Hepatic colon cancer metastases influence the white cell types trapped in liver sinusoids

1997 ◽  
Vol 56 ◽  
pp. 340-341
Author(s):  
S. Durowicz ◽  
B. Lukomska ◽  
E. Cybulska ◽  
W.L. Olszewski
Keyword(s):  
Colon Cancer ◽  
Cell Types ◽  
White Cell ◽  
Liver Sinusoids ◽  
Cancer Metastases

Two Unusual Sites of Colon Cancer Metastases and a Rare Thyroid Lymphoma

2001 ◽  
Vol 19 (15) ◽  
pp. 3574-3575 ◽  
Author(s):  
Elie B. Choufani ◽  
Harold L. Lazar ◽  
Kevan L. Hartshorn
Keyword(s):  
Colon Cancer ◽  
Thyroid Lymphoma ◽  
Cancer Metastases

Cytoplasmic c-erbB-2 expression is increased in human colon cancer metastases relative to primary tumors

2001 ◽  
Vol 120 (5) ◽  
pp. A258-A259
Author(s):  
Frank A. Sinicrope ◽  
Elizabeth Half-Onn ◽  
Michael G. Lemoine
Keyword(s):  
Colon Cancer ◽  
Human Colon ◽  
Human Colon Cancer ◽  
Primary Tumors ◽  
Cancer Metastases

Comparison of histopathology and RT-qPCR amplification of guanylyl cyclase C for detection of colon cancer metastases in lymph nodes

2010 ◽  
Vol 63 (6) ◽  
pp. 530-537 ◽  
Author(s):  
J. F. Haince ◽  
M. Houde ◽  
G. Beaudry ◽  
S. L'Esperance ◽  
G. Garon ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Lymph Nodes ◽  
Guanylyl Cyclase ◽  
Guanylyl Cyclase C ◽  
Cancer Metastases

scholarly journals MAPKAP Kinase-2 Drives Expression of Angiogenic Factors by Tumor-Associated Macrophages in a Model of Inflammation-Induced Colon Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Lucia Suarez-Lopez ◽  
Yi Wen Kong ◽  
Ganapathy Sriram ◽  
Jesse C. Patterson ◽  
Samantha Rosenberg ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Tumor Microenvironment ◽  
Tumor Progression ◽  
Chronic Inflammation ◽  
Cancer Progression ◽  
Tumor Angiogenesis ◽  
Cell Types ◽  
Adoptive Cell Transfer ◽  
Tumor Associated Macrophages

Chronic inflammation increases the risk for colorectal cancer through a variety of mechanisms involving the tumor microenvironment. MAPK-activated protein kinase 2 (MK2), a major effector of the p38 MAPK stress and DNA damage response signaling pathway, and a critical regulator of pro-inflammatory cytokine production, has been identified as a key contributor to colon tumorigenesis under conditions of chronic inflammation. We have previously described how genetic inactivation of MK2 in an inflammatory model of colon cancer results in delayed tumor progression, decreased tumor angiogenesis, and impaired macrophage differentiation into a pro-tumorigenic M2-like state. The molecular mechanism responsible for the impaired angiogenesis and tumor progression, however, has remained contentious and poorly defined. Here, using RNA expression analysis, assays of angiogenesis factors, genetic models, in vivo macrophage depletion and reconstitution of macrophage MK2 function using adoptive cell transfer, we demonstrate that MK2 activity in macrophages is necessary and sufficient for tumor angiogenesis during inflammation-induced cancer progression. We identify a critical and previously unappreciated role for MK2-dependent regulation of the well-known pro-angiogenesis factor CXCL-12/SDF-1 secreted by tumor associated-macrophages, in addition to MK2-dependent regulation of Serpin-E1/PAI-1 by several cell types within the tumor microenvironment.

scholarly journals Benzo(a)pyrene, an Active Product of Cigarette Smoke, Role in PLA2 Isoforms Activation in Colon Cancer

2018 ◽  
Vol 4 (Supplement 2) ◽  
pp. 193s-193s
Author(s):  
S. Sharma ◽  
S. Yadav ◽  
S. Rana ◽  
P. Avti ◽  
K.L. Khanduja
Keyword(s):  
Colon Cancer ◽  
Cell Viability ◽  
Cigarette Smoke ◽  
Membrane Integrity ◽  
Annexin V ◽  
Cell Types ◽  
Ros Generation ◽  
Dependent Manner ◽  
Colon Cells ◽  
Ht 29

Background and aim: One of the active combustion product of cigarette smoke, Benzo[a]pyrenes, role in pulmonary cancer is clearly understood. However, its role in gastrointestinal cancer including colon cancer is not clearly understood. Methods: In this study, benzo(a)pyrenes was treated to colon cells to evaluate its role in cell viability, cellular ROS, and gene expression of various PLA2 isoforms was evaluated by FACS and PCR. The identified PLA2 was silenced at the gene level to evaluate its role in cell viability and ROS generation. Results: B(a)P treatment at 1 µg/mL for 48 h to HCT-15 male colon cells significantly reduced the cell viability without affecting HT-29 female colon cells. Higher doses and longer treatment duration with B(a)P showed that female colon cells were highly sensitive than male colon cells. Annexin-V/PI staining for preapoptotic detection showed that B(a)P treatment increased the apoptosis in both the cell types in a concentration and time-dependent manner. The cytosolic ROS (cROS) and superoxide radical (SOR) formation in the female colon cells was significantly higher than male colon cells unlike the mitochondrial ROS (mtROS) production which was significantly higher in male colon cells. Treatment with B(a)P significantly upregulated the IID and IVA PLA2 isoform groups in HCT-15 male colon cells, whereas IB was upregulated in HT-29 female colon cells among the various PLA2 isozyme gene studied (IB, IID, III, IVA, IVB, IVC, VI, X, aiPLA2 and iPLA2). Gene silencing experiments targeting PLA2 IID and IVA in the HCT-15 male colon cells and IB in HT-29 female colon cells showed no effect with B(a)P treatment on the cell proliferation, apoptosis, membrane integrity and free radicals (ROS, mtROS, and SOR) generation. Conclusion: Targeting specific PLA2 isozymes in a cell-specific manner abolished the B(a)P-induced PLA2-mediated oxidative damage–related signaling pathways.

Two Unusual Sites of Colon Cancer Metastases and a Rare Thyroid Lymphoma

2001 ◽  
Vol 19 (15) ◽  
pp. 3576-3580 ◽  
Author(s):  
Ioannis Raftopoulos ◽  
Daniel Vanuno ◽  
Gregory Kouraklis
Keyword(s):  
Colon Cancer ◽  
Thyroid Lymphoma ◽  
Cancer Metastases
Sign in / Sign up

Export Citation Format

Share Document