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PubMed2002

Apoptotic markers for tumor recurrence: a minireview.

The control of apoptotic mechanisms is integral to many aspects of tumor biology and appears to be involved in the process of recurrence. Apoptosis serves as an essential mechanism to prevent the proliferation of cells with a higher mutation rate, thus tempering malignant transformation. Most antineoplastic therapies function by triggering apoptosis in sensitive cells. Resistance to treatment may result from specific inhibition of apoptotic signaling. Chemotherapy or radiation may increase the mutation rate and hasten tumor evolution in cancer cells that are resistant to apoptosis. Summarizing the current evidence regarding the usefulness of various apoptotic markers for predicting tumor recurrence, the most extensively studied appear to be bcl-2 and p53, as well as the apoptotic rate itself, with promising prognostic potential in several neoplasias. Investigative results, however, mostly refer to multiple single-center retrospective studies, awaiting validation by large prospective clinical trials. Despite initial optimism, it becomes apparent that the measurement of one or more gene products is inadequate to directly predict a phenomenon as complex as the clinical outcome. One of the challenges that is only beginning to be addressed is the combined assessment of traditional prognostic parameters and molecular biomarkers by creating models or equations to predict the likelihood of recurrence. Such screening of patients may help define prognostic categories and influence treatment decisions.

Animals↗

PubMed1997

Evidence of genetic progression in human gastric carcinomas with microsatellite instability.

Mutator phenotype tumors provide unique opportunities to unravel malignant progression because of various gene alterations acquired during clonal tumor evolution. Gastric carcinomas, which have been known to show frequent genetic instability, would be composed of initial gene alterations shared by most tumor areas and subsequent alterations restricted to particular tumor sites. To analyse the timing of genetic events, we examined separate sites of tumor tissue obtained from a given gastric carcinoma patient with microsatellite instability (MSI). Our study included 95 normal/tumor area pairs from 25 patients. Six of the 25 patients (24%) demonstrated various levels of MSI ranging from 7% (two of 30) to 97% (28 of 29) of markers tested in multiple tumor sites. Of the six patients, five manifested frameshift mutations in a tract of ten deoxyadenosines within transforming growth factor beta receptor type II and four demonstrated frameshift mutations in a tract of eight deoxyguanosines within BAX. These mutations were common to all tumor sites regardless of the various level of MSI phenotype, indicating initial events. Two of the six patients exhibited frameshift mutations in mononucleotide repeats of mismatch repair genes, hMSH3 and hMSH6, and the insulin-like growth factor II receptor in restricted tumor areas, indicating additional alterations. Insulin-like growth factor II receptor mutations appear to be caused by hMSH3 and hMSH6 mutations because the former mutations were confined to tumor portions with the latter two mismatch repair lesions. These results provide genetic progression evidence for gastric carcinomas of the mutator pathway. In this pathway, mismatch repair insufficiency initially targets mononucleotide tracts of transforming growth factor beta receptor type II and BAX. During tumorigenesis, primary mismatch repair failure may give rise to the secondary mismatch repair lesions, frameshift mutations of hMSH3 and hMSH6, which result in another tumorigenic mutation in the insulin-like growth factor II receptor.

Adult↗

PubMed1999

Clinical outcome of patients with anti-Hu-associated encephalomyelitis after treatment of the tumor.

OBJECTIVE: To evaluate 1) the effect of the tumor treatment on the clinical course of paraneoplastic encephalomyelitis (PEM) with anti-Hu antibodies, 2) the impact of immunotherapy on the tumor evolution, and 3) the outcome of the small cell lung cancer (SCLC) of PEM patients compared with that of patients without PEM. METHODS: The authors retrospectively analyzed 51 PEM patients (42 with SCLC, 9 with other tumors) who received antineoplastic treatment with (25 patients) or without (26) concomitant immunotherapy. Tumor response was assessed at the end of the antineoplastic treatment. Progression of PEM was defined as a change of at least 1 point in the Rankin scale measured at the onset and at the end of the tumor treatment. To evaluate the outcome of SCLC, 27 PEM patients with SCLC were matched one-to-one with SCLC patients without PEM for age, performance status, tumor stage, and type of antineoplastic treatment. RESULTS: Thirty-six (70%) patients were neurologically stable at the end of the tumor treatment. In a logistic regression analysis, tumor complete response was the only predictor of PEM stabilization (OR 7.07; 95% CI 1.68 to 29.76; p = 0.006). Immunotherapy did not modify the outcome of the tumor and PEM. Median survival was similar in SCLC patients with and without PEM, but the probability of survival at 30 months was higher in PEM patients with SCLC (OR 5.26; 95% CI 1.0004 to 27.6902; p = 0.03). CONCLUSIONS: Complete response of the tumor seems to have a favorable influence on the course of paraneoplastic encephalomyelitis (PEM). Concomitant immunotherapy does not adversely affect the tumor outcome. The small cell lung cancer of PEM patients may have a slightly better evolution than that of patients without PEM.

Adult↗

PubMed2004

Gene expression profiling of human adrenocortical tumors using complementary deoxyribonucleic Acid microarrays identifies several candidate genes as markers of malignancy.

The aim of this study was to identify predictor sets of genes whose over- or underexpression in human sporadic adrenocortical tumors would help to identify malignant vs. benign tumors and to predict postsurgical metastatic recurrence. For this, we analyzed the expression of 230 candidate genes using cDNA microarrays in a series of 57 well-characterized human sporadic adrenocortical tumors (33 adenomas and 24 carcinomas). We identified two clusters of genes (the IGF-II cluster containing eight genes, including IGF-II, and the steroidogenesis cluster containing six genes encoding steroidogenic enzymes plus eight other genes) whose combined levels of expression appeared to be good predictors of malignancy. This predictive value was as strong as that of the pathological score of Weiss. The analysis of the population of carcinomas (13 tumors) for genes whose expression would be strongly different between recurring and nonrecurring tumors allowed identification of 14 genes meeting these criteria. Among these genes, there are probably new markers of tumor evolution that will deserve additional validation on a larger scale. Taken together, these results show that the parallel analysis of the expression levels of a selected group of genes on microgram quantities of tumor RNA (a quantity that can be obtained from fine needle aspirations) appears as a complementary method to histopathology for the diagnosis and prognosis of evolution of adrenocortical carcinomas.

Adolescent↗

PubMed2006

Dynamic assessment of antiangiogenic therapy by monitoring both tumoral vascularization and tissue degeneration.

Tumor growth is dependent both on endothelial and tumor cells. The aim of this study was to investigate dynamically whether changes in tumor vasculature implicate tumor tissue degeneration during antiangiogenic therapies. In order to quantify intra-tumor vascularization and necrosis, we have used ultrasound technology. This study has identified essential parameters needed to quantify specifically and sensitively the number of microvessels and the extent of necrosis in xenografted human carcinomas during natural tumor evolution, using contrast-enhanced high-frequency ultrasonography with (HFCDUS) or without (HFUS) color Doppler. We showed that quantification of intra-tumor microvessels between HFCDUS and immunohistochemistry is correlated using an anti-CD31 antibody. Furthermore, quantification of tumor necrosis with HFUS was confirmed by histological examination of hematoxylin-eosin-saffranin-stained sections over the observation period. Subsequently, for the assessment of novel angiogenic inhibitors, HFCDUS and HFUS were used to elucidate the underlying dynamics linking vessel inhibition and tumor eradication. We describe a novel application for HFCDUS/HFUS that constitutes an effective, convenient, and non-invasive method for clinical assessment of angiogenic inhibitors. In conclusion, we showed that tumor cells abruptly became necrotic following an antivascular therapy, whereas untreated tumors were protected from degeneration by a significant blood supply.

Adenoviridae↗

PubMed1977

Effect of cyclophosphamide on syngeneic transplantation of adenovirus 12-transformed tumor cells in C3H/he mice.

We tested the cyclophosphamide effects against the growth of adenovirus-transformed cells and the subsequent tumor development in the syngeneic host. Cyclophosphamide did not show any effect on the tumor evolution when injected 24 and 6 hours before cell implantation. Cyclophosphamide injected 24 or 39 hours after cell implantation prevented or retarded the tumor growth. In mice bearing palpable tumors, it induced their complete regression in 85,7% of the animals, but did not effect the development of the homograft immunity.

Adenoviridae↗

PubMed1989

Ploidy of primary germ cell tumors of the testis. Pathogenetic and clinical relevance.

The ploidy of testicular germ cell tumors (GCT), a heterogeneous group of neoplasms, was studied by DNA flow cytometry. The DNA index for infantile yolk sac tumor (N = 10), seminomas (N = 20), and nonseminomas (N = 36), was: 1.91, 1.66, and 1.43, respectively. These values differed significantly one from another (p less than 0.01). The seminoma and nonseminoma components of combined tumors (N = 16) had a significantly different median DNA index of 1.61 and 1.40, respectively. Three of the 10 infantile yolk sac tumors, but only one of the 72 testicular GCT of adults were diploid. The consistent aneuploidy of testicular GCTs of adults might be helpful in the differential diagnosis of primary nongerm cell tumors of the testis, and in differentiating between metastases of testicular GCTs and primary extragonadal malignant GCTs. These data fit into a model of pathogenesis of testicular GCTs of adults in which all tumors, with the possible exception of spermatocytic seminoma, pass through a seminoma stage. Tumor evolution seems to result from net loss of chromosomes from a (near)tetraploid carcinoma in situ cell. The pathogenesis of infantile yolk sac tumor might be different from that of testicular GCTs of adults.

Aneuploidy↗

PubMed2001

Clinical and experimental progression of a new model of human prostate cancer and therapeutic approach.

We report the clinical evolution of a prostate cancer, metastasizing to lungs and bones, recurring locally, and escaping from anti-androgen therapy. Key event of biological progression of the patient's tumor was the coincidence of allelic imbalance accumulation and of bone metastases occurrence. The recurrent tumor was established as the transplantable xenograft PAC120 in nude mice, where it grew locally. PAC120 displayed the same immunophenotype of the original tumor (positive for keratin, vimentin, prostatic acid phosphatase, and Leu-7) and expressed human HOXB9, HOXA4, HER-2/neu, and prostate-specific antigen genes, as detected by reverse transcriptase-polymerase chain reaction. It formed lung micrometastases detected by mRNA expression of human genes. Cytogenetic analysis demonstrated numerous alterations reflecting the tumor evolution. PAC120 was still hormone-dependent; its growth was strongly inhibited by the new gonadotropin-releasing hormone antagonist FE 200486 but weakly by gonadotropin-releasing hormone superagonist D-Trp(6)-luteinizing-hormone releasing hormone (decapeptyl). Tumor growth inhibition induced by anti-hormone therapy was linked to the hormone deprivation degree, more important and more stable with FE 200486 than with D-Trp(6)-luteinizing-hormone releasing hormone. Surgical castration of mice led to tumor regressions but did not prevent late recurrences. Transition to hormone-independent tumors was frequently associated with a mucoid differentiation or with a neuroendocrine-like pattern. Independent variations of mRNA expression of HER-2/neu and prostate-specific antigen were observed in hormone-independent tumors whereas HOXB9 gene expression was constant. In conclusion, PAC120 xenograft, a new model of hormone-dependent prostate cancer retained the progression potential of the original tumor, opening the opportunity to study the hormone dependence escape mechanism.

Animals↗

PubMed1998

Telomere shortening in uterine leiomyomas.

OBJECTIVE: To gain a better understanding of proliferation control mechanisms in a common benign tumor, we investigated the mean telomere length and the clonality of uterine leiomyomas. STUDY DESIGN: Deoxyribonucleic acid from uterine leiomyomas and from the adjacent normal myometrium of 51 patients (total number of uterine leiomyomas 107; 28 patients with single leiomyoma, 23 patients with multiple leiomyomas ranging from 2 to 8 myoma nodules per case) was hybridized to a telomeric oligonucleotide probe by Southern blot and chemiluminescent detection. The mean telomere length was evaluated by densitometry. Clonality was assessed with use of the phosphoglycerokinase gene polymorphism. RESULTS: The mean telomere length was significantly shorter in uterine leiomyomas (median 7950 bp, interquartile range 7261 to 8372 bp) than in normal myometrium (median 9688 bp, interquartile range 8528 to 10535 bp) (P < .001). There was no correlation between tumor size and telomere attrition. Multiple uterine leiomyomas were found to have an independent clonal origin. CONCLUSIONS: Telomere attrition in uterine leiomyomas reflects enhanced proliferation activity in the course of tumor evolution. The basic telomere lengths differ in the myocytes from which the uterine leiomyomas originate, probably explaining the lack of correlation between telomere attrition and tumor size.

Adult↗

PubMed1997

Clinical evaluation and safety of loxiglumide (CCK-A receptor antagonist) in nonresectable pancreatic cancer patients. Italian Pancreatic Cancer Study Group.

The effects and safety of loxiglumide, a cholecystokinin-A (CCK-A) receptor antagonist, on advanced pancreatic cancer were investigated in humans. A perspective, controlled (2.4 g/day vs. placebo), randomized, double-blind, parallel-group study was performed in 64 patients affected by nonresectable histologically diagnosed pancreatic cancer. The patients were stratified according to sex and stage (A, T3/N0-N1/M0; B, T1-T2-T3/N0-N1/M1; C, relapse after surgical exeresis). Tumor size (by computed tomography scan) and mortality rate were evaluated as efficacy criteria. Clinical symptoms and physical signs, laboratory tests, and adverse reactions were checked every 6 weeks as efficacy/tolerability criteria. Forty-two male and twenty-two female patients were considered. A homogeneous distribution of the patients was demonstrated in the two treatment groups. Group C was not statistically evaluated for survival and tumor evolution because of its small number. Three patients dropped out for causes not related to the therapy. No toxic reactions to the drug were reported. Tumor size monitoring within groups A and B demonstrated a similar increase in both the loxiglumide and the placebo group. Survival in group A was higher than in group B (p = 0.0003). In group B, survival was lower in females (F) than in males (M) (F = 61.00 +/- 6.47 days, M = 140.44 +/- 22.15 days; p = 0.012), while survival by sex was similar in group A and in global analysis. Survival by treatment was similar for groups A and B. Survival by surgery was higher (p = 0.049) for surgical palliation than for nonoperated patients. The tumor grade affected survival but it did not vary by therapy. In conclusion, sure efficacy of loxiglumide in advanced pancreatic cancer was not demonstrated by our results. In consideration of its documented tumor growth inhibiting action, we suggest that loxiglumide be tested for recurrence prevention after resective surgery.

Double-Blind Method↗

PubMed2002

[Clinical implications of acoustic neuromas growth rate in volumetric study].

OBJECTIVE: The pattern of neuroma growth is of great importance in choosing the appropriate management. This paper tests the clinical impact of tumor growth rate assessed by volumetry. There is a conviction that some slowly growing tumors could be observed for many years. METHOD AND PATIENTS: Volume measurements were performed on T1- weighted MR images (spin echo sequences) after injection of gadolinium using a special dedicated software. The studied group included 17 patients in whom at least two MRI examinations were carried out and tumor growth was confirmed. The intervals between initial and the first follow-up examination were 14.2 months on the average. In 7 cases tumor evolution was observed in 2 periods (3 MRI studies) and in 4 cases in 3 periods (4 MRI studies). RESULTS: The growth rate depended on tumors volume and clinical stage (P<0.01). Small tumors can be observed more safely than advanced tumors because their increase in mass is lower. CONCLUSION: The observation with the tumoral volume measurements appears to be a useful and accurate tool to estimate the tumor growth rate. The growth rate is a major factor for choosing the appropriate management.

Follow-Up Studies↗

PubMedDate not supplied

The progression in astrocytic tumors.

Progression represents the qualitative tumor evolution during the time. Recently it received great consideration, mainly since the introduction of the neuroradiological imaging (CT and MRI). A series of 224 supratentorial astrocytic tumors of the juvenile and adult age have been analyzed: we found the morphological features of progression in 26% of them. These data introduce, perhaps, the most important information about progression: the "crisis" of the concept that low-grade tumors are stable lesions during the time.

Astrocytoma↗

PubMed2026

Mutational signature stratification of recurrent gliomas reveals distinct patterns of genomic traits.

BACKGROUND: Although temozolomide (TMZ) is widely used for glioma treatment, its therapeutic benefit is limited by acquired resistance and recurrence, facilitated by intratumor heterogeneity. Mutational signatures (MSs) inform tumor evolution and reveal alterations associated with treatment response. METHODS: We performed molecular analyses of 96 glioma recurrences with sufficient private single-nucleotide variants relative to their matched primary tumors, stratified by their dominant MS. RESULTS: Four groups were identified: MS11/TMZ-related (n = 38), MS1/5/aging-related (n = 32), MS6/15/21/26/microsatellite instability (MSI)-related (n = 13), and other MS-related recurrences (n = 13). MS11/TMZ-related recurrences showed higher acquired mutational counts than the other groups (1338 vs 59 (MS1/5/aging) vs 57 (MS6/15/21/26/MSI) vs 57 (other MSs); P < .01). Mutations in SYNE2, SZT2, and FBN3 were restricted to recurrences with dominant or second-dominant MS11/TMZ-related signature (n = 41), and 85% (35/41) harbored mutations in these genes. In MS11/TMZ-related recurrences with RNA sequencing data (n = 17), mRNA co-expression analyses identified SYNE2-ATAD5 and SZT2-MAPKBP1 associations. Among MS11/TMZ-related recurrences, MS23 was frequent (44%, 18/41) and associated with higher acquired mutational counts (2089 vs 1188; P = .018) and more IDH-wildtype tumors (67% vs 30%; P = .037). MAPKBP1 mutations were enriched in MS23-positive recurrences (56% (10/18) vs 0% (0/23); P < .001). MS1/5/aging-related recurrences showed more frequent acquired chromosome 16q losses (22% vs 8% (TMZ) vs 0% (MSI) vs 0% (other); P < .05), which were associated with an increased fraction of genome altered relative to 16q-diploid cases (15% vs 7%; P = .01). CONCLUSIONS: These findings show that MS-based stratification of recurrences refines molecular characterization after therapy and nominates candidate biomarkers and pathways for functional studies of treatment-associated glioma evolution.

mutational signatures↗

PubMed1997

Histopathological features of the Harderian glands in transgenic mice carrying MMTV/N-ras protooncogene.

The Harderian gland is a tubule-alveolar gland found within the orbit, on the posterior aspect of the eyeball. In mice, it is composed almost exclusively of secretory tubules and alveoli. The Harderian glands of transgenic mice, carrying the activated N-ras oncogene under the transcriptional control of the mouse mammary tumor virus long terminal repeat promoter (MMTV-LTR), were examined and compared to those of normal mice. Thirty transgenic mice provided by A. Pellicer (NYU) and 30 normal mice were examined in this study. Harderian glands were dissected, immersed in a formalin-based fixative, and embedded in paraffin. The sections of these glands were studied via histological techniques. Our results show that proliferative alterations in the Harderian glands of these transgenic mice are present even in the youngest animals. Such alterations correspond to different tumoral evolution stages, ranging from hyperplasia to wide tissue destruction. In the most advanced situations, these changes are accompanied by a glandular hypertrophy. Our results suggest a very high tumoral incidence in the Harderian glands of transgenic mice compared to normal mice. Tumors appear spontaneously in some areas, but not at the same time in the whole gland.

Animals↗

PubMed2000

The IgG Fc receptor, FcgammaRIIB, is a target for deregulation by chromosomal translocation in malignant lymphoma.

Rearrangement of chromosomal bands 1q21-23 is one of the most frequent chromosomal aberrations observed in hematological malignancy. The genes affected by these rearrangements remain poorly characterized. Typically, 1q21-23 rearrangements arise during tumor evolution and accompany disease-specific chromosomal rearrangements such as t(14;18) (BCL2) and t(8;14) (MYC), where they are thus thought to play an important role in tumor progression. The pathogenetic basis of this 1q21-23-associated disease progression is currently unknown. In this setting, we surveyed our series of follicular lymphoma for evidence of recurring 1q21-23 breaks and identified three cases in which a t(14;18)(q32;q21) was accompanied by a novel balanced t(1;22)(q22;q11). Molecular cloning of the t(1;22) in a cell line (B593) derived from one of these cases and detailed fluorescent in situ hybridization mapping in the two remaining cases identified the FCGR2B gene, which encodes the immunoreceptor tyrosine-based inhibition motif-bearing IgG Fc receptor, FcgammaRIIB, as the target gene of the t(1;22)(q22;q11). We demonstrate deregulation of FCGR2B leading to hyperexpression of FcgammaRIIb2 as the principal consequence of the t(1;22). This is evidence that IgG Fc receptors can be targets for deregulation through chromosomal translocation in lymphoma. It suggests that dysregulation of FCGR2B may play a role in tumor progression in follicular lymphoma.

Animals↗

PubMed2001

Comparative image and flow cytometric TUNEL analysis of fine needle samples of breast carcinoma.

The assessment of apoptosis in solid tumors is of interest because of its biological role in tumor evolution and response to therapy. A commonly used method for apoptosis measurement is the TUNEL 3' end-labeling technique, which has shown wide variations in results when applied to solid tumors. Thirty-one fine needle breast carcinoma samples were analyzed by fluorescent TUNEL assay and DNA content using image analysis and flow cytometry. TUNEL positivity, seen both in cells with apoptotic morphology and in a subset of morphologically normal cells, was categorized into five staining patterns and quantitated. Values for patterns of TUNEL-positive cells were compared with TUNEL positivity measured by flow cytometry. Flow cytometric quantitation showed a mean of 24.3% positive cells, which correlated (P < 0.02) with total positive cells (all patterns) measured by image (22.4%). Image analysis quantitation of morphologically apoptotic cells (4.2%) did not correlate with flow cytometric TUNEL positivity and the majority of TUNEL-stained cells were morphologically normal (17%). Image analysis allows discrimination of TUNEL-positive morphologically apoptotic and nonapoptotic cells, which are included in the total number of TUNEL-positive events measured by flow cytometry.

Apoptosis↗

PubMed2000

Intratumoral genetic heterogeneity and progression of endometrioid type endometrial adenocarcinomas.

OBJECTIVES: Development of genetic heterogeneity is one mechanism whereby tumors may acquire increasing aggressiveness during neoplastic progression. In this study we relate development of intratumoral genetic heterogeneity to invasion and metastatic spread of sporadic endometrioid (type I) endometrial adenocarcinomas. METHODS: Microsatellite unstable adenocarcinomas underwent detailed microsatellite allelotype mapping with reconstruction of neoplastic lineages using maximum parsimony analysis. RESULTS: Within individual patients, tumor allelotypes sometimes varied between regions of histologically identical tumor, indicating that genotypic variation may reflect differences inapparent by histology. Comparison of noninvasive (surface/luminal) with invasive (myometrial invasion or metastasis) carcinoma showed highly related genotypes in 3/8 cases in which the invasive component can be recognized as evolved from the superficial tumor lineage by progressive clonal selection. In 3/8 cases superficial and invasive genotypes independently evolved different sets of altered microsatellites, indicating either divergence at an early stage in tumor evolution or independent selection events. A total of 2/8 cases had random patterns of marker distribution between sampled areas that were not informative in delineating systematic relationships between surface and invasive tumor. CONCLUSIONS: We conclude from these results that endometrial tumor progression may occur through physical extension of existing clones or through creation of new subclones with altered growth properties. The latter occurs in about half of cases, where myometrial invasion may select for particular clones that are poorly represented on the luminal surface.

Alleles↗

PubMed2006

Stresses in growing soft tissues.

Biochemical processes of tissue growth lead to production of new proteins, cells, and other material particles at the microscopic level. At the macroscopic level, growth is marked by the change of the tissue shape and mass. In addition, the appearance of the new material particles is generally accompanied by deformation and, consequently, stresses in the surrounding material. Built upon a microscopic toy-tissue model mimicking the mechanical processes of mass supply, a simple phenomenological theory of tissue growth is used in the present work for explaining residual stresses in arteries and studying stresses around growing solid tumors/multicell spheroids. It is shown, in particular, that the uniform volumetric growth can lead to accumulation of residual stresses in arteries because of the material anisotropy. This can be a complementary source of residual stresses in arteries as compared to the stresses induced by non-uniform tissue growth. It is argued that the quantitative assessment of the residual stresses based on in vitro experiments may not be reliable because of the essential stress redistribution in the tissue samples under the cutting process. Concerning the problem of tumor growth, it is shown that the multicell spheroid or tumor evolution depends on elastic properties of surrounding tissues. In good qualitative agreement with the experimental in vitro observations on growing multicell spheroids, numerical simulations confirm that stiff hosting tissues can inhibit tumor growth.

Animals↗