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PubMed1989

Growth rate of acoustic neuromas.

During the past 25 years the authors have diagnosed over 1,600 acoustic neuromas. In almost all of the cases surgery for the removal of the tumor was performed shortly after the diagnostic tests. However in 35 cases one or more follow-up imaging studies was performed since the patients refused surgery, or surgery was not performed because of the poor general condition of the patients or the small size of the lesion, particularly in individuals of advanced age. In the latter group there was a clear understanding that surgery would be performed if the follow-up study showed progression of the lesion. In this paper the authors review the evolution of the tumor in the 35 cases, try to establish the rate of growth in cases where the tumor became larger, and correlate tumor evolution to patient's age and clinical findings.

Adolescent↗
PubMedDate not supplied

[Suppression of tumor immunity by electromagnetic fields and glucocorticoids in mice with implanted Ehrlich carcinoma].

INTRODUCTION: The immune system plays a major role in the origin, growth and evolution of tumors; factors that decrease the immune response in any way can cause higher tumor incidence and its faster or uncontrolled growth and evolution. MATERIAL AND METHODS: The research included 18 healthy male Han: NMRI mice, weighing between 25 and 30g, with ten-day-old tumor deposits, divided into three groups consisting of six mice each. The first group was continuously exposed to extremely low frequency electromagnetic fields (intensity 70-320 microT). The second group was treated with high doses of corticosteroids (dexamethasone). The control group was not treated with corticosteroids, nor was exposed to extremely low frequency electromagnetic fields. The exposure period lasted for ten days. The criteria used to evaluate tumor immunity were: histological findings of leukocyte infiltration around the tumor cells and white blood cell count. RESULTS: The control group presented with excellent immune response to tumor cells. Lymphoplasmacytic infiltrates widely surrounded the tumor. Numerous tumor cells showed signs of cell death. The results showed that exposure of animals to high doses of glucocorticoids resulted in extremely decreased leukocyte infiltration in the tumor tissue (single lymphocytes), while exposure to extremely low frequency electromagnetic fields significantly decreased leukocyte infiltration in comparison to the control group. Comparison of white blood cell count in treated groups revealed that the white blood cell count in both treated groups was decreased, compared with the control group. CONCLUSION: Extremely low frequency electromagnetic fields significantly suppress the immune response to tumor cells. Dexamethasone treatment resulted in almost complete absence of immune response to tumor cells. Electromagnetic fields and dexamethasone both decrease the white blood cell count.

Animals↗
PubMed1988

Existence of two distinct processes of chromosomal evolution in near-diploid colorectal tumors.

The comparison of all the karyotypes established in each of 18 near-diploid colorectal tumors made it possible to reconstruct a clonal evolution and to distinguish between early and late chromosomal aberrations. Because no abnormalities were observed in all tumors, and as even the most frequent changes, i.e., monosomy 17p and monosomy 18, may be present in mosaic, no chromosomal change can be regarded as a common primary event in the carcinogenetic process. However, the repeated occurrence of several changes favors the hypothesis of two karyotypic evolutionary processes. In most tumors, monosomy 17p and 18 were found, and the karyotypic evolution involved mainly several additional monosomies due to unbalanced rearrangements or losses that affect, by order of decreasing frequency, chromosomes 1p, 4, 14, 5q, 6q, 2p, and 11q, as well as gains of chromosomes 20, 8q, 13, 17q, and X. In this group of tumors, the mean number of chromosomes remains close to 46. In the other tumors, either only a monosomy 17p or a monosomy 18 was found and the karyotypic evolution involved essentially trisomies, resulting from gains with, by order of decreasing frequency, a preferential involvement of chromosomes 7, 8q, 13, 17q, 20, X, 2p, 5, and 16, the only additional recurrent deletion affecting chromosome 1p. In these tumors, the mean chromosome number is close to 51. Ten out of 11 polyploid sidelines emerged from monosomic-type tumors.

Chromosome Aberrations↗
PubMed1975

Refractoriness of lymph-node cells from tumour-bearing animals.

In vitro lymphocyte stimulation by mitomycin-C-blocked tumor cells has been used to demonstrate tumor-specific antigens in syngeneic murine systems and to follow the evolution of tumor immunity with the tumor-bearing state. Mitomycin-blocked tumor cells stimulated syngeneic lymphocytes from normal mice, from those bearing small tumors (less than 1 cm in diameter) and from tumor-immune mice, sensitized by tumor-cell inoculation and subsequent tumor removal, to undergo increased DNA synthesis as measured by the incorporation of tritiated thymidine. However, lymph-node cells from mice bearing tumors over 1 cm in diameter appeared to be maximally stimulated in vivo and incapable of further stimulation by the same tumor cells in vitro. This was reflected by the progressively increasing background levels of nucleic acid synthesis with the length of tumor-bearing and the size of the tumor. Although lymph-node cells from mice with large tumors did not respond to the same tumor cells in vitro, they did have normal responses to PHA. Within 7-14 days of surgical removal of the tumor, specific lymphocyte responsiveness and background activity returned to previous normal levels, but reinoculation with 10-6 tumor cells resulted in progressive tumor growth and loss of specific in vitro responsiveness when the second tumor had reached the critical size of 1 cm in diameter. Brief exposure of tumor-immune lymph-node cells to a soluble antigen extract of the same tumor resulted in a marked increase in DNA synthetic activity compared to that obtained after exposure to a different tumor extract, muscle extract or medium alone underwent stimulation when cultured with mitomycin-blocked tumor cells. However, normally responsive tumor-immune lymph-node cells, after brief exposure to a soluble antigen extract of the same tumor, initially underwent increased DNA synthesis, but were incapable of further stimulation by mitomycin-blocked tumor cells. Tumor antigen, alone or complexed with antibody, was also demonstrated in the sera of mice bearing large tumors and is thought to be responsible for the refractoriness of lymph-node cells from these mice to further stimulation in vitro. These experiments demonstrate that tumor size and the consequent antigen load to which the tumor-bearing animals is subjected have a profound effect on tumor-specific lymphocyte responsiveness.

Animals↗
PubMed2005

Estrogen receptor positivity in mammary tumors of Wnt-1 transgenic mice is influenced by collaborating oncogenic mutations.

The majority (75%) of human breast cancers express estrogen receptor (ER). Although ER-positive tumors usually respond to antiestrogen therapies, 30% of them do not. It is not known what controls the ER status of breast cancers or their responsiveness to antihormone interventions. In this report, we document that transgenic (TG) expression of Wnt-1 in mice induces ER-positive tumors. Loss of Pten or gain of Ras mutations during the evolution of tumors in Wnt-1 TG mice has no effect on the expression of ER, but overexpression of Neu or loss of p53 leads to ER-negative tumors. Thus, our results provide compelling evidence that expression of ER in breast cancer may be influenced by specific genetic changes that promote cancer progression. These findings constitute a first step to explore the molecular mechanisms leading to ER-positive or ER-negative mammary tumors. In addition, we find that ER-positive tumors arising in Wnt-1 TG mice are refractory to both ovariectomy and the ER antagonist tamoxifen, but lose ER expression with tamoxifen, suggesting that antiestrogen selects for ER-negative tumor cells and that the ER-positive cell fraction is dispensable for growth of these tumors. This is a first report of a mouse model of antiestrogen-resistant ER-positive breast cancers, and could provide a powerful tool to study the molecular mechanisms that control antiestrogen resistance.

Animals↗
PubMed2000

Centromere cleavage is a mechanism underlying isochromosome formation in skin and head and neck carcinomas.

Centromeric rearrangements, in the form of isochromosomes or whole-arm translocations, are the most common recurrent changes in head and neck and skin carcinomas. Little is known about the mechanisms behind the origin of these chromosome rearrangements. In the present study, one basal cell carcinoma and two squamous cell carcinomas of the head and neck were thoroughly studied by cytogenetic and fluorescence in situ hybridization techniques. All tumors showed intratumor heterogeneity in the form of cytogenetically related subclones (in all tumors) and unrelated clones (in one tumor). Assessment of karyotypic evolution in these tumors suggests that centromeric cleavage is a mechanism giving rise to isochromosomes. A similar mechanism may also be involved in the formation of whole-arm translocations.

Basal Cell Carcinoma↗
PubMed2004

Karyotypic evolution pathways in medulloblastoma/primitive neuroectodermal tumor determined with a combination of spectral karyotyping, G-banding, and fluorescence in situ hybridization.

Medulloblastomas (MBs) or primitive neuroectodermal tumors (PNETs) represent 15%-30% of pediatric brain tumors and are the most common brain tumors in children; they are rare in adults. Classification of these tumors is based on tissue morphology and is often controversial and problematic. Karyotypic analysis of these tumors using conventional cytogenetic methods is often a difficult process that may be hindered by a limited number of metaphase cells and poor chromosome morphology, often leading to only partial characterization of the chromosomal abnormalities. We investigated three primary human tumors and four cell lines (CHO-707, DAOY, D-341, and PFSK) utilizing a combination of conventional G-banding, spectral karyotyping (SKY), and fluorescence in situ hybridization (FISH) techniques. A high level of intratumoral heterogeneity was seen, with multiple numerical and structural chromosomal aberrations. The chromosomes most frequently involved in structural aberrations were chromosomes 1 (14 rearrangements), 7 (9 rearrangements), and 21 (9 rearrangements). The chromosomes most frequently involved in numerical aberrations were chromosomes 1, 12, and 13 (four cases) and chromosomes 14, 17, 19, 21, 22, and X (three cases). Numerous aberrant chromosomes were characterized only with the SKY analysis, and based on these findings multiple clones were identified, facilitating analysis of karyotypic evolution. The most frequent evolution mechanism was via polyploidization, followed by acquisition of additional numerical or structural aberrations (or both); however, the results showed that the karyotypic evolution process in these tumors is typically divergent and complex.

Adult↗
PubMed2002

Compilation of published comparative genomic hybridization studies.

The power of comparative genomic hybridization (CGH) has been clearly proven since the first paper appeared in 1992 as a tool to characterize chromosomal imbalances in neoplasias. This review summarizes the chromosomal imbalances detected by CGH in solid tumors and in hemopathies. In May of 2001, we took a census of 430 articles providing information on 11,984 cases of human solid tumors or hematologic malignancies. Comparative generic hybridization has detected a number of recurrent regions of amplification or deletion that allows for identification of new chromosomal loci (oncogenes, tumor suppressor genes, or other genes) involved in the development, progression, and clonal evolution of tumors. When CGH data from different studies are combined, a pattern of nonrandom genetic aberrations appears. As expected, some of these gains and losses are common to different types of pathologies, while others are more tumor-specific.

Chromosome Aberrations↗
PubMed2026

Liquid biopsy: a new window on the BRCA genes.

The Breast Cancer Susceptibility Gene (BRCA)-associated tumors represent a constantly evolving and intriguing scenario in oncology, in which the availability of novel systemic treatment, mainly including the poly (ADP-ribose) polymerase (PARP) inhibitors, has enabled an improved survival benefit in clinical subgroups. The expanding regulatory approvals of PARP inhibitors have inevitably reshaped the clinical indications for BRCA testing, moving the BRCA1/2 profiling from the traditional and preventive workflows to therapeutic paths. Despite advances in technology and treatment, substantial limitations remain in current genetic and genomic tools for the detection of deleterious BRCA1/2 variants. Germline and tumor tissue testing provide only a snapshot of a patient's disease, failing to capture the dynamic and longitudinal aspects of tumor clonal evolution. In this scenario, liquid biopsy (LB) profiling of BRCA1/2 genes, primarily as circulating tumor DNA, represents a highly active area of research potentially affecting many aspects of cancer screening, diagnosis, and monitoring in individuals who are carriers of BRCA1/2 deleterious variants. Beyond the attractive potential to surrogate the tumor tissue testing, to overcome the cancer spatial and temporal heterogeneity, and to monitor the tumor mutational profile over time, accurately detecting all clinically relevant BRCA genetic variants and epigenetic modifications using LB remains technically challenging.

BRCA1/2↗
PubMed2003

Pathogenesis of DNA repair-deficient cancers: a statistical meta-analysis of putative Real Common Target genes.

DNA mismatch repair deficiency is observed in about 15% of human colorectal, gastric, and endometrial tumors and in lower frequencies in a minority of other tumors thereby causing insertion/deletion mutations at short repetitive sequences, recognized as microsatellite instability (MSI). Evolution of tumors, including those with MSI, is a continuous process of mutation and selection favoring neoplastic growth. Mutations in microsatellite-bearing genes that promote tumor cell growth in general (Real Common Target genes) are assumed to be the driving force during MSI carcinogenesis. Thus, microsatellite mutations in these genes should occur more frequently than mutations in microsatellite genes without contribution to malignancy (ByStander genes). So far, only a few Real Common Target genes have been identified by functional studies. Thus, comprehensive analysis of microsatellite mutations will provide important clues to the understanding of MSI-driven carcinogenesis. Here, we evaluated published mutation frequencies on 194 repeat tracts in 137 genes in MSI-H colorectal, endometrial, and gastric carcinomas and propose a statistical model that aims to identify Real Common Target genes. According to our model nine genes including BAX and TGFbetaRII were identified as Real Common Targets in colorectal cancer, one gene in gastric cancer, and three genes in endometrial cancer. Microsatellite mutations in five additional genes seem to be counterselected in gastrointestinal tumors. Overall, the general applicability, the capacity to unlimited data analysis, the inclusion of mutation data generated by different groups on different sets of tumors make this model a useful tool for predicting Real Common Target genes with specificity for MSI-H tumors of different organs, guiding subsequent functional studies to the most likely targets among numerous microsatellite harboring genes.

Base Pair Mismatch↗
PubMed1996

[Ultrasonographic aspects of cystic papillary tumor of the pancreas. Apropos of 2 cases].

Cystic papillary pancreatic tumor is an infrequent neoplasm of unknown origin which is presented almost exclusively in young women. It is characterized by an anodyne clinical symptomatology with it frequently treated as an accidental finding. Ultrasonography and computerized axial tomography have a priority role in the study of this entity but the definitive diagnosis is based on the histologic findings. The treatment of choice is surgical removal and although it is a malignant tumor, good evolution is observed with recurrence not being expected. Two new cases of cystic papillary tumor are presented comparing the ultrasonographic appearance of the same with other pancreatic cystic neoplasms. Although the ultrasonographic findings are not characteristic they may be suggestive of papillary tumor.

Adult↗
PubMed2004

Pleomorphic hyalinizing angiectatic tumor: analysis of 41 cases supporting evolution from a distinctive precursor lesion.

The pleomorphic hyalinizing angiectatic tumor (PHAT) is a rare, low-grade neoplasm that features atypical stromal cells containing hemosiderin, partially thrombosed ectatic vessels with circumferential hyalinization, and a variable inflammatory infiltrate. Over the years, we have occasionally observed a monomorphic partially myxoid spindle cell component (provisionally termed "early PHAT") co-existing with classic PHAT. In some instances, this monomorphic lesion occurs by itself, suggesting an early stage in the evolution of PHAT. To explore this hypothesis and to better define the long-term behavior of PHAT, we have reviewed our experience with these lesions. Forty-one cases were identified from consultation files. They occurred chiefly in adults (median 51 years, range 10-79 years) of either sex (23 female, 18 male), ranged from 0.3 to 19.7 cm (median 5.6 cm), and involved the subcutis of the ankle/foot (N = 15), leg (N = 10), thigh (N = 6), and other sites. Thirteen tumors had been present for more than 1 year prior to biopsy. Fifteen tumors consisted entirely of typical PHAT. Twelve cases conformed to "early PHAT," lacked fully developed features of PHAT, and showed instead short fascicles of hemosiderin-stippled spindled cells that infiltrated fat and surrounded congeries of small, damaged vessels. With close scrutiny, all contained rare pleomorphic cells with intranuclear pseudo-inclusions, as seen in typical PHAT. Fourteen cases contained both classic and early PHAT, in variable proportions. Follow-up was available in 18 patients (mean 84 months, median 52 months; range 13-420 months). Six of 18 patients developed recurrences, 1 with classic PHAT, 1 with mixed early-classic PHAT, and 4 with early PHAT. Following resection, 16 are disease free and 2 have persistent disease. None has developed metastasis. Based on the histologic overlap between early and classic PHAT, the presence of early PHAT at the periphery of classic PHAT, and the admixture of both patterns within the same tumor, we conclude that early PHAT represents a precursor lesion for PHAT. It appears essentially identical to the lesion termed "hemosiderotic fibrohistiocytic lipomatous lesion," supporting the notion that the latter is a neoplastic rather than a reactive lesion. PHAT should be considered mesenchymal tumors of intermediate malignancy, given their high rate of (sometimes aggressive) local recurrence.

Adolescent↗
PubMed2002

How does blood oxygen level-dependent (BOLD) contrast correlate with oxygen partial pressure (pO2) inside tumors?

Blood oxygen level-dependent (BOLD) contrast-based functional MRI (fMRI) has been reported as a method to assess the evolution of tumor oxygenation after hyperoxic treatments, because of its sensitivity to changes in blood flow and deoxyhemoglobin content. However a number of questions remain: 1) In view of tumor heterogeneity, how good is the correlation between the MR parameters in gradient-echo imaging (signal intensity (SI) or effective transverse relaxation time (T(*)(2))) and local tumor oxygen partial pressure (pO(2))? 2) Is the magnitude of the change in SI or T(*)(2) a quantitative marker for variation in pO(2)? 3) Is initial T(*)(2) a good marker for initial pO(2)? To address these questions, murine tumors were imaged during respiratory challenges at 4.7 Tesla, using fiber-optic microprobes to simultaneously acquire tumor pO(2) and erythrocyte flux. The BOLD signal response (SI and T(*)(2)) was temporally correlated with changes in pO(2). However, the magnitude of the signal bore no absolute relation to pO(2) across tumors, i.e., a given change in SI corresponded to a 25 mmHg pO(2) change in one tumor, but to a 100 mmHg change in another. The initial T(*)(2) value did not reliably predict tumor oxygenation at the beginning of the experiment. In conclusion, the major advantages of the technique include noninvasiveness, high spatial resolution, and real-time detection of pO(2) fluctuations. Information afforded by the BOLD imaging technique is qualitative in nature and may be combined with other techniques capable of providing an absolute measure of pO(2).

Animals↗
PubMed2003

Cluster analysis of BOLD fMRI time series in tumors to study the heterogeneity of hemodynamic response to treatment.

BOLD-contrast functional MRI (fMRI) has been used to assess the evolution of tumor oxygenation and blood flow after treatment. The aim of this study was to evaluate K-means-based cluster analysis as a exploratory, data-driven method. The advantage of this approach is that it can be used to extract information without the need for prior knowledge concerning the hemodynamic response function. Two data sets were acquired to illustrate different types of BOLD fMRI response inside tumors: the first set following a respiratory challenge with carbogen, and the second after pharmacological modulation of tumor blood flow using flunarizine. To improve the efficiency of the clustering, a power density spectrum analysis was first used to isolate voxels for which signal changes did not originate from noise or linear drift. The technique presented here can be used to assess hemodynamic response to treatment, and especially to display areas of the tumor with heterogeneous responses.

Animals↗
PubMed1994

Cytogenetic aberrations in 188 benign and borderline adipose tissue tumors.

Chromosome studies of lipomas have revealed an extensive cytogenetic heterogeneity. To investigate the frequencies of previously recognized cytogenetic subgroups and to find out if more recurrent rearrangements can be identified, we have analyzed cytogenetically short-term tissue cultures of 237 samples from 188 adipose tissue tumors obtained from 142 patients. Only one of 58 tumors from 18 patients with multiple lipomas (more than two tumors) had karyotypic changes. Among the sporadic lipomas, 20 tumors had supernumerary ring chromosomes of unknown origin, 55 had different aberrations involving chromosome segment 12q13-15, 11 had changes of 6p or chromosome 13, but no rings or 12q13-15 changes, and 14 had various other aberrations. Ring chromosomes were found in all cytogenetically abnormal lipomas histologically classified as atypical and in nine tumors classified as typical lipoma or spindle cell lipoma. Recombinations between 12q13-15 and a few other bands or segments were seen more than once: 3q27-28 (15 tumors), 2p22-24 and 2q35 (four tumors), 1p32-34 and 13q12-14 (three tumors), and 5q33 (two tumors). Recombinations of 12q13-15 with 2q35 and 13q12-14 have not been described before. Of eight tumors with chromosome 13 aberrations, five had loss of 13q material. Aberrations of 12q13-15, 6p, and/or chromosome 13 were found simultaneously in nine tumors. Two to four samples from the same tumor were investigated in 29 tumors with clonal aberrations. Thirteen of these tumors displayed clonal evolution, also noted in another 17 tumors in which only one sample had been investigated. Thus clonal evolution occurred in 30% of the tumors and was particularly frequent in atypical lipomas.

Adolescent↗
PubMed1999

Striking increase of thin melanomas contrasts with stable incidence of thick melanomas.

OBJECTIVE: The aim of this study was to analyze the temporal evolution of melanoma incidence in the department of the Bas-Rhin, France, and to study the evolution of tumor thickness. DESIGN: Retrospective study including all histologically proven melanomas recorded at the cancer registry of the department of the Bas-Rhin between January 1980 and December 1992 and at the Cutaneous Histopathology Department of the University Hospitals, Strasbourg, between January 1980 and December 1997. SETTING: Population-based cancer registry and academic cutaneous histopathology department. PATIENTS: A total of 1254 patients with histologically proven melanomas. INTERVENTION: None. MAIN OUTCOME MEASURES: Temporal evolution of melanoma incidence and tumor thickness. RESULTS: The mean (SD) and median tumor thicknesses were 1.48 (1.59) mm and 0.87 mm, respectively, and they decreased during the study period. The increase in the number of melanomas was mainly related to an increase of superficial spreading melanomas in both sexes. The number of intermediate melanomas (1-2 mm) in both sexes and the number of melanomas with a Breslow index between 2 and 4 mm in women increased only slightly. The number of melanomas with a Breslow index greater than 2 mm in men and greater than 4 mm in women remained stable during the reference period. CONCLUSION: A striking increase in incidence of thin melanomas contrasts with a stable incidence of thick melanomas.

Adult↗
PubMed1983

Karyotype evolution in B-cell lymphoid malignancy with an 8;14 translocation.

To evaluate the significance of karyotypic evolution of tumor cells with an 8;14 translocation [t(8;14)(q24;q32)], we examined the clinicopathologic features and immunologic phenotypes of nine Japanese patients with various types of B-cell malignancy with the translocation. All these patients had structural rearrangements of the long arm of chromosome No. I (Iq) in a stem line or the subline of tumor cells with a t(8;14). The rearrangements were composed of a translocation involving Iq with other chromosomes and a tandem duplication of Iq, and they were exclusively associated with a partial trisomy for Iq. Two patients with diffuse large-cell lymphoma, whose tumor cells did not express surface immunoglobulins (s-Ig), had the Iq translocation in their highly complex karyotypes. Tumor cells from the other seven patients expressed s-Ig and the karyotypes were relatively simple. Among these patients, the Iq translocation was found in two patients with Burkitt's lymphoma, and the Iq duplication were observed in a stem line or the sublines from four patients with Burkitt's lymphoma-leukemia and one each with small non-cleaved-cell or diffuse large-cell lymphoma. Except for one patient in the stage of IE, these patients had a poor prognosis because of the clinical conversion of extranodal metastases in the earlier disease phase. These findings are compatible with those of Western patients with a t(8;14). Therefore, tumor cells marked primarily with a t(8;14) could have "major routes" in the karyotypic evolution, for which potentials should be recognized as clinical risk factors, and the morphologic presentation and the expression of surface immunoglobulins may be associated with the process of karyotypic evolution.

Adult↗