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PubMedDate not supplied

[Data concerning a case of long-term, asymptomatic, calcified cerebral tumor with late evolution of olfactory meningioma].

In a lot of 3 patients with olfactory meningioma, one patient drew particular attention by the particularities of its evolution, which was asymptomatic for a long time and atypical. The disease started at the age of 38 with asthenia, headaches, dizziness and X-ray images of left parasellar calcified brain tumour, without neurological signs of a focus at any of the repeated clinical or paraclinical examinations. After eight years focal signs appears: left pyramidal irritation, absences, left hyposmia, without altered visual acuity or conclusive scintigraphic and EEG alterations. Left carotid arteriography indicated a space-occupying process. The disease progressed slowly with left hemiparesis and corresponding effects. A diagnosis of "left olfactory meningioma" was established in the Neurosurgical Clinic, Bucharest. The situation deteriorated in 1977: total left anosmia, Jacksonian seizures, sometimes generalized, uncinate fits, paroxysmal headaches, amnesia disturbances and marked right hemiparesis. Recent scintigraphic and EEG alterations likewise lent support to a diagnosis of brain tumour. The existence of calcified, asymptomatic, trailing brain tumours, with an atypical and late evolution of unilateral olfactory meningioma, without Foster-Kennedy syndrome, demands from the beginning close surveillance and complex investigations, since a prolonged absence of anosmia and focal phenomena does not exclude the possibility of a meningioma of the olfactory groove, and may often lead to errors of diagnosis.

Adult↗
PubMed1998

[Giant mesenchymal tumor of the vulva with atypical clinical evolution].

Mixed mesenchymal tumors of the vulva are rare lesions. On other hand, aggressive angiomyxoma is a recently characterized neoplasm occurring principally in the pelvic soft-tissues and showing propensity for local recurrence. The benign soft-tissue tumors are small than malign neoplasm, mimicking and often are misdiagnosed as cysts of Bartholin's gland. In this report we describe one case of a benign, giant and atypical mixed mesenchymal tumor of the vulva and its particular clinical characteristics.

Adolescent↗
PubMed2006

Modeling the effects of vasculature evolution on early brain tumor growth.

Mathematical modeling of both tumor growth and angiogenesis have been active areas of research for the past several decades. Such models can be classified into one of two categories: those that analyze the remodeling of the vasculature while ignoring changes in the tumor mass, and those that predict tumor expansion in the presence of a non-evolving vasculature. However, it is well accepted that vasculature remodeling and tumor growth strongly depend on one another. For this reason, we have developed a two-dimensional hybrid cellular automaton model of early brain tumor growth that couples the remodeling of the microvasculature with the evolution of the tumor mass. A system of reaction-diffusion equations has been developed to track the concentration of vascular endothelial growth factor (VEGF), Ang-1, Ang-2, their receptors and their complexes in space and time. The properties of the vasculature and hence of each cell are determined by the relative concentrations of these key angiogenic factors. The model exhibits an angiogenic switch consistent with experimental observations on the upregulation of angiogenesis. Particularly, we show that if the pathways that produce and respond to VEGF and the angiopoietins are properly functioning, angiogenesis is initiated and a tumor can grow to a macroscopic size. However, if the VEGF pathway is inhibited, angiogenesis does not occur and tumor growth is thwarted beyond 1-2mm in size. Furthermore, we show that tumor expansion can occur in well-vascularized environments even when angiogenesis is inhibited, suggesting that anti-angiogenic therapies may not be sufficient to eliminate a population of actively dividing malignant cells.

Algorithms↗
PubMed2002

MRI of high-grade astrocytic tumors: early appearance and evolution.

The clinical management and prognosis of patients with diffusely infiltrating astrocytomas are dependent on neuropathological grading of the tumors. The characteristics of MR images of high-grade astrocytic tumors are well known, but the early MRI appearance and the MRI evolution of high-grade astrocytic tumors have rarely been examined. We retrospectively reviewed MR images obtained from 4 months to 3 years and 3 months before admission, as well as MR images on admission, for five patients with pathologically proven high-grade astrocytic tumors (two glioblastomas and three anaplastic astrocytomas). In two patients, neoplastic lesions were not detectable on initial MRI, even retrospectively. In the remaining three patients, however, hyperintense areas with little or no mass effect were demonstrated on T2-weighted imaging. These lesions were misinterpreted as non-neoplastic processes, such as ischemic lesion or infarction, or demyelinating processes. All tumors showed gadolinium enhancement on admission, that emerged from the previously existing hyperintense areas on T2-weighted images without gadolinium enhancement, except for one de novo glioblastoma. Development of a small central cyst without gadolinium enhancement was demonstrated in one case before the emergence of an enhancing area.

Adult↗
PubMed2004

Evolution of an orbital apex tumor over a decade.

We report the evolution of an orbital apex tumor that underwent spontaneous regression, followed several years later by rapid growth and loss of vision. A turkey farmer had a right apical lesion, initially thought to be an optic nerve meningioma. The mass spontaneously regressed over 2 years, with marked improvement of vision. Eight years later, the patient presented with loss of light perception and severe proptosis of the right eye from a massive orbital tumor that extended in the cavernous sinus. An eyelid-sparing orbital exenteration was performed. The pathologic diagnosis was diffuse large cell lymphoma. This case demonstrates that non-Hodgkin lymphoma of the orbital apex may resolve spontaneously or it may enlarge rapidly, degenerating into more aggressive forms.

Aged↗
PubMed2003

Genomic instability and tumor-specific alterations in oral squamous cell carcinomas assessed by inter-(simple sequence repeat) PCR.

PURPOSE: Genomic instability plays a major role in the genesis and progression of tumors, and in the evolution of tumor heterogeneity. To determine the role of genomic instability in the genesis and progression of oral cancer, we assessed the extent of genomic alterations in oral squamous cell carcinomas (OSCCs). EXPERIMENTAL DESIGN: We used the recently developed inter-(simple sequence repeat) PCR technique to quantitate genomic instability using matched tumor and normal OSCC samples (n = 25). The inter-repeat region bands of similar molecular size observed to be altered in more than one case were sequenced and analyzed to identify probable OSSC-associated specific genetic lesions. RESULTS: Of the four base-anchored, dinucleotide repeat-based primers used for the study, the most informative profile in OSCCs was generated by the (CA)(8)RG primer. Measurement of genomic instability index using the (CA)(8)RG primer revealed a high incidence of genomic instability in OSCCs. No significant correlation between the extent of alterations and stage or location of the tumor was observed. Sequencing analysis of the altered bands revealed gains/losses in several chromosomal regions. Of the matched tumor and corresponding normal tissue DNA studied, hitherto unreported losses were seen in 11p15 and 17q25 chromosomal regions. Sequencing of some of the tumor-specific altered regions indicated that they code for regions of UDP-GalNAc and hRAD 17 genes, which were lost (deleted) in oral cancer. CONCLUSIONS: Our results indicate that the extent of genomic instability in OSCC is not correlated to the tumor stage or location. For the first time, we have shown that chromosomal alterations detected by inter-(simple sequence repeat) PCR could be correlated to genes associated with cancer development.

Adult↗
PubMed1981

[Effects of the contamination by polychlorobiphenyls (PCBs) on the growth of the Ehrlich tumor in mice (author's transl)].

The effects of a 3-month experimental contamination with a commercial mixture of PCBs, DP5 (corresponding to Aroclor 1254) have been studied on groups of 25 SWISS female mice, at levels of 0, 10, 50 and 250 ppm added at feeding. After subcutaneous injection of 0,2 ml of Ehrlich's tumoral ascites liquid, the evolution of tumors as well as the mortality level, were different in the treated groups as compared to the control group. The percentages of mortality due to tumors were the following: control (0 ppm) = 50% 10 ppm = 5% 50 ppm = 5% 250 ppm = 35% Thus, contamination by PCBs seems to have protected these mice against the Ehrlich tumor. No decrease in body weight was noted neither were differences in size or appearance of the thymus and the spleen in the treated mice; an evident liver hypertrophy was noted in all PCB treated mice.

Animals↗
PubMed2026

Genomic characterization of aggressiveness in pituitary neuroendocrine tumors.

BACKGROUND: Aggressive evolution of PitNETs is rare; metastatic spread is even more. Defining aggressiveness and malignancy is challenging, subsequently hard to predict, and to understand. The aim was to provide a molecular definition of aggressiveness using genomic approaches. METHODS: PitNETs from 206 patients were included. Associations between 9 clinicopathological features of aggressiveness and PitNETs' omics were explored. Omics included transcriptome, DNA methylation, chromosomal alterations, and mutations. Clonal tumor evolution was monitored in 7 patients. RESULTS: Among the 9 clinicopathological features of aggressiveness, only rapid progression, progression after radiotherapy, Ki67/MIB1 proliferation index ≥10%, temozolomide treatment, metastases, and specific death were associated with specific omics signatures, while tumour maximal diameter ≥40 mm, cavernous, and sphenoid invasion were not. The omic signatures associated with these features of aggressiveness overlapped but remained distinct between corticotroph and mammo-somato-thyrotroph lineages. For each lineage, a common signature of aggressiveness was identified, associating a proliferative transcriptome signature and DNA hypermethylation. Alterations in specific genes were associated with aggressive features, including a novel PitNET gene, LRP1B, and known cancer genes (TP53, CDKN2A), while USP8 and GNAS alterations were not. Integration of gene alterations with methylome and transcriptome signatures isolated a subset of molecularly aggressive PitNETs. Molecular signatures were stable during the course of the disease, despite evolution toward aggressiveness and potential clonal divergence. CONCLUSION: This systematic analysis of clinicopathological features of aggressiveness using an integrated multiomic approach establishes a histomolecular definition of aggressiveness in PitNETs. Prospective cohort studies are needed to validate these molecular signatures and establish their prognostic value.

Humans↗
PubMedDate not supplied

Effect of homologous tumor DNA on the evolution of SV40-induced hamster sarcoma.

DNA extracted from SV40-induced hamster sarcoma (SV40--HS DNA) increased the survival length of animals carrying the homologous tumor and--in some cases--inhibited the development of the tumor. The efficacy of the preparation was directly proportional to the number of administrations; it did not necessarily depend on the amount of SV40--HS DNA per dose. SV40 DNA had no favourable effect on the evolution of the SV40-induced tumor, which suggests that viral DNA does not represent the active component of the SV40--HS DNA preparations. Some possible mechanisms of the effect of homologous tumor preparations are discussed.

Animals↗
PubMed2026

Overcoming cancer resistance in pancreatic cancer: toward dynamic precision oncology.

Pancreatic ductal adenocarcinoma (PDAC) remains a highly lethal malignancy, largely because of its profound and evolving therapeutic resistance. Resistance is not determined by a single molecular alteration but arises from interconnected mechanisms, including intrinsic resistance, treatment-induced adaptive resistance, acquired resistance, genomic evolution, clonal selection, cancer stemness, phenotypic plasticity, metabolic adaptation, and tumor microenvironment-mediated effects. Emerging therapeutic approaches targeting KRAS/RAS signaling, stromal and immune components, metabolic dependencies, and DNA damage repair pathways offer opportunities to address these mechanisms, although durable efficacy remains limited by biological heterogeneity and adaptive responses. In this review, we examine therapeutic resistance as an evolutionary and multidimensional process and summarize emerging strategies for overcoming resistance. We further propose a Dynamic Precision Oncology (DPO) framework that extends conventional precision oncology beyond baseline molecular profiling by integrating longitudinal assessment of tumor genomics, circulating tumor DNA, CA19-9, imaging, radiomics, and clinical characteristics. This framework emphasizes iterative detection and characterization of emerging resistance, mechanism-informed treatment adaptation, and subsequent reassessment rather than automatic treatment modification based on a single biomarker. DPO may provide a conceptual framework for integrating evolving tumor biology into treatment decision-making, while prospective studies are needed to validate biomarkers, define actionable thresholds, and determine whether longitudinal resistance-guided strategies improve clinical outcomes in PDAC.

Humans↗
PubMed2026

KDM6A loss enhances oxidative phosphorylation uncovering tissue-level convergent evolution.

The tumor suppressor KDM6A/UTX, a histone demethylase and a 2-oxoglutarate-dependent dioxygenase, is frequently lost in many cancer types. We show that KDM6A loss pervasively activates oxidative phosphorylation in several solid tumors, generating a pseudo-hyperoxic environment, opposite from the pseudo-hypoxia observed in VHL-mutated renal carcinomas. Mechanistically, KDM6A sustains the expression of the coil-coil domain gene CCDC3, which inhibits CREB1-driven transcription of the mitochondrial regulator PPARGC1A. In the hematological cancer multiple myeloma where KDM6A is frequently deleted, its loss similarly promotes oxidative phosphorylation, but via an alternative mechanism: the increased transfer of mitochondria from stromal to myeloma cells via tunneling nanotubes, triggered by the loss of the mTORC1 inhibitor TRAF3IP3. Beyond cancer, KDM6A regulates oxidative phosphorylation also during development and in adult tissues, engaging either the CCDC3-CREB1 or the TRAF3IP3-mTORC1 pathways. These mutually exclusive associations suggest a tissue-level convergent evolution, positioning KDM6A as a central modulator of mitochondrial activity through context-specific partners.

Journal Article↗