns of distribution and extracapsular invasion of cancer cells in the regional lymph nodes were linked to the survival rates for patients with advanced colorectal cancer who undergo a curative surgical resection. METHODS: Two hundred ninety-six surgically resected metastatic lymph nodes from 84 patients with node-positive colorectal cancer were microscopically examined. The distribution of cancer cells in the lymph nodes were grouped into two types: type A (> or =50 percent cancer) and type B (<50 percent cancer). The extracapsular invasion of cancer cells in the nodes were divided into three subgroups: pattern X (no evidence of cancer cell invasion into the adjacent tissue); pattern Y (less than five cancer cells were seen in the adjacent tissue); and pattern Z (more than five cancer cells invaded the adjacent tissue). The patients, based on these microscopic manifestations of metastatic patterns in the nodes, were divided into three groups: Group 1, patients with pattern X nodal metastases only; Group 2, patients with pattern Y and pattern (X + Y) nodal metastases; and Group 3, patients with pattern Z, pattern (X + Z), pattern (Y + Z), and pattern (X + Y + Z) nodal metastases. RESULTS: The survival rates and disease-free survival rates for patients with metastatic lymph nodes showing an extracapsular invasion pattern (Groups 2 and 3) were significantly worse than those for patients with metastatic nodes showing no extracapsular invasion pattern only (Group 1; P < 0.01). There was no significant difference for the above-cited survival rates among the groups classified according to the Dukes and TNM systems. CONCLUSIONS: It is the thesis of this article that the identification of extracapsular invasion of the metastatic lymph nodes can be taken as a useful prognostic sign in patients with resectable colorectal cancer.

Aged↗

PubMed2004

Molecular detection of MART-1, tyrosinase and MIA in peripheral blood, lymph nodes and metastatic sites of stage III/IV melanoma patients.

Melanoma lesions that develop in the same patient at different times or simultaneously at different locations may differ antigenically, because malignant melanoma is heterogeneous in terms of its biological, immunological and metastatic properties. The objective of this study was to characterize the molecular profiles of melanoma cells in peripheral blood, lymph nodes and metastatic tissues, employing the messenger RNA (mRNA) expression of tyrosinase, melanoma-inhibiting activity (MIA) and melanoma antigen recognized by T cells-1 (MART-1) as markers. Samples of cells propagated from metastatic sites were obtained from 17 stage III/IV melanoma patients and assayed by reverse transcriptase-polymerase chain reaction (RT-PCR), using specific primers for each marker. In eight patients, marker profiles were analysed in simultaneously obtained specimens of peripheral blood, lymph nodes and metastatic tissues originating from the same patient. Tyrosinase, MIA and MART-1 were expressed in 59%, 76% and 76% of the metastases, respectively. Simultaneously obtained specimens of peripheral blood, lymph nodes and metastatic tissues showed a high degree of homogeneity: 60%, 75% and 20% for tyrosinase, MIA and MART-1, respectively. Our findings suggest that the rather homogeneous expression pattern found in different tumour sites analysed in the same patient is of potential prognostic and therapeutic importance. Furthermore, melanoma lesions may be negative for the expression of antigens such as MART-1, and discrepancies in expression patterns between peripheral blood and metastatic tissues may occur, especially for this marker. Finally, our findings support the notion that molecular screening using an RT-PCR approach is appropriate in this kind of investigation.

Adult↗

PubMed1993

Relationships among tenascin expression, DNA ploidy patterns, and multidrug resistance gene product (P-glycoprotein) in human colon carcinoma.

Relationships among tenascin expression, DNA ploidy, and P-glycoprotein were examined in 81 primary human colon cancers and 61 metastatic lymph nodes. First, the DNA ploidy patterns of colon cancerous tissue surrounded (TN+) and not surrounded (TN-) by tenascin immunoreactivity were investigated. Then the expression of P-glycoprotein, one of two multidrug resistance gene products, was examined in TN+ and TN- colon cancer tissues by immunohistochemistry. Aneuploid DNA patterns were observed at high frequency in TN- colon cancer tissues (37/61) and metastatic lymph nodes (44/52). In contrast, diploid DNA patterns were observed predominantly in TN+ colon cancer tissues (50/56). Although P-glycoprotein expression was observed in primary TN+ and TN- colon cancer (9/81), the level of P-glycoprotein expression was not correlated with DNA aneuploidy in TN- colon cancer tissues. Overall, reduced tenascin expression was correlated well with DNA aneuploidy, but no significant correlation was found between DNA aneuploidy and P-glycoprotein appearing when cancer cells become resistant to several anti-cancer drugs. Thus, tenascin may play an important role in preventing colon cancer cells from invading surrounding tissues.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed1992

Significance of CD44 gene products for cancer diagnosis and disease evaluation.

With increasing emphasis on the early detection of cancer, the search is on for reliable markers that will be clinically helpful in the diagnosis of small tumours and in the assessment of their metastatic potential. This report presents evidence that an abnormal pattern of activity of the CD44 gene is a promising candidate for both of these purposes in various types of malignancy. By a mechanism known as alternative splicing this gene can produce different messenger RNA molecules (transcripts) which are detectable, after amplification, as separate bands in electrophoretic gels. In neoplasia many abnormal variant transcripts are produced. A previous finding in animal experiments, that one such variant might be important in metastasis, prompted our study of human tumour tissue, benign and malignant, and of corresponding normal tissues. We studied tumour tissue from 34 patients with neoplastic disease (mostly breast or colon cancer) and normal or non-malignant diseased breast or colonic tissue from 11 patients and peripheral blood leucocytes from 4 healthy volunteers. CD44 gene activity was studied by amplifying messenger RNA with the polymerase chain reaction (PCR) followed by electrophoresis and blot hybridisation. In malignant tissues there was gross overproduction of each of 9 or more alternatively-spliced large molecular variants in all samples, whereas in the control samples only the standard product was routinely detected with occasional minimal quantities of one or two small variants. Furthermore, the band pattern permitted differentiation between the 23 cases with metastatic tumours of the breast or colon and the 8 with no detectable metastases. Calibration studies seeding blood with tumour cells showed that the technique can detect as few as 10 tumour cells among 10(7) leucocytes (1 ml of blood). Analysis of CD44 splice variants may prove to have applications not just to the early detection of metastatic potential in surgical biopsy specimens but also, if our findings are confirmed, in readily available bodily fluids, to the early diagnosis of cancer in screening programmes, to the assessment of remaining disease in the body and to the early detection of recurrences.

Adult↗

PubMed1995

Clonal analysis of colorectal tumors using K-ras and p53 gene mutations as markers.

Mutations to the K-ras oncogene and p53 tumor suppressor gene are two of the most common genetic lesions in human cancers. In the present study we examined the clonality of colorectal tumors with respect to each of these genetic alterations. Screening for mutations was carried out using the polymerase chain reaction-based technique of single-strand conformation polymorphism. Eleven primary colorectal adenocarcinomas and two secondary adenocarcinomas were analyzed at four different sites within the tumor. Involved pericolic lymph nodes were collected from nine of these cases, a metastatic deposit in the liver was obtained in one case, and adjacent adenomatous lesions were collected in two cases. Seven tumors contained mutations in either the K-ras or p53 genes. In all cases, DNA derived from multiple sites within an individual tumor or metastatic deposits arising from that tumor showed the same pattern of gene mutation. Immunohistochemical staining for p53 protein overexpression also showed similar patterns of reactivity within individual tumors and their metastatic deposits. These results suggest that the major clonal expansion of colorectal carcinomas occurs after the acquisition of mutations in these genes. Our results also indicate that sampling errors are unlikely to occur in molecular studies aimed at defining the role of these genes in colorectal cancer progression.

Carcinoma↗

PubMed2001

Primary and metastatic lobular carcinoma of the breast.

Invasive lobular carcinoma of the breast is the second most common type of primary breast cancer, accounting for 8-14% of cases, but is often difficult to diagnose early. It typically shows a diffuse pattern of infiltration within the breast, resulting in a variety of often subtle radiological appearances. A similar infiltrative pattern is seen in its metastatic form, with involvement of the gastrointestinal tract, peritoneum, retroperitoneum, bone marrow, meninges and uterus occurring more frequently than with the more common infiltrating ductal carcinoma of the breast. This pictorial essay illustrates the spectrum of radiological appearances which may be encountered with both primary and secondary lobular carcinoma.

Aged↗