scholarly journals Cytological research of exophytic tumors of the bronchi and the growth pattern of lung cancer

2021 ◽  
Vol 4 ◽  
pp. 26-31
Author(s):  
Lidiya Bolgova ◽  
Tamara Tuganova ◽  
Anna Ponomarenko
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Growth Pattern ◽  
Treatment Method ◽  
Bronchial Mucosa ◽  
Preoperative Period ◽  
Entire Surface ◽  
Cytological Examination ◽  
Optimal Material

Background. The study of the growth of lung cancer (LC) has an important clinical significance for morphological verification, the choice of the treatment method, and the determining of prognosis. Investigation of this question allows to clarify the histogenesis of LC. The aim of our study was to compare the results of cytological studies of the material obtained during flexible bronchoscopy (FBS) and scrapings from the operated tumors of the bronchi to clarify the nature of LC growth. Design. To study the growth of tumors in the bronchi in relation to the bronchial mucosa, the cytological examination of the material obtained by FBS and scrapings from the surface of the operated bronchial tumors of 31 patients has been performed. Results. In the preoperative period, in the material of FBS, tumor cells were found only in 1/3 of patients. To obtain the optimal material from exophytic tumors of the bronchus, scrapings were carried out from the entire surface surgical material of the same patients. Cytological preparations of the obtained scrapings confirmed the presence of cancer cells in more than 1/3 of patients. In the rest of the observations, scrapings from the tumor surface contained only cells of the cylindrical epithelium. Conclusions. The cytological investigations made it possible to state that in 2/3 scrapings from surfaces of exophytic tumors of the bronchus contained only cells of the cylindrical epithelium; therefore, the tumors grow under it.

Synergy of nanodiamond-doxorubicin conjugates and PD-L1 blockade effectively turns tumor associated macrophages against tumor cells

2021 ◽  
Author(s):  
Huazhen Xu ◽  
Tongfei Li ◽  
Chao Wang ◽  
Yan Ma ◽  
Yan Liu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Lung Cancer Cells ◽  
Dependent Manner ◽  
Tumor Associated Macrophages ◽  
M1 Type

Abstract Background: Tumor-associated macrophages (TAM) are the most abundant stromal cells in the tumor microenvironment. Turning the TAM against their host tumor cells is an intriguing therapeutic strategy particularly attractive for patients with immunologically “cold” tumors. This concept was mechanistically demonstrated on in vitro human and murine lung cancer cells and their corresponding TAM models through combinatorial use of nanodiamond-doxorubicin conjugates (Nano-DOX) and a PD-L1 blocking agent BMS-1. Nano-DOX are an agent previously proved to be able to stimulate tumor cells’ immunogenicity and thereby reactivate the TAM into the anti-tumor M1 phenotype. Results: Nano-DOX were first shown to stimulate the tumor cells and the TAM to release the cytokine HMGB1 which, regardless of its source, acted through the RAGE/NF-κB pathway to induce PD-L1 in the tumor cells and PD-L1/PD-1 in the TAM. Interestingly, Nano-DOX also induced NF-κB-dependent RAGE expression in the tumor cells and thus reinforced HMGB1’s action thereon. Then, BMS-1 was shown to enhance Nano-DOX-stimulated M1-type activation of TAM both by blocking Nano-DOX-induced PD-L1 in the TAM and by blocking tumor cell PD-L1 ligation with TAM PD-1. The TAM with enhanced M1-type repolarization both killed the tumor cells and suppressed their growth. BMS-1 could also potentiate Nano-DOX’s action to suppress tumor cell growth via blocking of Nano-DOX-induced PD-L1 therein. Finally, Nano-DOX and BMS-1 achieved synergistic therapeutic efficacy against in vivo tumor grafts in a TAM-dependent manner. Conclusions: PD-L1/PD-1 upregulation mediated by autocrine and paracrine activation of the HMGB1/RAGE/NF-κB signaling is a key response of lung cancer cells and their TAM to stress, which can be induced by Nano-DOX. Blockade of Nano-DOX-induced PD-L1, both in the cancer cells and the TAM, achieves enhanced activation of TAM-mediated anti-tumor response.

scholarly journals Cytokine messenger RNA stability is enhanced in tumor cells

Blood ◽  
1991 ◽  
Vol 77 (8) ◽  
pp. 1787-1795 ◽  
Author(s):  
HJ Ross ◽  
N Sato ◽  
Y Ueyama ◽  
HP Koeffler
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Messenger Rna ◽  
Globin Gene ◽  
Rna Extraction ◽  
Human Tumor ◽  
Lung Cancer Cells ◽  
Hematopoietic Growth Factors ◽  
Cytokine Mrnas

Hematopoietic growth factors are produced by a number of human tumors. We extracted RNA from selected human tumor cells known to produce at least one hematopoietic growth factor and found high levels of abnormally stable cytokine messenger (m)RNA. Half-life experiments performed after preventing RNA synthesis by exposing cells to actinomycin D before RNA extraction showed stabilization of cytokine messages in tumor cells in liquid culture as well as in human tumor xenografts grown in mice. Exposure to the phorbol ester phorbol 12- myristate 13-acetate (TPA) caused enhancement of granulocyte-macrophage colony-stimulating factor (GM-CSF) message level in lung cancer cells and in control fibroblasts but elevated levels persisted far longer in the tumor cells. In normal cells, an AU-rich sequence in the 3′ untranslated region of cytokine mRNAs confers lability to the message. Although a beta-globin gene expression vector containing this region appears to produce unstable mRNA in lung cancer cells, cytokine mRNAs, which also contain this sequence, are very stable in the tumors we studied. This may indicate that another region of the cytokine mRNA molecule is of greater importance than the AU-rich region in determining mRNA stability in tumor cells.

Blood-compatible poly (2-methoxyethyl acrylate) for the adhesion and proliferation of lung cancer cells toward the isolation and analysis of circulating tumor cells

2016 ◽  
Vol 31 (4) ◽  
pp. 361-372 ◽  
Author(s):  
Takashi Hoshiba ◽  
Mayo Nikaido ◽  
Satomi Yagi ◽  
Iku Konno ◽  
Ayano Yoshihiro ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Circulating Tumor Cells ◽  
Lung Cancer Cells

Effects of Constitutive Production of Colony-Stimulating Factors by Human Lung Cancer Cells on Invasive Capacity.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4211-4211
Author(s):  
Yoshiki Uemura ◽  
Makoto Kobayashi ◽  
Hideshi Nakata ◽  
Tetsuya Kubota ◽  
Hirokuni Taguchi
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Cell Lines ◽  
Colony Stimulating Factor ◽  
Gelatinase Activity ◽  
Gm Csf ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Abstract In advanced clinical stage, many cases of lung cancer produce colony-stimulating factors (CSFs), including granulocyte-colony stimulating factor (G-CSF), granulocyte macrophage-colony stimulating factor (GM-CSF), and macrophage-colony stimulating factor (M-CSF). The biological properties of the overproduction of CSFs by tumor cells are not well understood. We previously found that CSFs produced by two lung cancer cell lines, OKa-C-1 and MI-4, which constitutively produce abundant amounts of G-CSF, GM-CSF, and M-CSF, stimulate the tumor’s own growth through an autoctine mechanism. In this study, we examined whether CSFs produced by tumor cells contribute to the invasion of the tumor itself. Invasive behaviors of the cancer cells were stimulated by exogenous CSFs but were suppressed by neutralizing antibodies against the CSFs. Matrix-degrading proteinases also are essential for successful tumor cell metastasis. Gelatin zymographs of conditioned media revealed two major bands of gelatinase activity at 68 and 92 kDa. The enzyme activities at 68 and 92 kDa were significantly enhanced in the presence of each CSF in the cell lines but were suppressed by the antibodies against the CSFs. The two gelatinase bands were characterized as matrix metalloproteinase (MMP)-2 and MMP-9, respectively. Our findings suggest that CSFs produced by tumor cells might be closely associated with the tumor invasion through gelatinase activation in CSF-producing lung cancer cells. In addition, an increase of invasion capacity and gelatinase activity by the CSFs might be mediated through the p44/42 mitogen-activated protein kinase (MAPK) signaling pathway. Figure Figure

scholarly journals Effects of conditioned media from murine lung cancer cells and human tumor cells on cultured myotubes

2020 ◽  
Vol 318 (1) ◽  
pp. E22-E32 ◽  
Author(s):  
Blas A. Guigni ◽  
Jos van der Velden ◽  
C. Matthew Kinsey ◽  
James A. Carson ◽  
Michael J. Toth
Keyword(s):  
Lung Cancer ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Lung Tumor ◽  
Control Cell ◽  
Human Tumor ◽  
Human Lung Tumor ◽  
Primary Cell Lines ◽  
Cultured Myotubes

Factors secreted from tumors/tumor cells are hypothesized to cause skeletal muscle wasting in cancer patients. We examined whether cancer cells secrete factors to promote atrophy by evaluating the effects of conditioned media (CM) from murine lung cancer cells and primary cultures of human lung tumor cells on cultured myotubes. We evaluated murine Lewis lung carcinoma (LLC) and KRASG12D cells, and primary cell lines derived from tumor biopsies from patients with lung cancer (hTCM; n = 6). In all experiments, serum content was matched across treatment groups. We hypothesized that CM from murine and human tumor cells would reduce myotube myosin content, decrease mitochondrial content, and increase mitochondrial reactive oxygen species (ROS) production. Treatment of myotubes differentiated for 7 days with CM from LLC and KRASG12D cells did not alter any of these variables. Effects of murine tumor cell CM were observed when myotubes differentiated for 4 days were treated with tumor cell CM and compared with undiluted differentiation media. However, these effects were not apparent if tumor cell CM treatments were compared with control cell CM or dilution controls. Finally, CM from human lung tumor primary cell lines did not modify myosin content or mitochondrial content or ROS production compared with either undiluted differentiated media, control cell CM, or dilution controls. Our results do not support the hypothesis that factors released from cultured lung cancer/tumor cells promote myotube wasting or mitochondrial abnormalities, but we cannot dismiss the possibility that these cells could secrete such factors in vivo within the native tumor microenvironment.

scholarly journals YAP1 mediates survival of ALK-rearranged lung cancer cells treated with alectinib via pro-apoptotic protein regulation

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Takahiro Tsuji ◽  
Hiroaki Ozasa ◽  
Wataru Aoki ◽  
Shunsuke Aburaya ◽  
Tomoko Yamamoto Funazo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Complete Remission ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Limited Information ◽  
Alk Inhibitors ◽  
Anaplastic Lymphoma ◽  
Alk Inhibitor ◽  
Apoptotic Protein ◽  
Tumor Remission

AbstractDespite the promising clinical efficacy of the second-generation anaplastic lymphoma kinase (ALK) inhibitor alectinib in patients with ALK-rearranged lung cancer, some tumor cells survive and eventually relapse, which may be an obstacle to achieving a cure. Limited information is currently available on the mechanisms underlying the initial survival of tumor cells against alectinib. Using patient-derived cell line models, we herein demonstrate that cancer cells survive a treatment with alectinib by activating Yes-associated protein 1 (YAP1), which mediates the expression of the anti-apoptosis factors Mcl-1 and Bcl-xL, and combinatorial inhibition against both YAP1 and ALK provides a longer tumor remission in ALK-rearranged xenografts when compared with alectinib monotherapy. These results suggest that the inhibition of YAP1 is a candidate for combinatorial therapy with ALK inhibitors to achieve complete remission in patients with ALK-rearranged lung cancer.

scholarly journals Cytokine messenger RNA stability is enhanced in tumor cells

Blood ◽  
1991 ◽  
Vol 77 (8) ◽  
pp. 1787-1795 ◽  
Author(s):  
HJ Ross ◽  
N Sato ◽  
Y Ueyama ◽  
HP Koeffler
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Messenger Rna ◽  
Globin Gene ◽  
Rna Extraction ◽  
Human Tumor ◽  
Lung Cancer Cells ◽  
Hematopoietic Growth Factors ◽  
Cytokine Mrnas

Abstract Hematopoietic growth factors are produced by a number of human tumors. We extracted RNA from selected human tumor cells known to produce at least one hematopoietic growth factor and found high levels of abnormally stable cytokine messenger (m)RNA. Half-life experiments performed after preventing RNA synthesis by exposing cells to actinomycin D before RNA extraction showed stabilization of cytokine messages in tumor cells in liquid culture as well as in human tumor xenografts grown in mice. Exposure to the phorbol ester phorbol 12- myristate 13-acetate (TPA) caused enhancement of granulocyte-macrophage colony-stimulating factor (GM-CSF) message level in lung cancer cells and in control fibroblasts but elevated levels persisted far longer in the tumor cells. In normal cells, an AU-rich sequence in the 3′ untranslated region of cytokine mRNAs confers lability to the message. Although a beta-globin gene expression vector containing this region appears to produce unstable mRNA in lung cancer cells, cytokine mRNAs, which also contain this sequence, are very stable in the tumors we studied. This may indicate that another region of the cytokine mRNA molecule is of greater importance than the AU-rich region in determining mRNA stability in tumor cells.

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