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PubMed1983

[Diffuse gingival plasmacytoma. Apropos of an case with an immunofluorescence and electron microscopy study].

A 5.1/2-year-old girl presented with an isolated diffuse gingival hypertrophy and an abnormal mobility of teeth (alveolysis on roentgenograms). The diagnosis of a plasmacytoma was suspected after pathological and immunohistological examinations of a gingival biopsy. Plasma cells were secreting monoclonal immunoglobulins (heavy chain IgA and light chain lambda), quite different from polyclonal secretions of a reactive plasmacytosis. The electron microscopic study demonstrated polymorphic plasma cells (well-differentiated, dysplastic or undifferentiated cells). The isolated nature of this tumor was confirmed by biological tests and radiological investigations. The extremely rare diffuse gingival locations of extraosseous solitary plasmacytomas was proved by a review of the published litterature. The evolution of such gingival tumors is unknown. It seems to be variable, and, perhaps, diffuse myelomas may develop later on (as in other sites of extra-osseous solitary plasmacytoma).

Child, Preschool↗
PubMed1995

[Biological profiles of malignant gliomas].

Specific and recurring chromosomal and genetic alterations have been identified in gliomas and could described a model of tumoral progression from benin glioma to glioblastoma multiforme. However, the heterogeneity of profiles of molecular alterations that have been observed in gliomas seems to reflect the variety of clinical evolutions which characterise those tumors. Loss of genetic material on chromosomes 17, 9 and 19, then of chromosome 10 have been associated to pathogenesis of glioma and a pejorative prognostic value have been attributed to the alteration of chromosome 10. Gliomas also express growth factors and growth factors receptors that may be important in promoting tumor growth, like Epidermal growth factor (EGF), fibroblast growth factors (FGF) and vascular endothelial growth factor (VEGF). Tumoral invasion which characterise also gliomas, may involve proteases like plasminogen activators (PA) and metalloproteases, under the regulation of specific receptors and inhibitors. PA inhibitor type 1 (PAI1), associated to the most aggressive form of gliomas, may also participate to tumoral neoangiogenesis. Description and understanding of these alterations may contribute to develop new treatment modalities in gliomas.

Chromosome Aberrations↗
PubMed1978

Application of a microchemical technique to the elucidation of enzyme activity profiles within single human mammary tumors.

An ultramicrochemical technique has been adapted to the evolution of enzyme profiles within individual human mammary tumors. Tandem observation of adjacent stained and lyophilized sections permitted dissection of microgram quantities of freeze-dried material within confirmed regions of malignancy. Enzymes frequently monitored to examine glycolytic, respiratory, and metastatic capacity were microanalyzed successfully: lactic dehydrogenase (LDH), phosphoglucose isomerase (PGI), malate dehydrogenase (MDH), acid phosphatase (AP), aldolase (ALD), glucose-6-phosphate dehydrogenase (G6PDH), pyruvate kinase (PK), alpha-glycerophosphate dehydrogenase (alpha-GOPDH), hexokinase (HK), and phosphofructokinase (PRK). All enzyme activities were higher in infiltrating ductal carcinomas than in fibroadenomas. Extracts of tumor cells mixed in varying proportions with brain or muscle extracts of rat evidenced no modification of expected activity. The technical adaptation described provided a sensitive methodology to resolve problems of relication, profile analysis, sample quantity, and selectivity within heterogeneous tissues.

Acid Phosphatase↗
PubMed1986

Promotion of pulmonary metastasis in mice by bleomycin-induced endothelial injury.

The passage of circulating tumor cells across the vascular wall is an important step in the evolution of cancer metastases. Since tumor cells attach preferentially to subendothelial matrix at sites of endothelial injury and retraction in vitro, we have used an established in vivo model of pulmonary endothelial damage to examine the effects of endothelial injury on the localization and metastasis of circulating tumor cells in vivo. C57BL/6 mice were given a single i.v. dose of bleomycin (120 mg/kg) or multiple i.p. injections (10 mg/kg, twice weekly for 6 wk). Five days after the single injection or 4 days after the last i.p. injection, 2 X 10(5) [131I] iododeoxyuridine-labeled fibrosarcoma cells or unlabeled cells were injected i.v. Two to 8 times as many labeled cells were found in the lungs of bleomycin-treated animals after 24 h. Two and 3 wk after injecting unlabeled fibrosarcoma cells, 1.4 to 5 times more metastatic lung colonies were counted in bleomycin-treated animals than in controls. Morphometric analysis of histological sections demonstrated that the percentage of lung area occupied by tumor in bleomycin-treated animals was between 4 and 16 times that of controls. Analysis of bronchoalveolar lavage fluids demonstrated 5-fold increases of total protein content and leakage of previously injected 125l-labeled albumin, indicating increased endothelial permeability. Electron microscopic examination of lungs of bleomycin-treated mice demonstrated endothelial retraction with exposure of the underlying basement membrane. Electron microscopy of [3H]thymidine-labeled tumor cells, located by autoradiography, demonstrated their attachment to exposed basal lamina. Data from these experiments in vivo support the hypothesis that endothelial damage can facilitate the metastasis of circulating tumor cells.

Animals↗
PubMed1997

Hourglass thoracic lipoma of infancy: case report and review of the literature.

The authors present a case of lipoma in infancy. A 12-year-old boy was referred for an asymptomatic fast-growing thoracic tumor of 1-month evolution. A simple chest x-ray showed an intra- and extrathoracic mass of extrapleural localization. Ultrasound scan and computed tomography studies were performed, and the diagnosis of an hourglass lipoma was confirmed by a fine-needle aspiration biopsy. Surgical excision of the tumor was performed and the pathological study reassessed the initial diagnosis of lipoma. The thoracic lipoma is a benign disease and has a good evolution after surgery.

Child↗
PubMed2005

p53 isoforms can regulate p53 transcriptional activity.

The recently discovered p53-related genes, p73 and p63, express multiple splice variants and N-terminally truncated forms initiated from an alternative promoter in intron 3. To date, no alternative promoter and multiple splice variants have been described for the p53 gene. In this study, we show that p53 has a gene structure similar to the p73 and p63 genes. The human p53 gene contains an alternative promoter and transcribes multiple splice variants. We show that p53 variants are expressed in normal human tissue in a tissue-dependent manner. We determine that the alternative promoter is conserved through evolution from Drosophila to man, suggesting that the p53 family gene structure plays an essential role in the multiple activities of the p53 family members. Consistent with this hypothesis, p53 variants are differentially expressed in human breast tumors compared with normal breast tissue. We establish that p53beta can bind differentially to promoters and can enhance p53 target gene expression in a promoter-dependent manner, while Delta133p53 is dominant-negative toward full-length p53, inhibiting p53-mediated apoptosis. The differential expression of the p53 isoforms in human tumors may explain the difficulties in linking p53 status to the biological properties and drug sensitivity of human cancer.

Alternative Splicing↗
PubMed1997

[Computerized tomography-guided needle biopsy for the diagnosis of pulmonary nodules: analysis of a series of 41 patients].

This study was aimed at assessing percutaneous biopsy under computerized tomography (CT) guidance, its results in terms of diagnostic value, factors contributing to its complications or success, and its indications. Results obtained from a series of 41 patients and data from previous clinical trials were compared. Patients who were not eligible due to either poor physical condition or a tumor that could not be reached were not included into the study. Various factors, ie, the tumor location, the size of the lesion, the distance between the lesion and the thoracic wall, and the type (histological and/or cytological) of samples, were analyzed. Results were evaluated according to the disease evolution or pathological findings. Tumoral cells were found in 23 samples. Eighteen samples were negative for malignancy, with eight benign lesions and ten false negative. Complications that occurred just after the biopsy were recorded. Failures and complication factors were analyzed and compared to those already described. CT-guided needle biopsy is an admitted alternative to thoracotomy, even for small nodules deeply located. The use of this technique should be discussed when fiberoptic endoscopy leads to negative results. Various tumors cannot be reached using CT-guided needle biopsy and this technique is more efficacious for bulky nodules. The thickness of lung parenchyma passed through does not seem to change the risk of pneumothorax. The use of laser guidance might help locate the tumor with more accuracy.

Adult↗
PubMed2026

Decoding glioblastoma evolution and heterogeneity through mechanistic modeling: implications for clinical translation.

Glioblastoma (GBM) is one of the most aggressive and lethal primary brain tumors in adults, characterized by dynamic clonal evolution and extensive genomic, cellular, spatial, and microenvironmental heterogeneity. Multi-omics studies have revealed that GBM follows complex evolutionary trajectories involving genetic, epigenetic, transcriptional, and immune-microenvironmental remodeling as tumors grow, adapt to the brain microenvironment, and acquire therapeutic resistance. Increasing evidence suggests that GBM may originate from aberrant neural stem or progenitor cells, including those residing in the subventricular zone, and that glioblastoma stem cells (GSCs) contribute to tumor propagation, heterogeneity, and recurrence. A key conceptual challenge is to reconcile hierarchical cancer stem cell models, in which GSCs are viewed as relatively stable tumor-propagating subpopulations, with dynamic state plasticity models, in which stem-like properties can be reversibly acquired or lost during transitions among proneural-like, mesenchymal-like, invasive, and therapy-tolerant states. Recent advances in single-cell profiling, spatial transcriptomics, lineage tracing, organoid culture, 3D bioprinting, genetically engineered models, and artificial intelligence (AI)-assisted computational modeling have substantially improved the ability to study these processes. However, no currently available model fully recapitulates human GBM heterogeneity, recurrence, treatment history, and tumor-microenvironment interactions. Therefore, model selection should be guided by clearly defined mechanistic questions rather than by reliance on any single platform. This review summarizes current advances in in vitro, ex vivo, in vivo, and computational models for studying GBM evolution and heterogeneity, and discusses how integrated model pipelines may improve preclinical drug testing, treatment-response prediction, and precision neuro-oncology.

Humans↗
PubMed2000

Molecular bases for the development of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC).

Hepatocellular carcinoma (HCC) is the most common histological form of primary liver cancer; the tumor cells having retained features of hepatocytic differentiation. It is important to emphasize the heterogeneity of the histological background on which the tumor develops. Most HCCs complicate the evolution of an active or inactive cirrhosis. However, some tumors occur on livers with minimal histological changes; the prevalence of such cases varies from one geographical region to the other; being much higher in the southern half of Africa (around 40% of HCCs) than in Asia, America and Europe, where at least 90% of HCCs are associated in the cirrhosis. This heterogeneity is probably a reflection of different environmental and genetic factors. A large number of epidemiological and molecular studies have indeed clearly demonstrated the prime importance of environmental factors to the development of primary liver cancers in humans. Chronic hepatitis B (HBV) and C (HCV) infections are major risk factors. This review will mainly analyse the impact of chronic HBV infection but it is important to emphasize the potential synergistic effects between HBV and HCV, as well as between viral infections and other environmental factors, such as alcohol, chemical carcinogens (see review by Dr Wogan) and other, still poorly defined, hormonal factors which may account for the higher incidence of the tumor in man. Finally the review by Dr Buendia highlights the emerging issue of liver-cancer genetics.

Apoptosis↗
PubMed2026

Dynamic evolution of chaperone-mediated autophagy is associated with tumor microenvironment remodeling and prognostic stratification in lung adenocarcinoma: insights from single-cell transcriptomics, ensemble machine learning, and experimental validation.

BACKGROUND: Lung adenocarcinoma (LUAD) shows prognostic heterogeneity, and tumor-node-metastasis (TNM) staging is limited for individualized management. Chaperone-mediated autophagy (CMA) maintains proteostasis, but its role during adenocarcinoma in situ (AIS)-minimally invasive adenocarcinoma (MIA)-invasive adenocarcinoma (IAC) progression remains unclear. METHODS: Single-cell RNA sequencing (scRNA-seq) data from GSE189357 and bulk transcriptomes from The Cancer Genome Atlas (TCGA)-LUAD and Gene Expression Omnibus (GEO) cohorts were integrated. CMA activity, cell-cell communication, weighted gene co-expression network analysis (WGCNA), tumor-normal differential expression, machine-learning survival modeling, tumor microenvironment (TME) features, drug sensitivity, and EPC1 function were analyzed. RESULTS: CMA-high tumor epithelial cells increased from AIS (58.1%) to MIA (65.7%) but declined in IAC (44.4%; p < 0.001). CMA-low cells preferentially received fibroblast-derived extracellular matrix cues. A CMA-negatively correlated module identified 69 core genes. Random survival forest (RSF) performed best among 117 machine-learning combinations (mean concordance index > 0.873). High-risk patients had worse survival across cohorts, and the risk score was independently associated with overall survival (hazard ratio = 16.013, 95% confidence interval: 9.579-26.768, p < 0.001). High-risk tumors showed proliferative activation and M0 macrophage enrichment, whereas low-risk tumors showed stronger immune-related signaling. EPC1 overexpression suppressed malignant phenotypes in A549 cells. CONCLUSION: CMA dynamics are associated with stromal and immune remodeling during LUAD progression. A CMA-based model provides robust prognostic stratification and may offer a basis for future TME-guided studies.

Chaperone-mediated autophagy↗
PubMed2002

The structural nature of chromosomal instability in colon cancer cells.

Biological and genetic cell heterogeneity is a landmark of most colorectal cancers and provides a frame for tumor progression as an evolutional process. Classical models have hypothesized that increased genetic instability may contribute to modulating and shaping malignant transformation. This is true for the small subset of colorectal cancers displaying microsatellite instability. For the rest of colorectal tumors, numerical and/or structural chromosomal alterations are the most prominent outcome of genetic disruption. These observations have prompted some investigators to hypothesize about the presence of chromosomal instability in these cells. To characterize chromosomal instability in cancer cells, we have analyzed genetic clonal divergence in three colorectal cancer cell lines considered to be archetypes in cancer research (HCT116, LoVo, and SW480). A dynamic setting was designed to allow the calculation of mutation rates. Comprehensive analyses at the chromosomal level revealed distinctive patterns of genetic divergence. Aneuploid SW480 cells displayed high rates of structural alterations (>100-fold) as compared with near diploid LoVo cells. Numerical alterations also occurred more frequently in SW480 cells but at low rates as compared with rearrangements in the chromosomically unstable SW480 cells. These results strengthen the role of structural instability in the generation of genetic heterogeneity in colorectal cancer.

Chromosome Aberrations↗
PubMed2002

[Evolution of surgical treatments in patients with borderline ovarian tumors].

OBJECTIVES: The aim of this study was to evaluate a type and range of primary operation of patients with borderline ovarian tumours. MATERIAL AND METHODS: The analysis included 129 patients operated for ovarian tumours of borderline malignancy in the Gynaecological Department of Medical University of Gdańsk between 1978-2000. The two types of primary operations were defined: conservative and radical. The dependency of type of operation on such factors as age of patients, parity, stage and histological type on was assessed. RESULTS: The group of 42 patients were treated with conservative surgery and 87 underwent radical treatment. 36 from 42 patients (85.7%) were treated by USO. A conservative surgery was mainly performed in young patients with mucinous borderline tumor in stage IA. The risk of recurrence was 4.8% in the group of patients treated conservatively and 8.0% in group of patients treated radically. 5-years survival was, 98.2% and 87.2% respectively. CONCLUSIONS: The type of the primary operation depends on age, parity, stage and histological type of borderline ovarian tumors. A conservative surgery is a proper treatment for young women with borderline ovary tumours in stage Ia. For older, perimenopausal women TAH with BSO is suggested.

Adult↗
PubMed1986

The evolution of clinical molecular genetics. Neuroblastoma as a model tumor.

The use of cytogenetics and molecular genetics to elucidate mechanisms underlying the pathogenesis of human cancer has led to important advances in our understanding of cancer etiology. The identification of a reciprocal (11;22) translocation in peripheral neuroectodermal tumors and N-myc amplification in classical childhood neuroblastoma provides new guidelines for the diagnostic evaluation of peripheral nervous system tumors. New approaches to the staging of these tumors are likely to include the evaluation of genetic alterations associated with tumor progression. Also, new therapeutic approaches will be focused on the modification of specific molecular targets responsible for neoplastic growth.

Cell Line↗