Angiotensin-converting enzyme and its association with outcome in lung cancer

Rømer, Frode K.

doi:10.1038/bjc.1981.21

Cited by 23 publications

(12 citation statements)

References 15 publications

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“…This finding was corroborated by others, demonstrating low serum ACE levels in patients with lung tumors as compared to patients with other pulmonary diseases or carcinomas [40, 41]. The lowest serum ACE levels correlated with poor prognosis and higher relapse rate [39, 42, 43] as well as metastatic disease, suggesting that quantification of serum ACE may be a prognostic indicator for lung cancer [44]. Further, ACE activity increased in patients with bronchial carcinoma following chemotherapy or radiotherapy [41, 43, 45] as well as in patients in clinical remission [44].…”

Section: Angiotensin Peptide Synthesizing Enzymes and Lung Cancersupporting

confidence: 72%

“…Romer found that the serum ACE levels were significantly lower in 141 patients newly diagnosed with primary lung cancer as compared to healthy controls [39]. This finding was corroborated by others, demonstrating low serum ACE levels in patients with lung tumors as compared to patients with other pulmonary diseases or carcinomas [40, 41].…”

Section: Angiotensin Peptide Synthesizing Enzymes and Lung Cancermentioning

confidence: 70%

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Angiotensin Peptides and Lung Cancer

Gallagher¹,

Cook²,

Soto-Pantoja³

et al. 2011

CCDT

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Lung cancer is a leading cause of death in both men and women, with over 1,000,000 new cases diagnosed worldwide annually and a 5-year survival rate of only 14%, a figure that has improved little in the past thirty years. This poor prognosis suggests a need for novel approaches for the treatment and prevention of lung cancer. The renin-angiotensin system is an established, primary regulator of blood pressure, homeostasis, and natriuresis; however, compelling evidence indicates that the angiotensin peptides also play a role in cell proliferation and inflammation. Angiotensin II is a vasoconstrictor, a mitogen, and an angiogenic factor, while angiotensin-(1-7) has vasodilator, anti-proliferative, and anti-angiogenic properties. This review focuses on studies examining the renin-angiotensin system in pulmonary cancers and whether clinical intervention of this pathway may serve as an effective chemotherapeutic and/or chemopreventive modality for lung cancer.

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Section: Angiotensin Peptide Synthesizing Enzymes and Lung Cancersupporting

confidence: 72%

Section: Angiotensin Peptide Synthesizing Enzymes and Lung Cancermentioning

confidence: 70%

Angiotensin Peptides and Lung Cancer

Gallagher¹,

Cook²,

Soto-Pantoja³

et al. 2011

CCDT

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“…In the following decades, it has been suggested that elevated serum ACE could be implicated with a worse prognosis for lung cancer and that this enzyme could be used as a prognostic indicator in this disease [9]. In other studies, the treatment with combined Ang II showed good clinical response in the patients with advanced gastrointestinal cancer and also with breast cancer [10] [11]. Between 1985 and 1990 several works showed that RAS components were correlated with other cancers (prostate, gastric, bladder, bronchial, breast, lung and neuroblastoma) [12] [13].…”

Section: Renin Angiotensin System and Cancermentioning

confidence: 99%

Renin Angiotensin System Components and Cancer: Reports of Association

Wolgien¹,

Correa²,

Breuel³

et al. 2016

JBM

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Objectives. The study assessed the existence and significance of associations between the expression of fifteen renin-angiotensin system component genes and lung adenocarcinoma. Materials and Methods. NCBI's built-in statistical tool, GEO2R, was used to calculate Student's í µí±¡-tests for the associations found in a DNA expression study of adenocarcinoma and matched healthy lung tissue samples. The raw data was processed with GeneSpring6 and then used to generate figures with and without Sidak's multiple comparison correction. Results. Ten genes were found to be significantly associated with adenocarcinoma. Seven of these associations remained statistically significant after correction for multiple comparisons. Notably, AGTR2, which encodes the AT 2 angiotensin II receptor subtype, was significantly underexpressed in adenocarcinoma tissue (í µí± < 0.01). AGTR1, ACE, ENPEP, MME, and PRCP, which encode the AT 1 angiotensin II receptor, angiotensin-converting enzyme, aminopeptidase N, neprilysin, and prolylcarboxypeptidase, respectively, were also underexpressed. AGT, which encodes angiotensinogen, the angiotensin peptide precursor, was overexpressed in adenocarcinoma tissue. Conclusion. The results suggest an association between the expression of the genes for renin-angiotensin system-related proteins and adenocarcinoma. While further research is necessary to conclusively demonstrate a link between the renin-angiotensin system and lung cancers, the results suggest that the renin-angiotensin system plays a role in the pathology of adenocarcinoma.

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“…Although individually low values were evenly distributed among the patients, it is known that some diseases (not included in this study) are associated with low enzyme activity, e.g. lung cancer [16] and some haematological and lymphatic malignancies [17]. A rather low SACE has also been reported in regional enteritis [22]; whereas a recent survey from our laboratory showed no difference from the reference series in yersinosis (SACE 27.7 i~ 6.5 kU/1, n = 7) or rheumatoid arthritis (SACE 22.2 f 4.6 kU/1, n = 21), these diseases being represented in this study.…”

Section: Patients Without Sarcoidosismentioning

confidence: 98%

The influence of prednisone on serum angiotensin-converting enzyme activity in patients with and without sarcoidosis

Rømer¹,

Jacobsen²

1982

Scand J Clin Lab Invest

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The influence of prednisone on S-angiotensin-converting enzyme (SACE) activity was examined by serial measurements in 20 non-sarcoidosis patients and 8 sarcoidosis patients on prednisone, compared with 26 patients and healthy controls not under treatment. All but the sarcoidosis patients had SACE within normal limits (12.0-36.8 kU/l). In the three groups initial or pretreatment SACE levels (mean +/- SD) were 20.1 +/- 5.7, 66.9 +/- 27.4 and 26.4 +/- 4.1 kU/l, respectively. Non-sarcoidosis patients on prednisone had a lower pretreatment SACE than untreated control persons, presumably due to the different diseases represented in the groups. During the observation period SACE was rather stable in untreated patients and also in the treated group as a whole. But in 12 patients with SACE greater than 18.2 kU/l (mean of reference series minus 1 SD) a significantly decreasing SACE was observed after 1 week of treatment, whereas SACE was unchanged in patients with lower pretreatment levels, suggesting that in these patients prednisone could not decrease any further a level which was already low. In sarcoidosis the elevated SACE declined, reaching a normal level after 4 weeks on prednisone. In the assay ACE was markedly inhibited by SQ 14,255 (Captopril), moderately by methylprednisolone in concentrations exceeding those generally used clinically, while no inhibition was seen using acetylsalicylic acid.

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Angiotensin-converting enzyme and its association with outcome in lung cancer

Cited by 23 publications

References 15 publications

Angiotensin Peptides and Lung Cancer

Angiotensin Peptides and Lung Cancer

Renin Angiotensin System Components and Cancer: Reports of Association

The influence of prednisone on serum angiotensin-converting enzyme activity in patients with and without sarcoidosis

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