Noninvasive discrimination of human normal cells and malignant tumor cells by phase-shifting laser microscopy

2010 ◽  
Vol 109 (5) ◽  
pp. 499-503 ◽  
Author(s):  
Ayako Tokumitsu ◽  
Shigeyuki Wakitani ◽  
Mutsumi Takagi
Keyword(s):  
Tumor Cells ◽  
Malignant Tumor ◽  
Phase Shifting ◽  
Normal Cells ◽  
Laser Microscopy

Cancer and Signaling Pathway Deregulation

2011 ◽  
pp. 369-379
Author(s):  
Yingchun Liu
Keyword(s):  
Cancer Patients ◽  
Tumor Cells ◽  
Malignant Tumor ◽  
Molecular Mechanisms ◽  
Complex Disease ◽  
Cancer Therapies ◽  
Normal Cells ◽  
Genetic Aberrations ◽  
Cancer Subtypes ◽  
Pathway Deregulation

Cancer is a complex disease that is associated with a variety of genetic aberrations. The diagnosis and treatment of cancer have been difficult because of poor understanding of cancer and lack of effective cancer therapies. Many studies have investigated cancer from different perspectives. It remains unclear what molecular mechanisms have triggered and sustained the transition of normal cells to malignant tumor cells in cancer patients. This chapter gives an introduction to the genetic aberrations associated with cancer and a brief view of the topics key to decode cancer, from identifying clinically relevant cancer subtypes to uncovering the pathways deregulated in particular subtypes of cancer.

CYTOLOGICAL AND IMMUNOCYTOCHEMICAL DIAGNOSIS OF TUMOR PLEURITIS

2017 ◽  
Vol 63 (6) ◽  
pp. 894-899
Author(s):  
Viktor Novik ◽  
A. Nefedova ◽  
Ye. Yakubo ◽  
O. Ivanov ◽  
Yekaterina Shalina ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Malignant Tumor ◽  
Cytological Study ◽  
False Negative ◽  
Unknown Primary ◽  
Cytological Examination ◽  
Immunocytochemical Studies ◽  
Negative Conclusion ◽  
Primary Localization

Cytological examination of smears from the sediment after centrifugation of pleural fluids was performed in 479 patients who underwent examination and treatment at our institution in 2014-2016. In 249 (52%) patients tumor cells were not detected in smears, in 230 (48%) observations a suspicion (28 observations) or a confident conclusion (202 observations) on the presence of malignant tumor cells in the exudates was cytologically expressed. In 38 cases immunocytochemical studies was additionally performed. In two observations a false-negative conclusion about the absence of tumor cells in smears was expressed. The sensitivity of the cytological study in the diagnosis of malignant pleuritis was 99.0%. Affirmative cytological conclusions on the presence of malignant pleuritis were given in 87.0% of observations, suspicious cytological responses - in 12.0% of cases. Immunocytochemical studies significantly expanded the possibilities of cytological research and were of great importance in the diagnosis of metastases of tumors of unknown primary localization.

The Role of Reactive Oxygen Species in Tumor Treatment and its Impact on Bone Marrow Hematopoiesis

2020 ◽  
Vol 21 (5) ◽  
pp. 477-498
Author(s):  
Yongfeng Chen ◽  
Xingjing Luo ◽  
Zhenyou Zou ◽  
Yong Liang
Keyword(s):  
Reactive Oxygen Species ◽  
Bone Marrow ◽  
Oxidative Damage ◽  
Tumor Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tumor Treatment ◽  
Normal Cells ◽  
Treatment And Prevention

Reactive oxygen species (ROS), an important molecule inducing oxidative stress in organisms, play a key role in tumorigenesis, tumor progression and recurrence. Recent findings on ROS have shown that ROS can be used to treat cancer as they accelerate the death of tumor cells. At present, pro-oxidant drugs that are intended to increase ROS levels of the tumor cells have been widely used in the clinic. However, ROS are a double-edged sword in the treatment of tumors. High levels of ROS induce not only the death of tumor cells but also oxidative damage to normal cells, especially bone marrow hemopoietic cells, which leads to bone marrow suppression and (or) other side effects, weak efficacy of tumor treatment and even threatening patients’ life. How to enhance the killing effect of ROS on tumor cells while avoiding oxidative damage to the normal cells has become an urgent issue. This study is a review of the latest progress in the role of ROS-mediated programmed death in tumor treatment and prevention and treatment of oxidative damage in bone marrow induced by ROS.

High-throughput concentration of rare malignant tumor cells from large-volume effusions by multistage inertial microfluidics

Lab on a Chip ◽  
2022 ◽  
Author(s):  
Nan Xiang ◽  
Zhonghua Ni
Keyword(s):  
Tumor Cells ◽  
High Throughput ◽  
Malignant Tumor ◽  
Large Volume ◽  
Concentration Factor ◽  
Pleural Effusions ◽  
Inertial Microfluidics ◽  
Low Concentration ◽  
Malignant Pleural Effusions ◽  
On Chip

On-chip concentration of rare malignant tumor cells (MTCs) in malignant pleural effusions (MPEs) with a large volume is challenging. Previous microfluidic concentrators suffer from a low concentration factor (CF) and...

scholarly journals Preferential expression of double-stranded ribonucleic acid in tumor versus normal cells: biological and clinical implications

Blood ◽  
1985 ◽  
Vol 66 (1) ◽  
pp. 39-46
Author(s):  
HM Kantarjian ◽  
B Barlogie ◽  
M Pershouse ◽  
D Swartzendruber ◽  
MJ Keating ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Cell Lines ◽  
Ribonucleic Acid ◽  
Flow Cytometric Analysis ◽  
Myelogenous Leukemia ◽  
Cycle Phase ◽  
Low Grade ◽  
Normal Cells ◽  
Normal Peripheral Blood ◽  
Rna Content

In an effort to develop a new tumor marker suitable for flow cytometric analysis, we examined the value of double-stranded ribonucleic acid (ds- RNA) measurements using propidium iodide after DN'ase treatment. Cellular ds-RNA content was evaluated both in experimental cell lines and in clinical specimens. Higher levels of ds-RNA were present in tumor cells as compared with normal cells. In tumor cells, fluorescence was intensely localized in the nucleolus and was more diffuse in the cytoplasm. Change of less than 10% in the ds-RNA levels was observed in cell lines as a function of cytokinetic determinants such as cycle phase, culture age, and cycle traverse rate. Tumor differentiation by dimethylsulfoxide resulted in a significant decrease in cellular ds-RNA content. For quantitative comparison of clinical material, a ds-RNA excess was defined in relationship to normal peripheral blood lymphocytes. ds-RNA excess greater than 30% was observed in only one of 34 normal tissues (3%) as compared with 124 of 201 neoplastic tissue samples (62%). This incidence was higher in patients with acute leukemia (76%), high-grade and intermediate-grade lymphoma (75%), and high tumor stage myeloma (83%), as compared with chronic leukemia (20%), low-grade lymphoma (25%), and intermediate or low tumor mass myeloma (43%). Prognostically, a high pretreatment ds-RNA excess in myeloma was associated with a lower remission rate. The persistence of ds-RNA excess in the bone marrow of patients with acute myelogenous leukemia in remission predicted for a shorter remission duration (seven v 22 months; P = .05). We conclude that ds-RNA excess, as readily measured objectively and quantitatively by flow cytometry, may have important diagnostic and prognostic implications for the management of patients with malignant disease.

scholarly journals VE-PTP participates in vasculogenic mimicry by preventing autophagic degradation of VE-cadherin

2019 ◽  
Author(s):  
Daniel Delgado-Bellido ◽  
Concepción Bueno-Galera ◽  
Angel Garcia-Diaz ◽  
F. Javier Oliver
Keyword(s):  
Endothelial Cells ◽  
Malignant Melanoma ◽  
Tumor Cells ◽  
Malignant Tumor ◽  
Vasculogenic Mimicry ◽  
P120 Catenin ◽  
Human Malignant Melanoma ◽  
Aberrant Phenotype ◽  
Autophagic Degradation ◽  
Vascular Expression

AbstractAberrant extra-vascular expression of VE-cadherin has been observed in metastasis associated with Vasculogenic Mimicry (VM); we have recently shown that in VM prone (VM+) tumor cells VE-cadherin is mainly in the form of pVE-cadherin in Y658 allowing an increased plasticity that potentiates VM development. As excessive VE-cadherin phosphorylation is regulated by the phosphatase VEPTP in endothelial cells in the current study we analysed its role in this aberrant phenotype in malignant tumor cells. We show that human malignant melanoma cells VM+, also express VE-PTP although at lower levels than endothelial cells. The complex VE-PTP/VE-Cadherin/p120-catenin act as a safeguard to prevent VE-cadherin degradation by autophagy. Indeed, silencing of VE-PTP results in complete degradation of VE-cadherin with the features of autophagy and increases the global p120 tyrosine phosphorylation status. In summary, we show that VE-PTP is involved in VM formation and disruption of VE-PTP/VE-Cadherin/p120 complex results in enhanced autophagy in aggressive VM+ cells.

scholarly journals Genes in Tumor Formation

2019 ◽  
Vol 3 (2) ◽  
pp. 18-22
Author(s):  
Isolde Riede
Keyword(s):  
Tumor Cells ◽  
Genome Instability ◽  
Tumor Formation ◽  
Normal Cells ◽  
Tumor Supressors ◽  
Somatic Pairing ◽  
Definition Of

With the definition of four gene classes, all differences between tumor cells and normal cells can be explained. Proliferative mutations induce a shortcut, forcing the cell to divide. They allow replication without control, induce somatic pairing defects of chromosomes and genome instability. Intact Tumor Supressors or mutant Switch Functions can inhibit this process. Oncogene mutations optimize the growth of the cells.

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