neoplastic cell
Recently Published Documents


TOTAL DOCUMENTS

390
(FIVE YEARS 85)

H-INDEX

45
(FIVE YEARS 4)

2022 ◽  
Vol 23 (2) ◽  
pp. 969
Author(s):  
Michał Wągrodzki ◽  
Andrzej Tysarowski ◽  
Katarzyna Seliga ◽  
Aneta Wojnowska ◽  
Maria Stepaniuk ◽  
...  

To validate the reliability and implementation of an objective diagnostic method for giant cell tumour of bone (GCTB). H3-3A gene mutation testing was performed using two different methods, Sanger sequencing and immunohistochemical (IHC) assays. A total of 214 patients, including 120 with GCTB and 94 with other giant cell-rich bone lesions, participated in the study. Sanger sequencing and IHC with anti-histone H3.3 G34W and G34V antibodies were performed on formalin-fixed, paraffin-embedded tissues, which were previously decalcified in EDTA if needed. The sensitivity and specificity of the molecular method was 100% (95% CI: 96.97–100%) and 100% (95% CI: 96.15–100%), respectively. The sensitivity and specificity of IHC was 94.32% (95% CI: 87.24–98.13%) and 100% (95% CI: 93.94–100.0%), respectively. P.G35 mutations were discovered in 2/9 (22.2%) secondary malignant GCTBs and 9/13 (69.2%) GCTB after denosumab treatment. We confirmed in a large series of patients that evaluation of H3-3A mutational status using direct sequencing is a reliable tool for diagnosing GCTB, and it should be incorporated into the diagnostic algorithm. Additionally, we discovered IHC can be used as a screening tool. Proper tissue processing and decalcification are necessary. The presence of the H3-3A mutation did not exclude malignant GCTB. Denosumab did not eradicate the neoplastic cell population of GCTB.


2022 ◽  
Vol 12 (1) ◽  
pp. 109
Author(s):  
Lucian Mărginean ◽  
Paul Andrei Ștefan ◽  
Andrei Lebovici ◽  
Iulian Opincariu ◽  
Csaba Csutak ◽  
...  

Due to their similar imaging features, high-grade gliomas (HGGs) and solitary brain metastases (BMs) can be easily misclassified. The peritumoral zone (PZ) of HGGs develops neoplastic cell infiltration, while in BMs the PZ contains pure vasogenic edema. As the two PZs cannot be differentiated macroscopically, this study investigated whether computed tomography (CT)-based texture analysis (TA) of the PZ can reflect the histological difference between the two entities. Thirty-six patients with solitary brain tumors (HGGs, n = 17; BMs, n = 19) that underwent CT examinations were retrospectively included in this pilot study. TA of the PZ was analyzed using dedicated software (MaZda version 5). Univariate, multivariate, and receiver operating characteristics analyses were used to identify the best-suited parameters for distinguishing between the two groups. Seven texture parameters were able to differentiate between HGGs and BMs with variable sensitivity (56.67–96.67%) and specificity (69.23–100%) rates. Their combined ability successfully identified HGGs with 77.9–99.2% sensitivity and 75.3–100% specificity. In conclusion, the CT-based TA can be a useful tool for differentiating between primary and secondary malignancies. The TA features indicate a more heterogenous content of the HGGs’ PZ, possibly due to the local infiltration of neoplastic cells.


2022 ◽  
pp. 52-113
Author(s):  
Abdullah A. A. Alghamdi ◽  
Amr Ahmed WalyEldeen ◽  
Sherif Abdelaziz Ibrahim

In cancer, angiogenesis is a hallmark necessary to supply sufficient nutrients for tumor growth and metastasis to distant sites. Therefore, targeting tumor angiogenesis emerges as an attractive therapeutic modality to retard neoplastic cell growth and dissemination using classes of anti-angiogenic drugs. However, multiple administrations of these drugs show adverse effects, precluding their long-term usage. Conventional chemotherapeutic drugs, natural compounds, carbon-based materials, inorganic and metallic elements, genes, siRNAs, shRNAs, and microRNAs can be incorporated into nanovehicles (e.g. polymers) for delivery to specific targets. This chapter reviews angiogenesis and the underlying molecular mechanisms that regulate this process. Furthermore, this chapter provides an overview on different formulations of nanoparticles or nanovectors that employed to combat cancer, with a special focus on their therapeutic potentials in the context of the suppressive effects on tumor angiogenesis process using in vitro and in vivo models of different tumor entities.


2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi132-vi133
Author(s):  
Hamed Akbari ◽  
Suyash Mohan ◽  
Jose A Garcia ◽  
Anahita Fathi Kazerooni ◽  
Chiharu Sako ◽  
...  

Abstract PURPOSE Multi-parametric MRI and artificial intelligence (AI) methods were previously used to predict peritumoral neoplastic cell infiltration and risk of future recurrence in glioblastoma, in single-institution studies. We hypothesize that important characteristics of peritumoral tissue heterogeneity captured, engineered/selected, and quantified by these methods relate to predictions generalizable in the multi-institutional ReSPOND (Radiomics Signatures for PrecisiON Diagnostics) consortium. METHODS To support further development, generalization, and clinical translation of our proposed method, we trained the AI model on a retrospective cohort of 29 de novo glioblastoma patients from the Hospital of the University of Pennsylvania (UPenn) (Male/Female:20/9, age:22-78 years) followed by evaluation on a prospective multi-institutional cohort of 84 glioblastoma patients (Male/Female:51/33, age:34-89 years) from Case Western Reserve University/University Hospitals (CWRU/UH, 25), New York University (NYU, 13), Ohio State University (OSU, 13), University Hospital Río Hortega (RH, 2), and UPenn (31). Features extracted from pre-resection MRI (T1, T1-Gd, T2, T2-FLAIR, ADC) were used to build our model predicting the spatial pattern of subsequent tumor recurrence. These predictions were evaluated against regions of pathology-confirmed post-resection recurrence. RESULTS Our model predicted the locations that later harbored tumor recurrence with sensitivity 83%, AUC 0.83 (99% CI, 0.73-0.93), and odds ratio 7.23 (99% CI, 7.09-7.37) in the prospective cohort. Odds ratio (99% CI)/AUC(99% CI) per institute were: CWRU/UH, 7.8(7.6-8.1)/0.82(0.75-0.89); NYU, 3.5(3.3-3.6)/0.84(074-0.93); OSU, 7.9(7.6-8.3)/0.8(0.67-0.94); RH, 22.7(20-25.1)/0.94(0.27-1); UPenn, 7.1(6.8-7.3)/0.83(0.76-0.91). CONCLUSION This is the first study that provides relatively extensive multi-institutional validated evidence that AI can provide good predictions of peritumoral neoplastic cell infiltration and future recurrence, by dissecting the MRI signal heterogeneity in peritumoral tissue. Our analyses leveraged the unique dataset of the ReSPOND consortium, which aims to develop and evaluate AI-based biomarkers for individualized prediction and prognostication, by moving from single-institution studies to generalizable, well-validated multi-institutional predictive biomarkers.


2021 ◽  
Vol 15 (3) ◽  
pp. 192-197
Author(s):  
Fernanda de Lima Correa ◽  
Luciana Wolfran ◽  
Aline de Marco Viott ◽  
Juliana das Chagas Goulart ◽  
Flávio Shigueru Jojima ◽  
...  

The transmissible venereal tumour (TVT) is one of the most frequent neoplasias in dogs. This tumour has specific characteristics, and it is exclusively of canines. Its transmission occurs through viable neoplastic cell transplantation when in contact with mucosa or unhealthy skin and rarely metastasise. This paper aims to report a rare presentation of pulmonary metastasis of widespread transmissible venereal tumours in a Blue Heeler dog. The patient was cachectic, dyspnoeic, and dehydrated and had multiple skin and pharynx nodulations. The cytology of all cutaneous nodulations showed round vacuolated cells with large eccentric nuclei and loose chromatin, which is compatible with TVT’s microscopic characteristics. Owing to the clinical evolution and reserved prognosis, the patient was euthanized. Necroscopy revealed a mass in the right pulmonary caudal lobe. The mass showed the same histopathologic characteristic of the others: not encapsulated infiltrative neoplastic proliferation of round vacuolated cells. The atypical manifestation of cutaneous metastasis and mainly pulmonary metastasis, in this case, denote the importance of TVT inclusion as a differential in cutaneous neoplasia, even if they show distant organ metastasis. Therefore, it emphasised the importance of cytology and histology in the diagnosis of nodular affections.


2021 ◽  
Vol 12 ◽  
Author(s):  
Edith Uetz-von Allmen ◽  
Guerric P. B. Samson ◽  
Vladimir Purvanov ◽  
Takahiro Maeda ◽  
Daniel F. Legler

Dendritic cells (DCs) are potent and versatile professional antigen-presenting cells and central for the induction of adaptive immunity. The ability to migrate and transport peripherally acquired antigens to draining lymph nodes for subsequent cognate T cell priming is a key feature of DCs. Consequently, DC-based immunotherapies are used to elicit tumor-antigen specific T cell responses in cancer patients. Understanding chemokine-guided DC migration is critical to explore DCs as cellular vaccines for immunotherapeutic approaches. Currently, research is hampered by the lack of appropriate human cellular model systems to effectively study spatio-temporal signaling and CCR7-driven migration of human DCs. Here, we report that the previously established human neoplastic cell line CAL-1 expresses the human DC surface antigens CD11c and HLA-DR together with co-stimulatory molecules. Importantly, if exposed for three days to GM-CSF, CAL-1 cells induce the endogenous expression of the chemokine receptor CCR7 upon encountering the clinically approved TLR7/8 agonist Resiquimod R848 and readily migrate along chemokine gradients. Further, we demonstrate that CAL-1 cells can be genetically modified to express fluorescent (GFP)-tagged reporter proteins to study and visualize signaling or can be gene-edited using CRISPR/Cas9. Hence, we herein present the human CAL-1 cell line as versatile and valuable cellular model system to effectively study human DC migration and signaling.


Author(s):  
Henna Myllymäki ◽  
Jeanette Astorga Johansson ◽  
Estefania Grados Porro ◽  
Abigail Elliot ◽  
Tessa Moses ◽  
...  

Metabolic rewiring is a critical hallmark of tumorigenesis and is essential for the development of cancer. Although many key features of metabolic alteration that are crucial for tumor cell survival, proliferation and progression have been identified, these are obtained from studies with established tumors and cancer cell lines. However, information on the essential metabolic changes that occur during pre-neoplastic cell (PNC) development that enables its progression to full blown tumor is still lacking. Here, we present an untargeted metabolomics analysis of human oncogene HRASG12V induced PNC development, using a transgenic inducible zebrafish larval skin development model. By comparison with normal sibling controls, we identified six metabolic pathways that are significantly altered during PNC development in the skin. Amongst these altered pathways are pyrimidine, purine and amino acid metabolism that are common to the cancer metabolic changes that support rapid cell proliferation and growth. Our data also suggest alterations in post transcriptional modification of RNAs that might play a role in PNC development. Our study provides a proof of principle work flow for identifying metabolic alterations during PNC development driven by an oncogenic mutation. In the future, this approach could be combined with transcriptomic or proteomic approaches to establish the detailed interaction between signaling networks and cellular metabolic pathways that occur at the onset of tumor progression.


2021 ◽  
Vol 11 (43) ◽  
pp. 90-100
Author(s):  
Akhmad Madaminov ◽  
Akbar Khasanov ◽  
Shuhrat Khatamov ◽  
Otabek Abdurakhmonov ◽  
Anvar Amonov ◽  
...  

Abstract According to scientific data, cancer is a very ancient disease, and along with the perfection of humanity it becomes more progressive. The development of technologies that detect molecular changes in the pathogenesis and subsequent development of carcinogenesis has led to the beginning of a new era in oncology. The cell cycle is tightly controlled by a group of protein kinases, including cyclin and cyclin-dependent kinases. These events occur in a strictly regulated time sequence supported by consistent restriction points. p53, p21, p16, retinoblastoma (and other proteins), cyclins and cyclin-related kinases repair DNA before the cell cycle enters the phase of synthesis and mitosis. Loss of regulatory activity of p53 and pRB, stable activation of E2F stimulates uncontrolled cell proliferation, leading to neoplastic cell growth. The Ras/Raf/MEK/ERK signalling pathway is also a complex network of sequentially activated proteins that play a major role in the onset and development of cancer. It can regulate not only the biological functions, such as cell proliferation, cycle regulation, cell differentiation, apoptosis and tissue formation, but it is also associated with tumor development. Stable mutations in the genome or defects in the epigenome lead to dysregulation in the normal biological cycle of the cell, underlying DNA chain damage or dysfunction in the control system, determined by various types of carcinogenic factors, both known and unknown.


Author(s):  
Jutishna Bora ◽  
Ishani Saha

Cancer genetics is the scientific discipline that investigates the genes and pathways that drive the development of cancer. Cancer geneticists use several approaches including the analysis of the genomes of cancer patients, and that of their tumors, to identify cancer genes. These studies are performed along with experiments in in vitro and in vivo models to decipher the mechanisms that drive tumorigenesis. Cancer geneticists aim to identify cancer genes, that when mutated, contribute towards cancer development by promoting tumor cell growth and by conferring upon a neoplastic cell the ability to evade the cell cycle and apoptosis checkpoints that might normally control their growth. Cancer geneticists are also interested in the networks and pathways that contribute to tumor development and the way cancer genes work together to market tumor evolution.


Cancers ◽  
2021 ◽  
Vol 13 (14) ◽  
pp. 3466
Author(s):  
Ismahane Belhabib ◽  
Sonia Zaghdoudi ◽  
Claire Lac ◽  
Corinne Bousquet ◽  
Christine Jean

Solid cancer progression is dictated by neoplastic cell features and pro-tumoral crosstalks with their microenvironment. Stroma modifications, such as fibroblast activation into cancer-associated fibroblasts (CAFs) and extracellular matrix (ECM) remodeling, are now recognized as critical events for cancer progression and as potential therapeutic or diagnostic targets. The recent appreciation of the key, complex and multiple roles of the ECM in cancer and of the CAF diversity, has revolutionized the field and raised innovative but challenging questions. Here, we rapidly present CAF heterogeneity in link with their specific ECM remodeling features observed in cancer, before developing each of the impacts of such ECM modifications on tumor progression (survival, angiogenesis, pre-metastatic niche, chemoresistance, etc.), and on patient prognosis. Finally, based on preclinical studies and recent results obtained from clinical trials, we highlight key mechanisms or proteins that are, or may be, used as potential therapeutic or diagnostic targets, and we report and discuss benefits, disappointments, or even failures, of recently reported stroma-targeting strategies.


Sign in / Sign up

Export Citation Format

Share Document