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PubMed1989

Alteration of tumour cell arrangement related to connective tissue stroma in metastatic brain tumours. Histological and immunohistochemical studies of 68 autopsy cases.

Tumour cell arrangements of a variety of 68 tumours metastatic to brain parenchyma and leptomeninges were compared histologically and immunohistochemically with those of the primary tumours in regard to their connective tissue stroma. In the brain parenchyma, more than 90% of 31 metastatic differentiated adenocarcinomas from various organs changed in cell arrangement from a tubular to a papillary pattern, in which tumour cells lined the increased perivascular connective tissue, rich in both type III collagen and fibronectin, the typical constituents of interstitial type extracellular matrices. Twelve (39%) and 3 of 31 cases were rearranged in a partially or completely tubular pattern respectively, within the metastatic nodules. Most of these neoplastic tubules were surrounded by diffusely proliferating connective tissue. Metastatic growth of carcinoma cells in the absence of supporting connective tissue in the nervous tissue was rare. A similar result was obtained for differentiated squamous cell carcinoma. In contrast, metastatic undifferentiated carcinoma and tumours with some neuro-ectodermal characteristics showed a sheet-like arrangement without pronounced connective tissue proliferation, similar to that of the primary tumours. In the leptomeninges, differentiated carcinoma cells were arranged in a tubular or a squamoid pattern and were frequently accompanied by marked stromal response. These results indicate that differentiated carcinomas require connective tissue stroma for metastatic growth, and that tumour cell arrangement in the brain varies depending upon the amount and distribution of proliferating connective tissue stroma. In undifferentiated carcinomas and tumours with neuro-ectodermal characteristics lacking stromal dependency, the tumor cell arrangement remains unchanged. The degree of stromal response to metastatic tumours in the brain parenchyma is related to the degree of epithelial differentiation.

Adenocarcinoma↗

PubMed2001

[Pathohistological findings in liver metastases].

Metastatic tumors are the most common malignancies of the liver. The frequency distribution of the primary tumor location site closely resembles the frequency distribution of primary cancers in general. Yet, due to the liver's filter function of the portal blood-stream, metastatic tumors of the gastrointestinal tract are overrepresented. Most metastatic tumors show a nodular growth pattern with a demarcation of the tumor by inflammatory or fibrous reactive tissue; a diffuse metastatic tumor spread within the sinusoids is uncommon. Metastatic liver tumors may be the first clinically detectable manifestation of an unknown primary tumor. In these cases, the histological and immunohistochemical pattern of the metastatic tumor cells may give a clue of the location of the corresponding primary tumor.

Adult↗

PubMedDate not supplied

Patterns of relapse and response to retreatment in patients with metastatic melanoma or renal cell carcinoma who responded to interleukin-2-based immunotherapy.

PURPOSE: The purpose of this study was to examine the pattern of relapse and the treatment of relapse with either surgery or repeat immunotherapy in patients with metastatic melanoma or renal cell carcinoma who had previously responded to interleukin-2-based therapy. PATIENTS AND METHODS: Over a 10-year period 1051 patients with metastatic melanoma or renal cell carcinoma were treated with interleukin-2-based immunotherapy at a single institution. One hundred fifty-nine patients who relapsed after an initial partial response or complete response to interleukin-2-based immunotherapy formed the study population for this retrospective review. Medical records, physical examination forms, and relevant radiographs were reviewed to determine response, relapse site(s), and response to treatment for relapse. RESULTS: Relapse after an initial response to interleukin-2-based therapy occurred in 84 (80%) of 105 patients with metastatic melanoma and in 75 (70%) of 107 patients with metastatic renal cell carcinoma. Relapse after an initial partial response involved 71 (97%) of 73 patients with metastatic melanoma and 55 (86%) of 64 patients with metastatic renal cell carcinoma. The initial site(s) of relapse after a partial response involved a new site(s), old site(s), or both old and new sites with relatively even distribution. Relapse after an initial complete response occurred in 13 (41%) of 32 patients with metastatic melanoma and in 20 (47%) of 43 completely responding patients with metastatic renal cell carcinoma. Surprisingly, the initial site of relapse after a complete response involved only new sites of disease in 70% of patients. Retreatment of relapses with the same interleukin-2-based therapy originally used was effective in only one (2%) of 54 selected patients, but a different interleukin-2-based therapy in 35 patients resulted in five responders (a 14% secondary response rate). Most re-responders, however, responded to treatment with tumor-infiltrating lymphocytes and interleukin-2, and only one of 20 patients responded to retreatment with interleukin-2 alone. Surgical metastasectomy with therapeutic intent in 25 selected melanoma patients and in 31 selected renal cell cancer patients resulted in a 2-year progression-free survival of 18% in patients with metastatic melanoma and 37% in patients with metastatic renal cell carcinoma. DISCUSSION: In patients with metastatic melanoma or renal cell carcinoma, tumor relapse was common after a partial response to an interleukin-2-based therapy and included previously identified sites of disease in most patients. Relapse after a complete response was less frequent and involved only new sites in a majority of patients. In selected patients who relapsed, repeat treatment with the same interleukin-2-based therapy that provided the initial response was rarely effective. However, with a different interleukin-2-based therapy, usually using tumor-infiltrating lymphocytes, repeat treatment induced secondary responses in some patients. In addition, salvage metastasectomy resulted in durable progression-free survival in selected patients.

Carcinoma, Renal Cell↗

PubMed1997

[Mechanism of regression of metastatic liver tumors in rats treated with angiogenesis inhibitor with special reference to apoptosis].

We examined the mechanism of the reduction of metastatic liver tumors in rats treated with angiogenesis inhibitor TNP-470 on the histological basis of patterns of tumor cell death. Metastatic tumors were developed by intravenous injection of AH-130 cell line, followed by a dose of TNP-470. Alteration in the size and number of metastatic liver tumors and its cell death pattern were analyzed. The number and size of the metastatic tumors at 2 weeks in untreated rats were larger than those in treated rats. The number of tumors in untreated rats decreased, whereas their size increased. All rats treated were alive and free from tumors after 4 weeks, although all untreated rats died of metastatic tumors. Necrosis was predominant in the tumors of untreated rats, while most tumors in treated rats showed apoptosis. Consequently, the metastatic tumor in untreated rats might grow faster than its angiogenesis, suggesting the occurrence of central necrosis due to apparent ischemia. On the other hand, the tumor in treated rats might be reduce a by weak ischemic stimulus, which triggers apoptosis.

Animals↗

PubMed1996

An in vitro invasion model for human renal cell carcinoma cell lines mimicking their metastatic abilities.

We developed a modified in vitro invasion assay system using monolayers of vascular endothelial cells. A type I collagen gel was formed in plastic dishes, and overlaid with type IV collagen. Calf pulmonary arterial endothelial (CPAE) cells were seeded onto these plates, and incubated until they reached confluence. Five human renal cell carcinoma cell lines with various metastatic potentials in vivo were then seeded on the monolayer CPAE cells, and their colony formation and invasion activities were examined for 9 days. At day 4, the highly metastatic cell lines increased the number of colony foci on monolayer CPAE cells several fold higher than their poorly metastatic counterpart. The horizontal spreading patterns were also different between poorly and highly metastatic cell lines. On day 9, the number of carcinoma foci that penetrated the monolayer of CPAE cells and type IV collagen sheets into type I collagen gels in highly metastatic cell lines greatly increased as compared with that of poorly metastatic cell lines. Our in vitro invasion assay using monolayer CPAE cells would be useful to evaluate protease activities and colony formation during invasion.

Animals↗

PubMed1990

Flow cytometric analysis of DNA content in laryngeal cancer.

DNA content was measured by flow-cytometric analysis in 30 paraffin embedded sections from patients with laryngeal squamous cell carcinoma. The morphological characteristics and N staging of the tumours as registered in their clinical charts were correlated with their DNA content. Eighty per cent of the tumours were found to have a predominantly aneuploid distribution of DNA values. There was no correlation between the N stage of the tumour or degree of cell differentiation and DNA content. A multiploid pattern correlates with non-metastatic laryngeal tumours and we suggest that this pattern may be a good indicator for biological activity.

Aneuploidy↗

PubMed1997

Common and variant gene fusions predict distinct clinical phenotypes in rhabdomyosarcoma.

PURPOSE: We evaluated the clinical features of the common PAX3-FKHR and variant PAX7-FKHR gene fusions observed in rhabdomyosarcoma. PATIENTS AND METHODS: Reverse-transcriptase polymerase chain reaction (RT-PCR) assays were used to detect the gene fusions in 34 cases of rhabdomyosarcoma. Clinical data were obtained retrospectively and compared with the molecular results. RESULTS: The PAX3-FKHR and PAX7-FKHR gene fusions were present in tumors from 18 and 16 patients, respectively. The group with a PAX7-FKHR fusion was younger (P = .01) and presented more often with an extremity lesion (82% v 22%; P = .001). PAX7-FKHR tumors were more often localized than PAX3-FKHR tumors (P = .03). In patients with metastatic disease at diagnosis, the patterns were different: PAX7-FKHR patients had metastatic disease that involved only bone (n = 2) and distant nodes (n = 2), while the PAX3-FKHR group had multiple sites involved, including bone (n = 7), marrow (n = 7), lungs (n = 3), distant nodes (n = 2), skin (n = 1), and brain (n = 1). No significant difference in relapse rate was observed. A trend toward improved overall survival in the PAX7-FKHR group was noted (P = .09). Event-free survival for this PAX7-FKHR group was significantly longer (P = .04). CONCLUSION: Our results suggest that the common PAX3-FKHR and the variant PAX7-FKHR fusions are associated with distinct clinical phenotypes. Identification of fusion gene status may be a useful diagnostic tool in rhabdomyosarcoma.

Adolescent↗

PubMed1998

Unique expression patterns and alterations in the intestinal protein villin in primary and metastatic pulmonary adenocarcinomas.

The identification of markers that distinguish primary pulmonary adenocarcinomas from pulmonary adenocarcinomas secondary to the digestive tract would be clinically important. Villin, a specific marker in digestive-tract malignancies, was evaluated in 57 pulmonary adenocarcinomas, six samples of proximal bronchial tissue, and five metastatic pulmonary adenocarcinomas (three colon and two esophageal adenocarcinomas) by using immunohistochemical and molecular analyses. Villin was expressed in 31.6% (18 of 57) of the pulmonary adenocarcinomas and showed either a diffuse cytoplasmic pattern (10.5%) or a primary cytoplasmic pattern with minor brush-border staining (21.1%). However, none of those samples demonstrated the primary brush-border staining pattern that was characteristic of all five of the metastatic digestive-tract adenocarcinomas. There was a significant difference in the positive brush-border staining pattern between the primary and metastatic pulmonary adenocarcinomas (P < 0.002). Villin protein was expressed in bronchial epithelial cells, and villin mRNA was detected by reverse transcription-polymerase chain reaction. Northern analysis demonstrated 3.5- and 2.7-kb villin mRNAs in villin protein-positive tumors, but villin mRNA was not detected in non-tumorous lung tissue, indicating the transcriptional upregulation of villin in lung tumors. An additional smaller-sized mRNA (1.8 kb) was observed in six of 10 pulmonary adenocarcinomas and in the bronchoalveolar carcinoma cell line A549. Two small villin mRNAs were cloned from the cell line A549 and were found to represent an alternatively spliced (exon 8-exon 14) 1.85-kb mRNA and a 1.8-kb mRNA that was missing a portion of the 5' region (exon 1-exon 9) of the native villin mRNA. These studies demonstrated that the pattern of villin expression and the presence of altered villin mRNAs may be useful markers for pulmonary adenocarcinomas as well as provide support for the potential origin of villin-expressing tumors from bronchial epithelial cells.

Adenocarcinoma↗

PubMed1999

Response of DNA ploidy to chemotherapy in primary and metastatic lesions in human osteosarcomas.

Primary and pulmonary metastatic and pulmonary metastatic tumors (two synchronous and seven metachronous metastases) in nine patients with osteosarcomas were studied by DNA cytofluorometry. All patients were treated with both pre and postoperative chemotherapy. The results showed that all five diploid osteosarcomas and three of the four aneuploid tumors did not markedly change their ploidy pattern after preoperative chemotherapy, and had almost the same ploidy patterns as the pulmonary metastatic lesions. Those eight tumors showed poor histologic response and chemoresistance by the doxorubicin binding assay. Only one aneuploid osteosarcoma showing good histologic response and chemosensitivity changed its ploidy pattern to diploid, with the disappearance of aneuploid tumor cells and its synchronous pulmonary metastatic tumor also showed conversion to a diploid pattern with massive tumor necrosis. It is evident that those tumors showing no change in their ploidy pattern after chemotherapy were resistant to the chemotherapy. Therefore, we conclude that regardless of whether the pulmonary metastatic tumors were synchronous or metachronous, they showed the same change in their ploidy pattern as well as their chemosensitivity as the primary human osteosarcoma from which they were derived.

Adolescent↗

PubMed1999

Cytogenetic analyses of secondary liver tumors reveal significant differences in genomic imbalances between primary and metastatic colon carcinomas.

To investigate if karyotypic features of secondary liver tumors may provide diagnostic information and if the cytogenetic patterns of primary and metastatic colorectal carcinomas (CRC) are different, 33 liver metastases were analyzed: 25 CRC, 4 small intestine carcinoids, 1 ovarian carcinoid, 1 lobular breast cancer, 1 head-and-neck squamous cell carcinoma, and 1 uveal malignant melanoma. Chromosomal aberrations were detected in 24 cases, whereas 5 had normal karyotypes and 4 were uninformative due to lack of mitoses. Trisomy 12 was detected in 2 small intestine carcinoids, suggesting that +12 may be of pathogenetic importance in this tumor type. The breast and head-and-neck carcinomas and the uveal melanoma displayed aberrations previously reported as characteristic in primary tumors, e.g., der(1;16) and deletion of 3p in the breast cancer, losses of 3p and 8p and partial gain of 8q in the head-and-neck carcinoma, and monosomy 3 and i(8)(q10) in the uveal melanoma, indicating that cytogenetic investigations provide important diagnostic information in secondary liver tumors. In the 18 CRC metastases with chromosomal abnormalities, the cytogenetic findings agreed well with previously reported primary CRC. Common numerical abnormalities included gains of chromosomes 7, 11, 13, and 20, and losses of Y, 4, 18, 21, and 22. Structural rearrangements most often affected chromosome bands 1p13, 1q10, 3p21, 5q10, 5q11, 7q10, 8q10, 8q11, 12q13, 16p13, 17p11, 20p13, 20p11, and 20q10, and frequently resulted in losses of 1p, 8p, and 17p, and gains of 5p, 6p, 7p, 8q, and 20q. Comparing the present cases with primary CRC previously analyzed in our department revealed that additional gains of 6p, 6q, 7p, and 20q, and losses of 1p, 4p, 4q, 8p, 18p, 18q, and 22 were more common (P < 0.05) in the metastases, suggesting that these genomic sites harbor genes of importance in the metastatic process of CRC.

Adult↗

PubMed1991

Flow cytometric DNA ploidy pattern in dysplastic mucosa, and in primary and metastatic carcinomas in patients with longstanding ulcerative colitis.

Eighty-nine fresh tissue samples from flat colonic mucosa, polypoid lesions, macroscopically evident carcinomas, and metastatic carcinomas from ten patients with longstanding ulcerative colitis (greater than or equal to 8 years duration) were analysed by DNA flow cytometry and light microscopy. Of a total of ten carcinomas found in six patients, six showed DNA aneuploidy. Three patients developed metastatic carcinomas, all with aneuploid cell populations with similar DNA indices as in the primary carcinoma. Furthermore, aneuploid cell populations with similar DNA indices often occurred, both in separate mucosa samples, as well as in mucosa and carcinoma samples, from the same patient. DNA aneuploidy was found in flat mucosa in five of the six patients with carcinoma, and in one of the four patients without carcinoma (P greater than 0.1). High grade dysplasia was found in only four of the six cases with carcinoma, indicating that high grade dysplasia is insufficient as marker for malignant development. DNA aneuploidy was found in 24% of the dysplastic mucosa samples, and in 18% of the non-dysplastic mucosa samples (n.s., both with regard to high and low grade dysplasia). Since abnormal DNA ploidy pattern was not confined to dysplastic epithelium only, DNA aneuploidy in flat mucosa may constitute an additional marker in the identification of patients at increased cancer risk who could benefit from a closer surveillance.

Adult↗

PubMed2006

Distribution of nodal metastases after chemotherapy in nonseminomatous testis cancer: a possible indication for limited dissection.

OBJECTIVE: To assess the clinical and pathological findings of patients treated by bilateral retroperitoneal lymph node dissection (RPLND) after chemotherapy, to identify a subset for whom modified template nodal resection might be contemplated, as bilateral RPLND is the treatment of choice in patients with residual retroperitoneal disease after chemotherapy for nonseminomatous germ-cell tumour (GCT). PATIENTS AND METHODS: The medical records were reviewed of 50 consecutive patients who had RPLND after chemotherapy between 1996 and 2005. Bilateral template RPLND was performed uniformly. Extracted lymph nodes were surgically stratified into three distinct anatomical zones by two sagittal planes running in front of the aorta and the inferior vena cava. The pathological findings were correlated with the side of the primary lesion and the extent of metastatic disease before chemotherapy. RESULTS: Pathological assessment of the resected lymph nodes revealed teratoma in 28 patients (56%), viable carcinoma in three (6%), and necrosis or fibrosis in 19 (38%). All clinical stage Is, IIA and IIB left-sided primary tumours followed a predictable pattern of spread constricted to a modified left-sided template. Patients with clinical stage IIC and III, or right-sided primary tumour, had a less predictable metastatic pattern, having crossover metastases to the contralateral template. CONCLUSION: Bilateral RPLND should be considered as the reference standard in patients with metastatic GCT and residual retroperitoneal mass after completing chemotherapy. However, the present data suggest that a modified template dissection might be considered even after chemotherapy in patients with left-sided primary tumours and limited nodal involvement at presentation.

Adolescent↗

PubMed1998

Postoperative radiation for squamous cell carcinoma metastatic to cervical lymph nodes from an unknown primary site: outcomes and patterns of failure.

BACKGROUND: This retrospective study assesses the outcomes and patterns of failure in patients with squamous cell carcinoma metastatic to cervical lymph nodes from an unknown primary site treated with combined surgery and postoperative radiotherapy. METHODS: One hundred thirty-six patients with squamous cell carcinoma metastatic to cervical lymph nodes from an unknown primary source were treated postoperatively with radiotherapy at the University of Texas M. D. Anderson Cancer Center between the years 1968 and 1992. Stage distribution was: N1, 31 patients; N2a, 49; N2b, 25; N2c, 3; N3, 18; and Nx, 10. Thirty-nine patients had excisional biopsies only, 64 patients underwent modified neck dissections, and 33 had radical neck dissections. Extracapsular extension was present in 87 cases. Fifty-nine patients had multiple nodes involved. The median duration of follow-up for surviving patients was 8.7 years. RESULTS: Twelve patients, all with extracapsular nodal disease, developed regional relapse. The 5-year actuarial rates of regional relapse in patients with and without extracapsular nodal disease were 16% and 0%, respectively (p = .004). Nine patients (22%) with extracapsular disease and multiple nodes relapsed compared with three patients (7%) with extracapsular disease and a solitary node (p = .02). None of the patients treated with excisional biopsy and radiotherapy relapsed regionally. No statistically significant relationship between dose, treatment duration, time interval between surgery, and the start of radiotherapy and relapse was detected. The 2-, 5-, and 10-year actuarial disease-specific survival rates were 82%, 74%, and 68%, respectively. Fourteen patients developed cancers in head and neck mucosal sites; six of these cancers were located in unirradiated tissues. CONCLUSIONS: Relapse occurred infrequently in patients treated with excisional biopsies and postoperative radiotherapy. Extracapsular extension and multiple nodes were associated with worse regional control and disease-specific survival. These results appear consistent with those expected for patients with advanced neck disease and a known primary site, and the absence of a primary site should not exclude patients from studies aiming to improve outcomes in patients with extensive neck disease from a head and neck squamous cell cancer. We continue to recommend radiation to the necks and pharyngeal axis for patients suspected of having residual microscopic disease following surgery for squamous cell carcinoma metastatic to the neck from an unknown primary site.

Adult↗

PubMed1990

Comparison of DNA content in gastric cancer cells between primary lesions and lymph node metastases.

Cytophotomtric DNA contents of tumor cells in primary lesions and the corresponding metastatic lymph nodes were compared in 61 cases of gastric cancer to determine whether the DNA content remains stable during lymph node metastasis. The DNA distribution patterns were grouped into three types, according to the proportion of aneuploid cell population. Changes in DNA patterns between primary and metastatic lesions were evident in 36 of 61 patients (59.0%); in the remaining 25 (41.0%), the same DNA distribution patterns were noted for both lesions. In 33 of these 36, DNA pattern in the primary carcinoma was transformed into a more narrowly scattered one in the metastatic lesion of the lymph node. Mean and modal values and the frequency of cells over tetraploid (4c) or hexaploid (6c) were significantly higher in the primary lesion compared with findings in the metastatic lesions. This reduction in DNA content in the metastatic lesions was a more frequent occurrence in differentiated (18 of 23) than in undifferentiated adenocarcinoma (15 of 35) (P less than 0.01). Therefore, in primary lesions with a widely scattered DNA ploidy, the tumor cells with a smaller DNA ploidy frequently metastasized to lymph nodes, particularly in cases of a differentiated carcinoma. Such observations may be pertinent in future designing of treatment protocols.

Adenocarcinoma↗

PubMed1986

Carbohydrate-binding proteins of tumor lines with different growth properties. II. Changes in their pattern in clones of transformed rat fibroblasts of differing metastatic potential.

A tumor model system of clones of myeloproliferative sarcoma virus (MPV)-transformed rat fibroblasts (NRK) with different growth properties and metastatic potential was studied. The relationship between metastatic behavior and composition of carbohydrate-binding proteins (lectins) was analyzed by affinity chromatography. The metastatic variant differs qualitatively from its parental clone in the presence of galactoside-binding proteins at apparent molecular weight of 42 kDa. The alpha-glucosyl-binding proteins at apparent molecular weights of 67 kDa and 53 kDa and a galactoside-binding protein of apparent molecular weight of 34 kDa, however, are not detectable in the metastatic variant in comparison to its parental clone. In this respect the parental clone shows closer resemblance to the clone 5-8#1 with different growth properties and low metastatic potential than to its own metastatic variant. Furthermore, only the parental clone has a melibiose- and a mannan-binding protein of an apparent molecular weight of 64 kDa and 14 kDa, respectively. Rosette formation as model system for intercellular interaction reveals differences in the inhibition pattern with sugar between the two clones 5-8#1 and 5-20#20, whereas the metastatic variant 5-20#20 (s) exhibits drastically reduced capability to form rosettes. Initial experiments demonstrate the feasibility of drug targeting to transformed fibroblasts via carbohydrate-binding proteins.

Animals↗

PubMed1992

DNA content in primary tumours and lymph node metastases in colorectal adenocarcinoma.

In 18 consecutive patients operated on for colorectal carcinoma of Dukes' stage C, the DNA patterns were determined in multiple samples of the primary tumours and in all detected lymph node metastases. Single-cell microspectrophotometry on Feulgen-stained smears of fine-needle aspirates was used. When the most aggressive DNA pattern was considered representative, 12 primary tumours (67%) were designated as aneuploid. The frequency of aneuploidy among the metastases was almost the same (63%). In 15 cases (83%) the DNA patterns displayed by the metastatic lymph nodes were also found in the corresponding primary tumour, while in the remaining three cases (17%) the DNA pattern in the lymph node metastases was not seen in any of the multiple samples from the primary tumour. The observed tumour DNA heterogeneity may reflect either the multicellular origin of the tumour cells or the continuous evolution and progression of a neoplasm of unicellular origin, and may partly explain the dissimilarities between the DNA patterns of the primary tumour and the lymph node metastases. Biopsy samples from a number of metastatic lymph nodes are therefore required to ensure representativeness and to permit an adequate analysis of the prognostic role of the DNA ploidy status in lymph node metastases from colorectal cancer.

Adenocarcinoma↗

PubMed2002

Radiosurgery for residual or recurrent nonfunctioning pituitary adenoma.

OBJECT: Nonfunctioning pituitary adenomas comprise approximately 30% of all pituitary tumors. The purpose of this retrospective study is to evaluate the efficacy and role of gamma knife radiosurgery (GKS) in the management of residual or recurrent nonfunctioning pituitary adenomas. METHODS: A review was conducted of the data obtained in 42 patients who underwent adjuvant GKS at the University of Pittsburgh between 1987 and 2001. Prior treatments included transsphenoidal resection, craniotomy and resection, or conventional radiotherapy. Endocrinological, ophthalmological, and radiological responses were evaluated. The duration of follow-up review varied from 6 to 102 months (mean 31.2 months). Fifteen patients were observed for more than 40 months. The mean radiation dose to the tumor margin was 16 Gy. Conformal radiosurgery planning was used to restrict the dose to the optic nerve and chiasm. Tumor control after GKS was achieved in 100% of patients with microadenomas and 97% of patients with macroadenomas. Gamma knife radiosurgery was equally effective in controlling adenomas with cavernous sinus invasion and suprasellar extension. No patient developed a new endocrinological deficiency following GKS. One patient's tumor enlarged with an associated decline in visual function. Another patient experienced a deterioration of visual fields despite a decrease in tumor size. CONCLUSIONS: Gamma knife radiosurgery can achieve tumor control in virtually all residual or recurrent nonfunctioning pituitary adenomas. Dose sparing facilitates tumor management even when the adenoma is close to the optic apparatus or invades the cavernous sinus.

Adenoma↗

PubMed1998

Disseminated growth of murine plasmacytoma: similarities to multiple myeloma.

Murine plasma cell tumors share a number of common features with human multiple myeloma, suggesting their possible use as a model for this disease. However, one major difference between the two is the peritoneal localization of murine tumors as opposed to bone marrow residence of malignant plasma cells in early stages of multiple myeloma. We have thus examined the ability of murine plasmacytoma to produce disseminated growth similar to that seen in myeloma or other lymphoid neoplasias. Of four murine cell lines evaluated, all were demonstrated to effect highly metastatic disease involving multiple organs, although variation was observed between lines. A temporal analysis was accordingly performed with the S107 line to assess the pattern of cellular localization. Both light microscopy and PCR analysis revealed that engraftment of plasma cells occurs first in the bone marrow, followed by dissemination to other sites including the spleen, lung, and liver. Cells passaged in vivo through the bone marrow display an entirely different metastatic pattern with no homing preference to bone marrow or any other organ, suggesting the occurrence of a phenotypic change. Microscopic osteolytic lesions were observed adjacent to plasma cell tumor masses in the bone marrow, indicating early stages of bone disease. These findings demonstrate previously unrecognized similarities between the murine and human diseases and suggest the use of this in vivo model for experimental approaches to the treatment of human disease.

Animals↗