Atypical adenomatous hyperplasia of lung: its incidence and analysis of clinical, glycohistochemical and structural features including newly defined growth regulators and vascularization

Kayser, Klaus; Nwoye, Johnson Obiefune; Kosjerina, Zdravko; Goldmann, Torsten; Vollmer, Ekkehard; Kaltner, Herbert; André, Sabine; Gabius, Hans‐Joachim

doi:10.1016/s0169-5002(03)00289-7

Cited by 29 publications

(24 citation statements)

References 40 publications

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“…We and others have shown that MIF is markedly overexpressed in lung cancer [1][2][3] and nearly all other common solid tumors; eg, breast, 4 -8 ovarian, 9,10 prostate, 6 -8 bladder, 11,12 and colon cancer, 13 as well as melanoma. 14,15 In lung cancer MIF expression is associated with increased production of angiogenic CXC chemokines both in vitro, 16 and in vivo.…”

Section: Discussionmentioning

confidence: 99%

“…We have shown that macrophage migration inhibitory factor (MIF) induces expression of angiogenic CXC chemokines by tumor-associated monocytes, and that MIF-dependent expression of angiogenic CXC chemokines is one of several major pathways by which lung cancer tumors induce an angiogenic environment. We and others have shown that MIF is markedly overexpressed in lung cancer [1][2][3] and nearly all other common solid tumors; eg, breast, 4 -8 ovarian, 9,10 prostate, 6 -8 bladder, 11,12 and colon cancer, 13 as well as melanoma. 14,15 In lung cancer MIF expression is associated with increased production of angiogenic CXC chemokines both in vitro, 16 and in vivo.…”

mentioning

confidence: 99%

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Expression of CD74, the Receptor for Macrophage Migration Inhibitory Factor, in Non-Small Cell Lung Cancer

McClelland

Zhao

Carskadon

et al. 2009

The American Journal of Pathology

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Macrophage migration inhibitory factor (MIF) is a multifunctional cytokine that is overexpressed in lung cancer. The MIF receptor was recently discovered and found to be the invariant chain of the HLA class II molecule, CD74. We hypothesized that the expression of this receptor-ligand pair in lung cancer is associated with the angiogenic activity and level of CXC chemokine expression in human specimens of non-small cell lung cancer. We, therefore, performed immunolocalization of CD74 and compared it with the localization of MIF in non-small cell lung cancer to determine their respective locations, as well as the relationship between the co-expression of MIF-CD74 and angiogenic CXC chemokines with tumor angiogenesis. We found intense CD74 expression by immunohistochemistry in 57 of 70 tumors with minimal to no staining in the remaining 13 tumors. Comparing the localization of CD74 with its putative ligand, MIF, we found that CD74 and MIF were co-expressed in tumors in close proximity, and that co-expression of the MIF-CD74 pair was associated with both higher levels of tumor-associated angiogenic CXC chemokines (ie, the ELR score) and greater vascularity compared with tumors in which MIF-CD74 co-expression was not present. We also found that MIF induced angiogenic CXC chemokine expression in an autocrine manner in vitro , a function that was specifically inhibited by antibodies to CD74. (Am J Pathol

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Expression of CD74, the Receptor for Macrophage Migration Inhibitory Factor, in Non-Small Cell Lung Cancer

McClelland

Zhao

Carskadon

et al. 2009

The American Journal of Pathology

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“…Furthermore, MIF is overexpressed in human lung adenocarcinomas (33,34), and mutations of ras are estimated to occur in up to 50% of lung cancers (35). We determined whether there was a positive level of regulation of MIF expression and secretion by immortalizing and transforming oncogenes in lung bronchioalveolar epithelial cells.…”

Section: Mif Is Overexpressed In Premalignant and Malignant Bronchialmentioning

confidence: 99%

Regulation of Human Lung Adenocarcinoma Cell Migration and Invasion by Macrophage Migration Inhibitory Factor

Rendon

Roger

Teneng

et al. 2007

Journal of Biological Chemistry

100

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Macrophage migration inhibitory factor (MIF) is expressed and secreted in response to mitogens and integrin-dependent cell adhesion. Once released, autocrine MIF promotes the activation of RhoA GTPase leading to cell cycle progression in rodent fibroblasts. We now report that small interfering RNAmediated knockdown of MIF and MIF small molecule antagonism results in a greater than 90% loss of both the migratory and invasive potential of human lung adenocarcinoma cells. Correlating with these phenotypes is a substantial reduction in steady state as well as serum-induced effector binding activity of the Rho GTPase family member, Rac1, in MIF-deficient cells. Conversely, MIF overexpression by adenovirus in human lung adenocarcinoma cells induces a dramatic enhancement of cell migration, and co-expression of a dominant interfering mutant of Rac1 (Rac1 N17 ) completely abrogates this effect. Finally, our results indicate that MIF depletion results in defective partitioning of Rac1 to caveolin-containing membrane microdomains, raising the possibility that MIF promotes Rac1 activity and subsequent tumor cell motility through lipid raft stabilization.

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“…1A) and has been shown to be typically a well-defined oval or round shape [19]. It can be either solitary or multifocal and is typically less than 5 mm in size, although case reports have shown AAH as large as 2 cm [20,21]. The ground-glass density represents atypical pneumocytes proliferating within the alveolar septa (Fig.…”

Section: Atypical Adenomatous Hyperplasiamentioning

confidence: 99%

Subsolid pulmonary nodules: CT–pathologic correlation using the 2011 IASLC/ATS/ERS classification

et al. 2015

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Atypical adenomatous hyperplasia of lung: its incidence and analysis of clinical, glycohistochemical and structural features including newly defined growth regulators and vascularization

Cited by 29 publications

References 40 publications

Expression of CD74, the Receptor for Macrophage Migration Inhibitory Factor, in Non-Small Cell Lung Cancer

Expression of CD74, the Receptor for Macrophage Migration Inhibitory Factor, in Non-Small Cell Lung Cancer

Regulation of Human Lung Adenocarcinoma Cell Migration and Invasion by Macrophage Migration Inhibitory Factor

Subsolid pulmonary nodules: CT–pathologic correlation using the 2011 IASLC/ATS/ERS classification

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