Lipocalin‐2 is associated with modulation of disease phenotype in a patient with concurrent <i>JAK2</i>‐V617F and <i>BCR‐ABL</i> mutation

Nadarajan, Veera Sekaran; Ang, Chow-Hiang; Bee, Ping Chong

doi:10.1111/j.1600-0609.2011.01712.x

Cited by 4 publications

(2 citation statements)

References 11 publications

(20 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…With regard to CML, inhibition of the constitutive tyrosine kinase activity of p210 BCR-ABL [ 51 ] with imatinib alleviates the hyperproliferation-induced symptoms [ 52 ]. Furthermore, serum levels of NGAL are significantly higher in CML patients than in healthy individuals [ 44 , 45 , 53 , 54 ]. If CML patients achieve complete molecular remission after imatinib therapy, NGAL serum levels fall and are significantly lower than during the full-blown disease [ 44 , 53 ].…”

Section: Ngal As a Biomarker In Cancermentioning

confidence: 99%

Revisiting Neutrophil Gelatinase-Associated Lipocalin (NGAL) in Cancer: Saint or Sinner?

Bauvois

Susin

2018

Cancers

View full text Add to dashboard Cite

Human neutrophil gelatinase-associated lipocalin (NGAL) is a glycoprotein present in a wide variety of tissues and cell types. NGAL exists as a 25 kDa monomer, a 46 kDa homodimer (the most abundant form in healthy subjects) and a 130 kDa disulfide-linked heterodimer bound to latent matrix metalloproteinase-9. Dysregulated expression of NGAL in human malignancies suggests its value as a clinical marker. A growing body of evidence is highlighting NGAL’s paradoxical (i.e., both beneficial and detrimental) effects on cellular processes associated with tumor development (proliferation, survival, migration, invasion, and multidrug resistance). At least two distinct cell surface receptors are identified for NGAL. This review (i) summarizes our current knowledge of NGAL’s expression profiles in solid tumors and leukemias, and (ii) critically evaluates the beneficial and detrimental activities of NGAL having been documented in a diverse range of cancer-derived cell lines. A better understanding of the causal relationships between NGAL dysregulation and tumor development will require a fine analysis of the molecular aspects and biological role(s) of NGAL both in primary tumors and at different stages of disease. Having an accurate picture of NGAL’s contribution to tumor progression is a prerequisite for attempting to modulate this protein as a putative therapeutic target.

show abstract

Section: Ngal As a Biomarker In Cancermentioning

confidence: 99%

Revisiting Neutrophil Gelatinase-Associated Lipocalin (NGAL) in Cancer: Saint or Sinner?

Bauvois

Susin

2018

Cancers

View full text Add to dashboard Cite

show abstract

“…Our study provides the first evidence that the co-expression of NGAL-R and CD38 is a high-value target in CLL. Beyond CLL, the expression rates of CD38 and NGAL-R are high in other tumors such as acute and chronic myeloid leukemias [ 47 , 48 , 49 , 50 ], epithelial carcinomas (esophagus, liver, kidney, endometrial carcinomas) [ 13 , 24 , 51 , 52 , 53 , 54 , 55 ] and gliomas [ 51 , 56 ]. Although these studies separately showed elevated expressions of CD38 and NGAL-R, it is very likely that both antigens are co-expressed in these tumors, and therefore suggest that a combination of anti-CD38/NGAL-R Abs may offer new therapeutic options for the management of these cancers.…”

Section: Discussionmentioning

confidence: 99%

The Value of Neutrophil Gelatinase-Associated Lipocalin Receptor as a Novel Partner of CD38 in Chronic Lymphocytic Leukemia: From an Adverse Prognostic Factor to a Potential Pharmacological Target?

Bauvois,

Chapiro,

Quiney

et al. 2023

Biomedicines

View full text Add to dashboard Cite

Chronic lymphocytic leukemia (CLL) is characterized by the accumulation of neoplastic B lymphocytes that escape death, and correlates with the expression of negative prognostic markers such as the CD38 antigen. Although certain new drugs approved by the US Food and Drug Administration improve the clinical outcome of CLL patients, drug resistance and disease relapse still occur. Like CD38, neutrophil gelatinase-associated lipocalin receptor (NGAL-R) is frequently overexpressed in CLL cells. Here, we evaluated the concomitant surface expression of NGAL-R and CD38 in leukemic blood cells from 52 CLL patients (37 untreated, 8 in clinical remission, and 7 relapsed). We provide evidence of a positive correlation between NGAL-R and CD38 levels both in the interpatient cohorts (p < 0.0001) and in individual patients, indicating a constitutive association of NGAL-R and CD38 at the cell level. Patients with progressing CLL showed a time-dependent increase in NGAL-R/CD38 levels. In treated CLL patients who achieved clinical remission, NGAL-R/CD38 levels were decreased, and were significantly lower than in the untreated and relapsed groups (p < 0.02). As NGAL-R and CD38 participate in CLL cell survival, envisioning their simultaneous inhibition with bispecific NGAL-R/CD38 antibodies capable of inducing leukemic cell death might provide therapeutic benefit for CLL patients.

show abstract

Chronic neutrophilic leukemia with plasma cell dyscrasia: friends or relatives?

Erber

Reilly

2013

Leukemia & Lymphoma

View full text Add to dashboard Cite

Lipocalin‐2 is associated with modulation of disease phenotype in a patient with concurrent JAK2‐V617F and BCR‐ABL mutation

Cited by 4 publications

References 11 publications

Revisiting Neutrophil Gelatinase-Associated Lipocalin (NGAL) in Cancer: Saint or Sinner?

Revisiting Neutrophil Gelatinase-Associated Lipocalin (NGAL) in Cancer: Saint or Sinner?

The Value of Neutrophil Gelatinase-Associated Lipocalin Receptor as a Novel Partner of CD38 in Chronic Lymphocytic Leukemia: From an Adverse Prognostic Factor to a Potential Pharmacological Target?

Chronic neutrophilic leukemia with plasma cell dyscrasia: friends or relatives?

Contact Info

Product

Resources

About