Induction of apoptosis in leukemic cell lines treated with captopril, trandolapril and losartan: A new role in the treatment of leukaemia for these agents

Iglesia, Silvia de la; López-Jorge, C E; Gómez‐Casares, María Teresa; Castellano, Angelina Lemes; Cabrera, Pedro Martin; Brito, Jezabel López; Cabrera, Alexia Suárez; Labarta, T. Molero

doi:10.1016/j.leukres.2008.09.029

Cited by 42 publications

(26 citation statements)

References 44 publications

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“…Angiotensin II supported VEGF production and angiogenesis in xenografts of ovarian cancer cells (Suganuma et al 2005) and AT1 receptor blockade inhibited both of these actions in xenografts of ovarian and gastric tumour cells (Suganuma et al 2005, Huang et al 2008. AT1 receptor blockade also inhibited angiogenesis in murine Lewis lung tumours (Imai et al 2007) and through this means enhanced the effectiveness of radiation treatment in murine melanoma (Ohnuma et al 2009, Otake et al 2009) and in murine renal tumours (Miyajima et al 2009). However, in in vivo studies in which S-180 murine sarcoma cell tumours were developed in AT1a receptor null mice, angiogenesis, along with VEGF expression, was both reduced and partially refractory to AT1 receptor blockade when compared with normal tissue.…”

Section: Angiogenesismentioning

confidence: 97%

“…However, in in vivo studies in which S-180 murine sarcoma cell tumours were developed in AT1a receptor null mice, angiogenesis, along with VEGF expression, was both reduced and partially refractory to AT1 receptor blockade when compared with normal tissue. Hence, host angiotensin II activity is instrumental in supporting angiogenesis in host stromal cells in addition to any effect it has on the cancer cells themselves (Fujita et al 2002, 2005, Imai et al 2007.…”

Section: Angiogenesismentioning

confidence: 99%

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The renin–angiotensin system in the breast and breast cancer

Vinson¹,

Barker²,

Puddefoot³

2011

Endocrine-Related Cancer

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Much evidence now suggests that angiotensin II has roles in normal functions of the breast that may be altered or attenuated in cancer. Both angiotensin type 1 (AT1) and type 2 (AT2) receptors are present particularly in the secretory epithelium. Additionally, all the elements of a tissue renin-angiotensin system, angiotensinogen, prorenin and angiotensin-converting enzyme (ACE), are also present and distributed in different cell types in a manner suggesting a close relationship with sites of angiotensin II activity. These findings are consistent with the concept that stromal elements and myoepithelium are instrumental in maintaining normal epithelial structure and function. In disease, this system becomes disrupted, particularly in invasive carcinoma. Both AT1 and AT2 receptors are present in tumours and may be up-regulated in some. Experimentally, angiotensin II, acting via the AT1 receptor, increases tumour cell proliferation and angiogenesis, both these are inhibited by blocking its production or function. Epidemiological evidence on the effect of expression levels of ACE or the distribution of ACE or AT1 receptor variants in many types of cancer gives indirect support to these concepts. It is possible that there is a case for the therapeutic use of high doses of ACE inhibitors and AT1 receptor blockers in breast cancer, as there may be for AT2 receptor agonists, though this awaits full investigation. Attention is drawn to the possibility of blocking specific AT1-mediated intracellular signalling pathways, for example by AT1-directed antibodies, which exploit the possibility that the extracellular N-terminus of the AT1 receptor may have previously unsuspected signalling roles.

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Section: Angiogenesismentioning

confidence: 97%

Section: Angiogenesismentioning

confidence: 99%

The renin–angiotensin system in the breast and breast cancer

Vinson¹,

Barker²,

Puddefoot³

2011

Endocrine-Related Cancer

View full text Add to dashboard Cite

show abstract

“…A seminal epidemiological study demonstrated that patients taking angiotensin-converting-enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) were at decreased risk of developing some types of cancers [7]. Several studies have provided evidence that RAS signaling regulates angiogenesis, invasion, cell survival and cell proliferation [8][9][10][11]. The effects on cell survival and proliferation are both direct, by effects on tumor and stromal cells, and also indirect, by modulating the growth of endothelial cells during angiogenesis [8].…”

Section: Introductionmentioning

confidence: 99%

Dual targeting of angiotensin receptors (AGTR1 and AGTR2) in epithelial ovarian carcinoma

Park

Choi

et al. 2014

Gynecologic Oncology

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“…Angiotensin II receptors have been shown to be present in hematopoietic progenitor cells[10], and components of the renin angiotensin system (RAS) are expressed in the bone marrow microenvironment of AML cells and are postulated to exert a regulatory function by participating in autocrine and paracrine loops[11]. Interestingly, treatment of certain AML cell lines with ACE inhibitors or ARBs results in inhibition of cell growth and promotion of apoptosis associated with decreased c-myc expression[12]. With regards to beta blockers, the non-selective beta blocker carvedilol is a very potent inhibitor of the myeloid leukemia K562 cells[13], whereas propranolol exerts a cytotoxic effect on the monocyte cell line U937[14].…”

Section: Introductionmentioning

confidence: 99%

The effect of calcium channel blockers on the outcome of acute myeloid leukemia

Chae

Dimou

Pierce

et al. 2014

Leukemia & Lymphoma

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The effect of calcium channel blockers (CCBs), beta blockers and angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) on the prognosis of patients with acute myeloid leukemia (AML) is largely unknown. We collected data on the use of these medications on 1043 patients with AML excluding promyelocytic leukemia diagnosed and treated at MD Anderson Cancer Center between 2000 and 2012. Treatment with either amlodipine or diltiazem predicted a worse overall survival (HR 1.6 95% CI 1.22-2.06, p<0.0001). There was no difference in survival depending on whether the patients were taking beta blockers, ACE inhibitors or ARBs. The effect of CCBs on survival was independent from the NCCN risk classification, age, performance status, response to treatment, year of diagnosis and CD34 levels, assessed by flow cytometry (HR=1.39, 95% CI 1.05-1.80, p=0.02). Treatment with either amlodipine or diltiazem predicts worse survival in patients with AML independent of known prognostic factors.

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Induction of apoptosis in leukemic cell lines treated with captopril, trandolapril and losartan: A new role in the treatment of leukaemia for these agents

Cited by 42 publications

References 44 publications

The renin–angiotensin system in the breast and breast cancer

The renin–angiotensin system in the breast and breast cancer

Dual targeting of angiotensin receptors (AGTR1 and AGTR2) in epithelial ovarian carcinoma

The effect of calcium channel blockers on the outcome of acute myeloid leukemia

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