Patterns of practice of androgen deprivation therapy combined to radiotherapy in favorable and unfavorable intermediate risk prostate cancer. Results of The PROACT Survey from the French GETUG Radiation Oncology group
urpose: The medium-risk (IR) prostate cancer (PCa) are a heterogeneous group in terms of prognosis. For unfavorable or favorable IR PCa treated with radiotherapy, the remnants of the optimal strategy to be defined. In routine practice, doctor’s decision to propose hormonal therapy (HT) is controversial. PROACT survey aims to evaluate patterns and preferences of daily practice in France at this IR population.
Materials and Methods: A questionnaire was distributed to member web 91 French radiotherapy centers of the Groupe d’Etude des Tumeurs Uro-Genitales (GETUG). The questionnaire included four sections on: (i) specialists who prescribe treatment and multidisciplinary decision (MTD) validation; (Ii) the definition of patient subsets IR; (Iii) the parameters of radiotherapy; (Iv) regarding the practice patterns of cardiovascular (CV) and (iv) a metabolic evaluation. Descriptive presentation of the results is used.
Results: Among the 82 responses (90% of the centers), HT schedule and irradiation techniques validated by a particular board meeting in 54% and 45% of the center, respectively. Three-quarters (76%) of centers identify a subset of patients with IR to specific strategies. The majority of the center considers PSA> 15 (77%) and / or Gleason 7 (4 + 3) (87%) for the definition of IR unfavorable. Overall, 41% of the center is carried out systematically evaluate CV before HT prescription while 61% only consider CV history / status in defining the type of HT. LHRH agonists is often prescribed in both favorable (70%) and unfavorable (98%) patients with IR. Finally, weight loss (80%), metabolic profile (70%) and CV status (77%) of patients considered for follow-up under HT.
Conclusion: To the best of our knowledge, this is the first survey on practices in IR PCa HT. PROACT survey showed that three-quarters of respondents identified a subset of IR-patients in adjusting therapy. CV status of patients considered in guiding decisions HT, duration and type of .
Two professions against two killer diseases: reason, organizations, and the initial experience cardio-oncology services
Background: Cardiovascular disease (CV) is the most common factor affecting the prognosis in cancer patients. Cardio-oncology (CO) service has been developed to solve this problem. The lack of results regarding patient demographics and clinical findings applicable and available data is limited to the services CO evaluate patients undergoing chemotherapy only.
Purpose: To demonstrate initial experience CO service was conducted in a tertiary oncology centers. Methods: CO Service is designed to include two major domains: general and consulting CO electrotherapy. Patients who are referred to a collection service CO with basic demographics, type of cancer, the reason for referral, cardiac evaluation, and initial clinical results were included in this observational study.
Results: All cancer patients referred to our CO service between March 2016 and December 2019 included in this study. A total of 2,762 (77% female) patients at a mean (SD) age of 62 (12) years referenced (63% on the basis of hospitalization) for public consultation.
The most frequent diagnosis was breast cancer (66%). In 18% of patients, the reason for referral to services CO is the treatment of cancer-related complications CV. A total of 652 patients (515 patients with cardiac implantable electronic device (CIED) eligible for radiotherapy (RT), 48 patients with diagnosed CIEDs by magnetic resonance imaging (MRI), and 89 patients with cancer treated with surgery CIED) were evaluated by a team CO- CIED. During the 5872 session of the RT total, two dangerous interactions and no other complications during MRI and surgery were recorded.
Diet Association Quality With Survival Among People With Metastatic Colorectal Cancer at the Cancer and Leukemia Group B and the Southwest Oncology 80 405 Experiment
Importance: Diet has been associated with survival in patients with stage I to III colorectal cancer, but the data in patients with metastatic colorectal cancer are limited.
Objective: To examine the relationship between diet quality and overall survival among individuals with metastatic colorectal cancer.
Design, setting, and participants: This study is a prospective cohort study of patients with metastatic colorectal cancer enrolled in the Cancer and Leukemia Group B (Alliance) and the Southwest Oncology Group 80 405 trials between 27 October 2005 and 29 February 2012, and followed up through January 2018 ,
Exposure: Participants completed a validated food frequency questionnaire within 4 weeks after starting first-line treatment for metastatic colorectal cancer. Diet categorized according to the Alternative Healthy Eating Index (AHEI), Alternative Mediterranean Diet (AMED) score, diet Approaches to Stop Hypertension (DASH) score, and Western and prudent dietary pattern derived using principal component analysis. Participants were classified into sex-specific quintiles.
The main results and measures: multivariable hazard ratio (HR) and 95% CI for overall survival.
Description: VEGF R2 (mouseFlk1 gene), VEGF R1 (Flt1) and VEGF R3 (Flt4) belong to the class III subfamily of receptor tyrosine kinases (RTKs). All three receptors contain seven immunoglobulinlike repeats in their extracellular domains and kinase insert domains in their intracellular regions. The expression of VEGF R1, 2, and 3 is almost exclusively restricted to the endothelial cells. These receptors are likely to play essential roles in vasculogenesis and angiogenesis. Mouse VEGF R2 cDNA encodes a 1367 amino acid (aa) precursor protein with a 19 aa signal peptide. Mature VEGF R2 is composed of a 743 aa extracellular domain, a 22 aa transmembrane domain, and a 583 aa cytoplasmic domain. In contrast to VEGF R1 which binds both PlGF and VEGF with high affinity, VEGF R2 binds VEGF but not PlGF with high affinity. The solube receptor was used as a an antigen.
Description: VEGF R1 (Flt-1), VEGF R2 (KDR/Flk-1), and VEGF R3 (Flt-4) belong to the class III subfamily of receptor tyrosine kinases (RTKs). All three receptors contain seven immunoglobulin-like repeats in their extracellular domain and kinase insert domains in their intracellular region. They are best known for regulating VEGF family-mediated vasculogenesis, angiogenesis, and lymphangiogenesis. They are also mediators of neurotrophic activity and regulators of hematopoietic development. VEGF R2 is thought to be the primary inducer of VEGF-mediated blood vessel growth, while VEGF R3 plays a significant role in VEGF-C and VEGF-D-mediated lymphangiogenesis.
Description: VEGF R1 (Flt-1), VEGF R2 (KDR/Flk-1), and VEGF R3 (Flt-4) belong to the class III subfamily of receptor tyrosine kinases (RTKs). All three receptors contain seven immunoglobulin-like repeats in their extracellular domain and kinase insert domains in their intracellular region. They are best known for regulating VEGF family-mediated vasculogenesis, angiogenesis, and lymphangiogenesis. They are also mediators of neurotrophic activity and regulators of hematopoietic development. VEGF R2 is thought to be the primary inducer of VEGF-mediated blood vessel growth, while VEGF R3 plays a significant role in VEGF-C and VEGF-D-mediated lymphangiogenesis.
Description: VEGF R2 (mouseFlk1 gene), VEGF R1 (Flt1) and VEGF R3 (Flt4) belong to the class III subfamily of receptor tyrosine kinases (RTKs). All three receptors contain seven immunoglobulinlike repeats in their extracellular domains and kinase insert domains in their intracellular regions. The expression of VEGF R1, 2, and 3 is almost exclusively restricted to the endothelial cells. These receptors are likely to play essential roles in vasculogenesis and angiogenesis. Mouse VEGF R2 cDNA encodes a 1367 amino acid (aa) precursor protein with a 19 aa signal peptide. Mature VEGF R2 is composed of a 743 aa extracellular domain, a 22 aa transmembrane domain, and a 583 aa cytoplasmic domain. In contrast to VEGF R1 which binds both PlGF and VEGF with high affinity, VEGF R2 binds VEGF but not PlGF with high affinity. The solube receptor was used as a an antigen.
Description: The antibody recognizes mouse vascular endothelial growth factor receptor 2, alos known as CD309, VEGFR2, KDR, protein tyrosine kinase receptor flk-1, and fetal liver kinase-1. Flk-1 is a member of the tyrosine protein kinase family, sub-family CSF-1/PDGF, that contains a single pass transmembrane receptor with a protein kinase domain and seven immunoglobulin-like domains in the extracellular region. Flk-1 is expressed at high levels in adult heart, lung, kidney, brain, and skeletal muscle; other tissues express at lower levels. Flk-1 is a receptor for VEGF-A or fully processed VEGF-C; ligand binding plays a key role in vascular development and vascular permeability.
Description: Disruption of the precise balance of positive and negative molecular regulators of blood and lymphatic vessel growth can lead to myriad diseases. Although dozens of natural inhibitors of hemangiogenesis have been identified, an endogenous selective inhibitor of lymphatic vessel growth has not to our knowledge been previously described. A splice variant of the gene encoding vascular endothelial growth factor receptor-2 (VEGFR-2) that encodes a secreted form of the protein, designated endogenous soluble VEGFR-2 (esVEGFR-2/KDR) has been described. The endogenous soluble esKDR inhibits developmental and reparative lymphangiogenesis by blocking VEGF-C function. Tissue-specific loss of esKDR in mice induced, at birth, spontaneous lymphatic invasion of the normally alymphatic cornea and hyperplasia of skin lymphatics without affecting blood vasculature. Administration of esKDR inhibited lymphangiogenesis but not hemangiogenesis induced by corneal suture injury or transplantation, enhanced corneal allograft survival and suppressed lymphangioma cellular proliferation. Naturally occurring esKDR thus acts as a molecular uncoupler of blood and lymphatic vessels; modulation of esKDR might have therapeutic effects in treating lymphatic vascular malformations, transplantation rejection and, potentially, tumor lymphangiogenesis and lymphedema. Recombinant human esKDR generated by alternative splicing consist of the first 6 Ig-like loops followed by the unique C-terminal end: GMEASLGDRIAMP.
Mouse VEGFR-2/Flk-1 (native), soluble Recombinant Protein
Description: Disruption of the precise balance of positive and negative molecular regulators of blood and lymphatic vessel growth can lead to myriad diseases. Although dozens of natural inhibitors of hemangiogenesis have been identified, an endogenous selective inhibitor of lymphatic vessel growth has not to our knowledge been previously described. A splice variant of the gene encoding vascular endothelial growth factor receptor-2 (VEGFR-2) that encodes a secreted form of the protein, designated endogenous soluble VEGFR-2 (esVEGFR-2/KDR) has been described. The endogenous soluble esKDR inhibits developmental and reparative lymphangiogenesis by blocking VEGF-C function. Tissue-specific loss of esKDR in mice induced, at birth, spontaneous lymphatic invasion of the normally alymphatic cornea and hyperplasia of skin lymphatics without affecting blood vasculature. Administration of esKDR inhibited lymphangiogenesis but not hemangiogenesis induced by corneal suture injury or transplantation, enhanced corneal allograft survival and suppressed lymphangioma cellular proliferation. Naturally occurring esKDR thus acts as a molecular uncoupler of blood and lymphatic vessels; modulation of esKDR might have therapeutic effects in treating lymphatic vascular malformations, transplantation rejection and, potentially, tumor lymphangiogenesis and lymphedema. Recombinant human esKDR generated by alternative splicing consist of the first 6 Ig-like loops followed by the unique C-terminal end: GMEASLGDRIAMP.
Description: VEGF R1 (Flt-1), VEGF R2 (KDR/Flk-1), and VEGF R3 (Flt-4) belong to the class III subfamily of receptor tyrosine kinases (RTKs). All three receptors contain seven immunoglobulin-like repeats in their extracellular domain and kinase insert domains in their intracellular region. They are best known for regulating VEGF family-mediated vasculogenesis, angiogenesis, and lymphangiogenesis. They are also mediators of neurotrophic activity and regulators of hematopoietic development. Human VEGF R2 is thought to be the primary inducer of VEGF-mediated blood vessel growth, while VEGF R3 plays a significant role in VEGF-C and VEGF-D-mediated lymphangiogenesis.
Description: Endothelial cells express three different vascular endothelial growth factor (VEGF) receptors, belonging to the family of receptor tyrosine kinases (RTKs). They are named VEGFR-1 (Flt-1), VEGFR-2 (KDR/Flk-1), VEGFR-3 (Flt-4). Their expression is almost exclusively restricted to endothelial cells, but VEGFR-1 can also be found on monocytes, dendritic cells and on trophoblast cells. The flt-1 gene was first described in 1990. The receptor contains seven immunoglobulin-like extracellular domains, a single transmembrane region and an intracellular splited tyrosine kinase domain. Compared to VEGFR-2 the Flt-1 receptor has a higher affinity for VEGF but a weaker signaling activity. VEGFR-1 thus leads not to proliferation of endothelial cells, but mediates signals for differentiation. Interestingly a naturally occuring soluble variant of VEGFR-1 (sVEGFR-1) was found in HUVEC supernatants in 1996, which is generated by alternative splicing of the flt-1 mRNA.
Description: Quantitative sandwich ELISA kit for measuring Mouse Vascular endothelial cell growth factor receptor 2, VEGFR-2/Flk-1 in samples from serum, plasma. A new trial version of the kit, which allows you to test the kit in your application at a reasonable price.
Description: Quantitative sandwich ELISA kit for measuring Mouse Vascular endothelial cell growth factor receptor 2, VEGFR-2/Flk-1 in samples from serum, plasma. Now available in a cost efficient pack of 5 plates of 96 wells each, conveniently packed along with the other reagents in 5 separate kits.
Results: In a cohort study of 1284 individuals with metastatic colorectal cancer, the median age was 59 (interquartile range [IQR]: 51-68) years, body mass index, the average was 27.2 (IQR, 24.1 to 31, 4), 521 (41%) were women, and in 1102 (86%) were white. There are 1100 deaths during a median follow-up of 73 months (IQR, 64-87 months). We observed an inverse relationship between a score of AMED and the risk of death (HR quintile 5 vs first quintile, 0.83; 95% CI, 0.67 to 1.04; P = 0.04 for trend), but the estimate is not statistically significant point , None of the other diet or pattern values associated with overall survival.
Conclusion and relevance: In this prospective analysis of patients with metastatic colorectal cancer, diet quality were assessed at start of first-line treatment for metastatic disease was not associated with overall survival.