Time filter

Source Type

News Article | April 21, 2017
Site: www.rdmag.com

A new potential early-stage lung cancer detection method has emerged, which focuses on changes in the composition of the breath In a Max Planck Institute for Heart and Lung Research study comprised of 138 healthy volunteers and cancer patients, a breath test—which detected the presence of traces of RNA molecules that are altered by cancer growth— correctly determined the health status of 98 percent of participants. “The breath test could make the detection of early-stage lung cancer easier and more reliable, but it will not completely supplant conventional techniques,” Guillermo Barreto, a Working Group Leader at the Max Planck Institute, said in a statement. “However, it can complement other techniques for detecting early cancer stages and reduce false-positive diagnoses.” The researchers analyzed RNA molecules from lung tissue into expired breath, which is not identical in every cell. The research team observed that cancerous and healthy cells contain different amounts of GATA6 and NKX2 genes, RNA variants. The researchers were able to isolate RNA molecules, which have an extremely low concentration in expired breath but are also frequently highly fragmented. Lung cancer is known for its insidious and largely symptom-free onset, which often remains unnoticed, causing the majority of lung cancer patients to pass away within five years of the diagnosis. According to the study, lung cancer is the leading cause of cancer-related deaths worldwide. High-risk groups, including heavy smokers, are routinely given CAT scans in the U.S., but patients can also be wrongly classified as having the disease from this method. Scientists will now contribute to future clinical trials, while seeking licensing partners to develop the breath test to maturity and market it with the Max Planck Innovation, a technology transfer organization. The researchers will also attempt to use RNA profiles for the early detection of other diseases, making tiny changes to produce tissue profiles that reveal diseased cells and allow for rapid treatment. The study was published in EMBO Molecular Medicine.


News Article | April 21, 2017
Site: www.rdmag.com

A new potential early-stage lung cancer detection method has emerged, which focuses on changes in the composition of the breath In a Max Planck Institute for Heart and Lung Research study comprised of 138 healthy volunteers and cancer patients, a breath test—which detected the presence of traces of RNA molecules that are altered by cancer growth— correctly determined the health status of 98 percent of participants. “The breath test could make the detection of early-stage lung cancer easier and more reliable, but it will not completely supplant conventional techniques,” Guillermo Barreto, a Working Group Leader at the Max Planck Institute, said in a statement. “However, it can complement other techniques for detecting early cancer stages and reduce false-positive diagnoses.” The researchers analyzed RNA molecules from lung tissue into expired breath, which is not identical in every cell. The research team observed that cancerous and healthy cells contain different amounts of GATA6 and NKX2 genes, RNA variants. The researchers were able to isolate RNA molecules, which have an extremely low concentration in expired breath but are also frequently highly fragmented. Lung cancer is known for its insidious and largely symptom-free onset, which often remains unnoticed, causing the majority of lung cancer patients to pass away within five years of the diagnosis. According to the study, lung cancer is the leading cause of cancer-related deaths worldwide. High-risk groups, including heavy smokers, are routinely given CAT scans in the U.S., but patients can also be wrongly classified as having the disease from this method. Scientists will now contribute to future clinical trials, while seeking licensing partners to develop the breath test to maturity and market it with the Max Planck Innovation, a technology transfer organization. The researchers will also attempt to use RNA profiles for the early detection of other diseases, making tiny changes to produce tissue profiles that reveal diseased cells and allow for rapid treatment. The study was published in EMBO Molecular Medicine.


News Article | April 20, 2017
Site: www.biosciencetechnology.com

“Inhale deeply ... and exhale.” This is what a test for lung cancer could be like in future. Scientists at the Max Planck Institute for Heart and Lung Research in Bad Nauheim have developed a method that can detect the disease at an early stage. To this effect, they investigated the presence of traces of RNA molecules that are altered by cancer growth. In a study on healthy volunteers and cancer patients, the breath test correctly determined the health status of 98 percent of the participants. The method will now be refined in cooperation with licensing partners so that it can be used for the diagnosis of lung cancer. Most lung cancer patients die within five years of diagnosis. One of the main reasons for this is the insidious and largely symptom-free onset of the disease, which often remains unnoticed. In the USA, high-risk groups, such as heavy smokers, are therefore routinely examined by CAT scan. However, patients can be wrongly classified as having the disease. Together with cooperation partners, researchers at the Max Planck Institute for Heart and Lung Research have now developed a breath test that is much more accurate. In their research, the diagnosis of lung cancer was correct in nine out of ten cases. The method is therefore reliable enough to be used for the routine early detection of lung cancer. The researchers analyzed RNA molecules released from lung tissue into expired breath, noting differences between healthy subjects and lung cancer patients. Unlike DNA, the RNA profile is not identical in every cell. Several RNA variants, and therefore different proteins, can arise from one and the same DNA segment. In healthy cells, such variants are present in a characteristic ratio. The scientists discovered that cancerous and healthy cells contain different amounts of RNA variants of the GATA6 and NKX2 genes. Cancer cells resemble lung cells in the embryonic stage. The researchers developed a method to isolate RNA molecules. Not only is their concentration in expired breath extremely low, but they are also frequently highly fragmented. The researchers then investigated the RNA profile in subjects with and without lung cancer and from these data established a model for diagnosing the disease. In a test of 138 subjects whose health status was known, the test was able to identify 98 percent of the patients with lung cancer. 90 percent of the detected abnormalities were in fact cancerous. “The breath test could make the detection of early-stage lung cancer easier and more reliable, but it will not completely supplant conventional techniques,” says Guillermo Barreto, a Working Group Leader at the Max Planck Institute in Bad Nauheim. “However, it can complement other techniques for detecting early cancer stages and reduce false-positive diagnoses.” The scientists will contribute to future large-scale clinical trials. Together with the technology transfer organization Max Planck Innovation, they are seeking licensing partners to develop the breath test to maturity and market it. They also hope to use RNA profiles for the early detection of other diseases. Tiny changes could produce tissue profiles, akin to an RNA fingerprint, that reveal diseased cells and allow for rapid treatment.


Gunther S.,Max Planck Institute for Heart and Lung Research
Cell stem cell | Year: 2013

Skeletal muscle contains Pax7-expressing muscle stem or satellite cells, enabling muscle regeneration throughout most of adult life. Here, we demonstrate that induced inactivation of Pax7 in Pax7-expressing cells of adult mice leads to loss of muscle stem cells and reduced heterochromatin condensation in rare surviving satellite cells. Inactivation of Pax7 in Myf5-expressing cells revealed that the majority of adult muscle stem cells originate from myogenic lineages, which express the myogenic regulators Myf5 or MyoD. Likewise, the majority of muscle stem cells are replenished from Myf5-expressing myogenic cells during adult life, and inactivation of Pax7 in Myf5-expressing cells after muscle damage leads to a complete arrest of muscle regeneration. Finally, we demonstrate that a relatively small number of muscle stem cells are sufficient for efficient repair of skeletal muscles. We conclude that Pax7 acts at different levels in a nonhierarchical regulatory network controlling muscle-satellite-cell-mediated muscle regeneration. Copyright © 2013 Elsevier Inc. All rights reserved.


Boettger T.,Max Planck Institute for Heart and Lung Research | Braun T.,Max Planck Institute for Heart and Lung Research
Circulation Research | Year: 2012

The discovery of the regulatory role of noncoding RNAs, and micro (mi)RNAs in particular, has added a new layer of complexity to our understanding of cardiovascular development. miRNAs regulate and modulate various steps of cardiovascular morphogenesis, cell proliferation, differentiation, and phenotype modulation. miRNAs simultaneously regulate multiple targets, and many miRNAs can bind to the same target, allowing for a complex pattern of regulation of gene expression. miRNA families are continuously added during evolution paralleling the increased complexity of the cardiovascular system in vertebrates compared with invertebrates. Several lines of evidence suggest that the appearance of miRNAs is at least in part responsible for the formation of complex organ systems and stable regulatory mechanisms in vertebrates. We review the current understanding of miRNAs during cardiovascular development. Further progress in this area will help to decipher quantitative changes in gene expression that provide robustness to cellular phenotypes and regulatory options to diseases processes. miRNAs might also provide clues to better understand congenital heart defects, which are the most common birth defects in human newborns. © 2012 American Heart Association, Inc.


Understanding in vivo regeneration of complex structures offers a fascinating perspective for translation into medical applications. Unfortunately, mammals in general lack large-scale regenerative capacity, whereas planarians, newts or Hydra can regenerate complete body parts. Such organisms are, however, poorly annotated because of the lack of sequence information. This leads to limited access for molecular biological investigations. In the last decade, high throughput technologies and new methods enabling the effective generation of transgenic animals have rapidly evolved. These developments have allowed the extensive use of niche model organisms as part of a trend towards the accessibility of a greater panel of model species for scientific research. The case study that follows provides an insight into the impact of high throughput techniques on the landscape of models of regeneration. The cases presented here give evidence of alternative stem cell maintenance pathways, the identification of new protein families and new stem cell markers. Regeneration of complex structures is a capability mastered by a small number of niche model organisms. Although such organisms are poorly annotated, current technologies allow the extensive use of such organisms. Representative studies give evidence of alternative stem cell maintenance pathways, new protein families, and new stem cell markers. © 2014 WILEY Periodicals, Inc.


Ofermanns S.,Max Planck Institute for Heart and Lung Research
Science Translational Medicine | Year: 2012

The antiatherogenic drug nicotinic acid (niacin) has antidyslipidemic ef ects independent of free fatty acid suppression mediated by its receptor HCA2 (GPR109A) (Lauring et al., this issue).


Sawamiphak S.,Max Planck Institute for Heart and Lung Research | Kontarakis Z.,Max Planck Institute for Heart and Lung Research | Stainier D.Y.R.,Max Planck Institute for Heart and Lung Research
Developmental Cell | Year: 2014

Vertebrate hematopoietic stem cells (HSCs) emerge in the aorta-gonad-mesonephros (AGM) region from "hemogenic" endothelium. Here we show that the proinflammatory cytokine interferon-γ (IFN-γ) and its receptor Crfb17 positively regulate HSC development in zebrafish. This regulation does not appear to modulate the proliferation or survival of HSCs or endothelial cells, but rather the endothelial-to-HSC transition. Notch signaling and blood flow positively regulate the expression of ifng and crfb17 in the AGM. Notably, IFN-γ overexpression partially rescues the HSC loss observed in the absence of blood flow or Notch signaling. Importantly, IFN-γ signaling acts cell autonomously to control the endothelial-to-HSC transition. IFN-γ activates Stat3, an atypical transducer of IFN-γ signaling, in the AGM, and Stat3 inhibition decreases HSC formation. Together, our findings uncover a developmental role for an inflammatory cytokine and place its action downstream of Notch signaling and blood flow to control Stat3 activation and HSC emergence. © 2014 Elsevier Inc.


Kostin S.,Max Planck Institute for Heart and Lung Research
Journal of Cellular and Molecular Medicine | Year: 2010

The existence of a new type of interstitial cells in the heart namely, interstitial Cajal-like cells (ICLC), has been described for the first time by Hinescu and Popescu in 2005. This study was then followed by an ascending trend of publications regarding the morphology, phenotype and distribution of myocardial ICLC in diverse species including human patients. Recently the new term 'telocytes' has been proposed for cells formerly known as ICLC, and the term 'telopodes' has been proposed for the prolongations of these cells. The identification of these cells is based on ultrastructural criteria. In addition, telocyters/telyopodes can be identified by several complementary approaches including methylene blue vital staining, silver impregnation and immunoreactivity against CD117/c-kit, vimentin, etc. This point of view presents critical data existing in literature, as well as own results, which unequivocally provide compelling evidence that telocytes are a new distinct cellular entity of myocardial interstitium. Several presumable functions of the myocardial telocytes are discussed: (i) intercellular signalling, (ii) cardiac repair/remodelling and (iii) stem cell nursing in cardiac renewal. © 2010 The Authors Journal compilation © 2010 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.


Wirth A.,Max Planck Institute for Heart and Lung Research
Biochimica et Biophysica Acta - Molecular Basis of Disease | Year: 2010

Arterial hypertension is a multifactorial disease that is characterised by increased peripheral vascular resistance often accompanied by smooth muscle cell hypertrophy and proliferation. Rho kinases (ROCKs) are the most extensively studied effectors of the small G-protein RhoA and abnormalities in RhoA/ROCK signalling have been observed in various cardiovascular disease including hypertension. The RhoA/ROCK-pathway is a key player in different smooth muscle cell functions including contractility, proliferation and migration. Furthermore, there is extensive crosstalk between RhoA/ROCK- and NO-signalling. Therefore, not only ROCK inhibitors but also NO-donators or pleiotropic agents like statins exert their beneficial effects on the cardiovascular system at least in part via Rho/Rho-kinase. © 2010 Elsevier B.V.

Loading Max Planck Institute for Heart and Lung Research collaborators
Loading Max Planck Institute for Heart and Lung Research collaborators