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- Table of Contents
7 Citations 16 Q&As
Facts about Insulin-like growth factor-binding protein 7.
Binds IGF-I and IGF-II with a relatively low affinity.
Stimulates prostacyclin (PGI2) production.Stimulates cell adhesion. .
Human | |
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Gene Name: | IGFBP7 |
Uniprot: | Q16270 |
Entrez: | 3490 |
Belongs to: |
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No superfamily |
angiomodulin; FSTL2; IBP-7; IGFBP7; IGFBP-7; IGFBP-7PGI2-stimulating factor; IGFBP-7v; IGFBPrp1; IGFBP-rp1; insulin-like growth factor binding protein 7; insulin-like growth factor-binding protein 7; MAC25 protein; Mac25; MAC25IGF-binding protein 7; Prostacyclin-stimulating factor; PSF; PSFAGM; TAF; Tumor-derived adhesion factor
Mass (kDA):
29.13 kDA
Human | |
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Location: | 4q12 |
Sequence: | 4; NC_000004.12 (57030773..57110385, complement) |
Secreted.
Boster Bio: The latest tumor marker for B-lineage ALL cells, IGFBP7 has many promising uses in the diagnosis of a variety of diseases. We'll explore IGFBP7's potential role as a tumor marker in lung adenocarcinoma as well as the necessity of RRT for patients suffering from the disease.
Researchers discovered that IGFBP7 is a new indicator in patients with high risk myeloma. It functions as a receptor for insulin-like growth factors (IGF). The protein is also involved in regulating the levels of the pro-angiogenic factor-beta-secretase inhibitor TIMP-2. This study is solely focused on predicting eGFR for patients with MM, without regard to clinically relevant covariates.
Researchers have discovered that IGFBP7 is a gene that is coexpressed in AML and T–ALL. IGFBP7 may play a role in the survival and proliferation of cancerous leukemic cells. The bone marrow cells, which make the protein, known as bone marrow stromal cells, are also vital components of bone.
The researchers attributed the finding to variations in protein expression among patients with RI. The study identified IGFBP-7 levels that were higher in the urine and serum of RI patients. Although the source of the protein's exact origin is unknown, IGFBP7 levels were higher in patients receiving maintenance chemotherapy than in patients receiving stem cell transplant. These findings suggest that IGFBP7 might be able to block the inhibitory effects of bone-morphogenetic protein which could explain the link between tumor burden and symptomatic disease.
The authors conducted a series of non-routine laboratory tests to evaluate the relationship between IGFBP7 and the levels of NT proBNP and IL-6 as well as NGAL. These tests were conducted on 73 patients suffering from high risk myeloma or no-symptomatic myeloma. They also observed a negative correlation between serum IGFBP-7 and TIMP-2 levels in urine.
These findings suggest that IGFBP7 could be a novel indicator for high-risk myeloma. This protein has been linked to diseases that require immune surveillance and homeostasis. This study may provide a conceptual framework to help with risk assessment. It will be very useful to identify patients suffering from this mutation to improve the treatment of their illness.
It is not known the role that IGFBP-7 plays in MM, but it appears to play a role in the process of causing renal damage. The study of the molecule will be required to confirm its role in the progression of the disease. It's still a possible biomarker in nephropathy, though its presence in the kidneys suggests a connection with diabetic nephropathy or primary myeloma.
The present study demonstrates that IGFBP7 levels are a plausible indicator of the need for RRT. Although not directly predictive of the need for RRT, the levels of TIMP-2, serum creatinine, and IGFBP7 were useful in risk classification. The C-statistics of these biomarkers were improved when they were paired with serum creatinine. The results of this study suggest that a combination of these biomarkers could be a better predictor of the need for RRT.
The sensitiveness and specificity were calculated using the bivariate model of normality with log-transformed sensitivities as well as specificities. The overall analysis was based on several cutoff points. The statistical tests were paired and P0.05 was considered significant. Stata 12.0 software was used for all statistical analyses. The results are comparable to previous studies. The results support the notion that IGFBP7 could predict the need for RRT in Boster Bio.
Urine samples were taken at four 12 and 24 hours post-surgery as well as during the first week of ICU stay. All studies used a commercial Nephro-Check kit. The most common cutoff values were 2.0.3ng/mL2/1000. However, the cutoff values for moderate-to-severe AKI decreased to 38%.
In a recent study researchers discovered that IGFBP-7 levels and NGAL were better predictors of survival than NGAL. NGAL and IGFBP-7 did not have any significant influence on predicting mortality, however both markers were predictive of need for RRT. These findings are encouraging but further research is required. The results of this study are published in Boster Bio.
Although there's no evidence to determine the predictive power of these biomarkers, it can be concluded that TIMP-2 levels and IGFBP7 levels are reliable predictors of RRT. The authors found that TIMP-2 and IGFBP-7 levels were significantly higher after surgery TIMP-2 significantly improved the prediction of the need for RRT at stage three AKI levels as well as NGAL levels.
IGFBP7 and TIMP-2 are both important biomarkers of stress in the cellular. Their combined expression was associated with a delay in functioning of the graft. AUC of ROC of 0.541 (95% 95% confidence interval: 0.441 to 0.807) showed an extremely strong correlation with delayed graft function within the first 24 h following kidney transplant. Additionally, TIMP-2 and IGFBP7 are highly accurate in predicting the necessity for RRT in Boster Bio.
Studies have previously demonstrated that IGFBP7 promotes osteogenesis in bone-derived tissues, a process associated with myeloma bone disease. Primary BMSCs were cultured in osteogenic media for 21 days and their expression of IGFBP7 was measured using quantitative PCR. We also assessed the alkaline phosphatase activity of primary BMSCs on days 7 and 14 of differentiation compared to control cells.
We then investigated whether IGFBP7 interferes with the growth of B-lineage ALL cells by inhibiting the expression of CD47 by BMSCs. We co-cultured primary MM cells human BMSC TERT+ cells (BMSC TERT+) in the presence or absence of HMCLs. We found that rhIGFBP7 significantly hindered the proliferation of primary MM cells. We also observed that the expression of IGFBP7 was significantly lower in BM samples compared with those from healthy donors.
These results show that IGFBP7 suppresses asparaginase activity in B-lineage ALL cells via creating DNA methylation. In this study, IGFBP7 expression was decreased in malignant plasma cells (MPCLs). In addition, the expression of IGFBP7 was lower than that in normal B-lineage ALL cells, suggesting that myeloma-like cells are not dependent on antagonistic BMP activity.
Another study demonstrated that inhibition of the NF-kB signaling pathway repressed asparaginase-resilection in B-lineage ALL cells. The inhibitors of this pathway also affected the cell's chemoprotective function. In addition, IGFBP7 inhibition inhibits the activity integrins in leukemia cells.
A number of studies have implicated IGFBP7 in many cancers, including colon cancer. Recent studies have revealed that high levels of IGFBP7 are associated with poor outcomes. In addition, IGFBP7 expression has also been associated with the development of colorectal cancer, and the inhibition of IGFBP7 prevented the growth and development of the colon.
We found that in 71% of cases of ETP-ALL, asparaginase-resisistance in B-lineage ALL was associated with a monoclonal rearrangement of T-cell receptor genes. Additionally, the analysis of IGFBP7 gene mutations revealed no significant differences between the T-ALL subgroups. It is important to study the therapeutic potential of other agents for treating T-ALL.
It has been proven that tumors can infiltrate lymphatic vessels via the IGFBP7 gene. This pathway is involved in lymphangiogenesis, which is the process through cancer cells migrate from one site to the next. Lymphangiogenesis is closely linked to metastasis. In lung cancers tumor cells, tumor cells may trigger lymphangiogenesis by secreting the VEGF-C, VEGF-D, and VEGF-R-3.
Serum IGFBP7 was significantly higher in patients suffering from ESCC than in healthy controls. The difference was statistically significant for patients suffering from ESCC and those with lung cancer in the early stages, regardless of age or stage. This study has shown that the IGFBP7 is a sensitive and specific tumor marker for predicting the presence of lymphatic metastases in lung adenocarcinoma.
IGFBP7 is a growth hormone found in all human cells. Despite its abundant presence in healthy tissues, IGFBP7 is up-regulated in certain forms of lung cancer. It is also believed to be a dual role player in cancer because it can function as both a tumor suppressor and as an oncogene that alters the susceptibility of cells to chemotherapy agents.
IGFBP7 is also a potential tumor marker to predict the presence of lymph nodes in patients with lung adenocarcinima. It is linked to lymphatic tissue infiltrating tumor cells. Researchers are currently looking into whether IGFBP7 is a tumor marker for lymphatic metastases in patients with lung cancer.
The IGFBP7 gene, which is highly expressed in the lymphatic system of lung cancer, correlates with favorable nodal status. It's not beneficial for patients' recurrence free survival. Although IGFBP7 has been linked with favorable prognosis for lung tumors Adenocarcinoma, its angiogenic function may be in contradiction to its role in tumor suppression.
Researchers used Human Genome Microarrays (HGM) to compare gene expression profiles in lung cancer. They identified 181 genes that were 2-fold more frequent in patients with lung cancer. Patients with lung adenocarcinoma also had significantly higher levels of a variety of membrane proteins that are closely associated with metabolic disease and also the endocrine system.
PMID: 7694637 by Murphy M., et al. Identification and characterization of genes differentially expressed in meningiomas.
PMID: 7980422 by Yamauchi T., et al. Purification and molecular cloning of prostacyclin-stimulating factor from serum-free conditioned medium of human diploid fibroblast cells.
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