scispace - formally typeset
Search or ask a question

Answers from top 10 papers

More filters
Papers (10)Insight
Hence, pharmacologically targeting mutant ras oncogenes could conceivably suppress solid tumor growth in vivo, in part, by inhibiting tumor-induced angiogenesis.
Thus, oncogenes may cause complex changes in the ability of GBM cancer cells to interact with the coagulation system, thereby exacerbating its influence on angiogenesis and disease progression.
Recent data indicate that developmental and tumor angiogenesis can be induced by cellular oncogenes, leading to the enhanced activity of molecules stimulating angiogenesis.
The results suggest that dominantly acting ras oncogenes may contribute to the growth of solid tumors in vivo not only by a direct effect on tumor cell proliferation but also indirectly, i. e., by facilitating tumor angiogenesis.
However, activated oncogenes might also facilitate angiogenesis by down-regulating endogenous inhibitors of angiogenesis.
Although activated oncogenes increase tumor cell proliferation and decrease their apoptosis, these activities are not sufficient to expand tumor mass beyond a microscopic size.
Oncogenes must also induce tumor angiogenesis for expansion of tumor mass.
We propose that normalization of the vascular network by targeting oncogenes in the tumor cells might lead to more efficient and sustained therapeutic effects compared to therapies targeting tumor vessels.
Thus, oncogenes can impact several interconnected aspects of cellular growth, survival, and angiogenesis.

Related Questions

Types of Oncogenes?4 answersOncogenes are altered versions of proto-oncogenes that are involved in the regulation of cell growth and are activated by mutation, chromosomal rearrangement, or gene amplification. Approximately 20 different oncogenes have been reproducibly activated in various types of malignancies, including breast, colon, lung, pancreatic, and thyroid carcinomas, leukemias, and lymphomas. These oncogenes can serve as potential markers for early detection of cancer, depending on the stage of tumor development at which they are activated. In addition to deregulating cell proliferation or suppressing apoptosis, oncogenes may also play a role in cell lineage determination and the behavior of cancer stem cells. Alterations in the expression of oncogenes, tumor suppressor genes, and apoptosis-inducing genes are frequently observed in cancer cells and can impact the development and maintenance of malignant phenotypes. Restoring the normal function of these genes has shown promise as an effective means of cancer therapy, although effective delivery of these genes to cancer cells is crucial.
What is the role of angiogenesis in the progression of glioma tumors?5 answersAngiogenesis plays a crucial role in the progression of glioma tumors. Glioblastoma multiforme (GBM), a highly invasive and vascularized brain tumor, relies on angiogenesis for growth and survival. Angiogenic factors such as vascular endothelial growth factor (VEGF) and angiopoietins (Ang-1, Ang-2, and Ang-4) promote tumor angiogenesis and contribute to GBM progression. The formation of a microvascular network provides oxygen, nutrients, and growth factors to glioma cells, facilitating their proliferation, survival, and invasion. Abnormal activation of tumor angiogenesis and the mutation of isocitrate dehydrogenase are associated with higher anaplasia levels in anaplastic gliomas. Anti-angiogenesis therapies, such as targeting VEGF or using anti-angiogenic antibodies like bevacizumab, have shown clinical efficacy in GBM treatment by inhibiting tumor angiogenesis. However, therapeutic resistance and the activation of alternative angiogenesis pathways remain challenges in GBM treatment. Understanding the molecular basis of angiogenesis and identifying novel angiogenic factors may provide new therapeutic targets for controlling glioma progression.
What are most famous angiogenic motifs that have been studied recently?5 answersThe most famous angiogenic motifs that have been studied recently include the VHHQKLVFF sequence found in Abeta peptides, the C-terminal cystine knot motifs present in key angiogenic regulators such as Slit3, von Willebrand factor, platelet-derived growth factor-B, and VEGF-A, and the vascular endothelial growth factor (VEGF) which guides the growth of new blood vessels. These motifs have been shown to play important roles in angiogenesis, which is the formation and sprouting of new blood vessels from pre-existing vascular structures. The Abeta peptide sequence VHHQKLVFF has been found to exhibit potent anti-angiogenic effects and may have clinical relevance as an anti-angiogenic agent. The C-terminal cystine knot motifs, particularly those found in connective tissue growth factor (CCN2/CTGF), have been shown to promote angiogenesis and have therapeutic potential for antiangiogenesis. VEGF has been extensively studied for its role in guiding the growth of new blood vessels.
What are angiogenic motifs?3 answersAngiogenic motifs are sequences within proteins that play a role in the process of angiogenesis, which is the formation of new blood vessels from existing ones. These motifs can be found in various angiogenic factors and are involved in initiating specific events within the complex cascade of pathways that lead to angiogenesis. However, the exact nature and characteristics of angiogenic motifs are still being studied.
Does VEGF inhibit angiogenesis?10 answers
Does angiogenesis inhibit tumor growth?10 answers

See what other people are reading

What is the expression of c-Myc in prostatic cancer immunohistochemistry?
5 answers
The expression of c-Myc in prostatic cancer immunohistochemistry varies based on different parameters. Studies show that c-Myc overexpression diminishes the androgen receptor (AR) transcriptional program in prostate cells, accelerating cancer progression towards metastasis. In muscle-invasive urothelial carcinoma of the bladder, nuclear c-Myc expression correlates with poor prognostic factors and tumor invasion patterns. Additionally, c-Myc plays a crucial role in immortalizing human prostate epithelial cells, contributing to prostate cancer development without the need for additional genetic lesions. Furthermore, c-Myc is implicated in regulating the expression and activity of androgen receptor isoforms in castration-resistant prostate cancer, suggesting its potential as a therapeutic target. High c-Myc levels are significantly associated with elevated HIF-1α expression, suggesting a potential biomarker role in prostate cancer characterization.
What role do hepatic stellate cells play on T cells form pancreatic cancer by means of memory?
4 answers
Hepatic stellate cells (HSCs) have been shown to exert immunosuppressive effects on T cells in the context of cancer. Studies have demonstrated that activated HSCs induce T-cell hyporesponsiveness, leading to T-cell anergy and increased regulatory T (Treg) cell populations, ultimately facilitating immune evasion by cancer cells. Additionally, in the case of pancreatic cancer, pancreatic stellate cells (PSCs) have been found to suppress the function of natural killer (NK) cells in the tumor microenvironment, potentially contributing to immune suppression. These findings collectively suggest that stellate cells, whether hepatic or pancreatic, play a crucial role in modulating immune responses, including T-cell functions, within the tumor microenvironment, thereby influencing the immune surveillance and anti-tumor responses in cancer settings.
Which are the roles of NRP1 in endothelial cells in the hypothalamus?
5 answers
Neuropilin 1 (NRP1) plays crucial roles in endothelial cells within the hypothalamus. In the context of the mature brain, NRP1 interacts with the 65 kDa isoform of Sema3A, guiding axonal sprouting in hypothalamic neurons that secrete gonadotropin-releasing hormone (GnRH). Additionally, NRP1 is involved in promoting blood vessel growth independently and synergistically with VEGFR2 pathways, modulating angiogenesis and vascular permeability. Furthermore, NRP1 proteolytic cleavage generates C-terminal domain NRP1 proteins in endothelial cells, which regulate VEGF-induced phosphorylation of VEGFR2 and endothelial cell motility, impacting angiogenesis. These findings collectively highlight NRP1's multifaceted functions in endothelial cells within the hypothalamus, influencing axonal growth, vascular development, and signaling pathways critical for physiological processes.
What is extravasation in metastatis?
4 answers
Extravasation in metastasis refers to the crucial step where cancer cells exit the bloodstream at distant sites to establish new colonies. This process involves cancer cells adhering to vascular endothelial cells, crossing vessel walls, and interacting with circulating platelets, leukocytes, and the local tissue microenvironment. Understanding the molecular mechanisms governing extravasation is essential for developing effective anti-metastasis strategies. Recent studies have highlighted the significance of extravasation inhibition as a promising approach for treating cancer metastasis. By visualizing cancer extravasation stages and identifying key molecules involved, researchers aim to discover new therapeutic targets to impede this critical step in the metastatic cascade.
What is known about the role of hypoxia in mRNA regulation in breast cancer?
8 answers
Hypoxia, a common feature in the tumor microenvironment of breast cancer, significantly influences mRNA regulation, affecting cancer progression and patient survival. The transcription factor CCAAT/enhancer binding protein-α (C/EBPα), known for its role in cell differentiation and proliferation, is down-regulated under hypoxic conditions in T-47D breast cancer cells. This down-regulation involves both transcriptional repression and decreased mRNA stability, mediated by hypoxia-inducible factor (HIF)-1α. Furthermore, hypoxia impairs the type I interferon (IFN) pathway, crucial for immune response against tumors, by suppressing mRNA and protein expressions of key components in this pathway, including sensors, adaptors, and transcription factors, in a manner that is independent of HIF1/2α. The expression of hypoxia-inducible factors (HIFs), particularly HIF-1, is pivotal in adapting solid tumors to hypoxic conditions, influencing the expression of genes involved in cancer progression. RNA sequencing studies reveal that hypoxia leads to differential expression of genes related to glycolysis, proliferation, growth, and migration in T47D breast cancer cells. Hypoxia also appears to modulate the expression of APOBEC3A and APOBEC3B, enzymes involved in mutation and tumor progression, suggesting a complex interaction between hypoxia and genetic variability within tumors. Long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs) are also regulated by hypoxia, playing roles in tumorigenesis and cancer progression. NDRG1-OT1, a hypoxia-induced lncRNA, is upregulated under hypoxic conditions and promotes tumor growth and migration, acting as a miRNA sponge. Similarly, hypoxia-related circRNAs are involved in the progression, angiogenesis, metabolic reprogramming, and stemness maintenance of breast cancer. Single-cell and bulk sequencing data have been utilized to construct hypoxia-related prognostic signatures, highlighting the importance of hypoxia in breast cancer prognosis. The role of hypoxia-associated lncRNAs in breast cancer underscores their potential as diagnostic and prognostic tools, further emphasizing the critical impact of hypoxia on mRNA regulation in breast cancer.
What is the role of ruberythrin?
5 answers
Rubrerythrins play a crucial role in oxidative stress protection in various organisms. These non-heme iron proteins are involved in scavenging peroxides, providing defense against oxidative damage. Rubrerythrins are particularly essential in anaerobic environments, where they help protect against hydrogen peroxide and dioxygen sensitivity. The protein structure of rubrerythrins includes a Fe-S center that aids in electron transfer, contributing to their catalytic reduction of intracellular hydrogen peroxide. Rubrerythrins have evolved in response to changing environmental conditions, with different lineages adapting to varying oxygen concentrations and temperatures. Overall, rubrerythrins are vital components in the defense mechanisms of organisms against oxidative stress, showcasing their significance in maintaining cellular homeostasis and survival in challenging environments.
What cells produce Il-6 in peridontal tissue?
5 answers
IL-6 in periodontal tissues is primarily produced by human periodontal ligament fibroblasts (HPLF) and gingival fibroblasts, which are stimulated by pro-inflammatory cytokines such as IL-1 and TNF-alpha. Additionally, IL-4- and IL-6-producing cells have been identified in periodontal disease tissues, with a higher percentage of IL-4+ cells in periodontal lesions compared to gingivitis tissues. Furthermore, IL-35 has been shown to inhibit IL-6 production in human periodontal ligament cells (HPDLCs) stimulated with IL-17A, suggesting a regulatory role in controlling IL-6 levels in periodontal tissues. Overall, these findings highlight the involvement of various cell types and cytokines in the production of IL-6 within the complex microenvironment of periodontal tissues.
Why trypan blue is added to cell culture haemocytometer?
4 answers
Trypan blue is added to cell culture haemocytometer for cell viability assessment and counting. It is a widely used dye that stains dead cells blue, allowing for easy differentiation between live and dead cells under a microscope. The combination of trypan blue with a haemocytometer is considered the standard approach to estimate cell population density and assess viability in 2D and 3D cultures. This method provides a rapid and convenient way to determine the overall viability of cells in a culture before experiments or to quantify cell death post-treatment with cytotoxic agents. Additionally, trypan blue staining can be adapted for in situ staining of adherent cells on ELISA plates, offering a practical tool for preliminary cell viability assessment in high-throughput settings.
What is the current state of research on Pomiferin as an antineoplastic agent?
4 answers
Pomiferin, a natural product from Osage Orange, has shown promising potential as an antineoplastic agent. It has been identified as an autophagy activator that overcomes innate and acquired drug resistance in cancer. Additionally, heteroleptic copper(II) complexes containing pomiferin have demonstrated significant cytotoxicity against various cancer cell lines, including cisplatin-resistant ovarian carcinoma. Furthermore, studies on ponicidin, a diterpenoid similar to pomiferin, have highlighted its antioxidant and anticancer properties, suggesting the potential of pomiferin as a cancer chemotherapeutic agent. Moreover, mangiferin, another natural compound, has been explored for its anti-cancer properties and bioavailability enhancement strategies, indicating the promising nature of natural compounds like pomiferin in cancer treatment. Overall, research indicates that pomiferin holds great promise as an effective agent in combating cancer.
How does reregulation of the MAPK signalling pathway affect tumorigenesis?
4 answers
The dysregulation of the Mitogen-Activated Protein Kinase (MAPK) signaling pathway significantly impacts tumorigenesis by influencing various aspects of cancer development and progression. Abnormalities in the MAPK pathway, including hyperactivation of ERK1 and ERK2, play a crucial role in promoting cancer cell growth, invasion, metastasis, and angiogenesis. Studies have shown that modulating the MAPK pathway through polyphenolic compounds from dietary sources can suppress cancerous cell growth, induce cell death, alter immunity, and block angiogenesis, thereby inhibiting tumorigenesis. Additionally, the inhibition of MAPK signaling pathways has been demonstrated to disrupt tumor vasculature, leading to the suppression of renal cell carcinoma growth. The re-regulation of the MAPK pathway through various interventions holds promise for developing effective strategies to combat cancer progression.
How do matrix metalloproteinases affect bone metastases?
5 answers
Matrix metalloproteinases (MMPs) play a crucial role in bone metastases. MMP-2 is associated with aggressive breast cancer growth in bone, promoting tumor progression and bone destruction. MMP-2's dysregulation can lead to osteolytic effects, either through excessive activation in late-stage cancers or loss-of-function mutations causing skeletal developmental disorders. MMPs, including MMP-2, facilitate cancer metastasis by degrading the extracellular matrix, aiding in invasion and metastatic spread. Specifically, MMP-13 has been linked to breast cancer bone metastasis by promoting osteoclastogenesis. Targeting MMPs, such as with selective inhibitors like BMMPIs, shows promise in reducing tumor growth, bone destruction, and promoting tumor apoptosis in bone metastatic breast cancer. These findings highlight the significant impact of MMPs on bone metastases and the potential for targeted therapies in managing this aspect of cancer progression.