Cancer is being cured- The aberancy of the Cytokine Cycle is abated

 Lifted from Fierce Publications

Novartis ($NVS) picked up an FDA breakthrough therapy designation for its in-development treatment for blood cancer, guaranteeing the company preferred access to top regulators as it prepares to file for approval.

The agency has added PKC412 to its breakthrough program, which is meant to accelerate the process for treatments that could change the standard of care in particularly underserved diseases.

Novartis' drug is an oral therapy designed to treat patients with a form of acute myeloid leukemia, or AML. PKC412, also known as midostaurin, works by blocking multiple enzymes key to cancer growth in the roughly one-third of AML patients who have mutations in their FLT3 genes. In Phase III data presented at the American Society of Hematology meeting last year, the drug charted a median overall survival of 74.7 months, beating out the 25.6 months seen on placebo alone.

Novartis said it's on track to submit PKC412 for global regulatory approvals in the first half of this year, working with Invivoscribe Technologies to develop a companion diagnostic that can screen AML patients for FLT3 mutations.

AML accounts for about 25% of all adult leukemias, according to Novartis, and has the lowest survival rate.

"For more than 25 years, medical developments have been limited for AML patients and the chemotherapy treatment strategy has essentially remained unchanged," Novartis oncology chief Alessandro Riva said in a statement. "We look forward to working closely with the FDA to bring PKC412 (midostaurin), the first potential AML targeted therapy, to patients as quickly as possible."

Novartis is also developing PKC412 in mast cell leukemia and myelodysplastic syndrome

JAK Inhibition

                             JAK inhibition

                                           Insight

 The complete Cytokine cycle must be illucidated  in order for in part results to make sense.

This was jacked from Fierce newsletter on stock info.

JAK inhibition for solid tumors flops, forcing Incyte to pull the plug on a slate of trials

Thursday, February 11, 2016 | By John Carroll

Incyte CEO Hervé Hoppenot

Jakafi has failed to help patients in a late-stage study for pancreatic cancer, and Incyte feels that it now has all the data it needs to prove that a JAK1 inhibitor is the wrong way to go in solid tumors.

Just ahead of its annual numbers release, Incyte reported today that it is slamming the brakes on a range of studies for Jakafi as well as the experimental INCB39110, another JAK1. Already halted on one colon cancer trial failure, Incyte is ending the Phase III pancreatic cancer study, a separate midstage trial in colorectal cancer, a Phase II for breast and lung cancers and a dose-ranging trial for INCB39110 in pancreatic cancer.

Shares of Wilmington, DE-based Incyte ($INCY) plunged 23% on the news of the setback.

Incyte, though, still believes that the drug's impact on the tumor microenvironment, a key target in oncology, is worth studying in combination studies using Merck's checkpoint inhibitor Keytruda, as well as its in-house IDO1 inhibitor and PI3k drug. INCB39110 plus osimertinib, AstraZeneca's next-generation EGFR inhibitor, will also stay in the pipeline.

Back in the summer of 2013, evidence of some success using Jakafi against pancreatic cancer spurred a 33% spike in the biotech's share price, encouraging CEO Hervé Hoppenot to tell reporters some months later that the company's shares were undervalued. At the time the company's shares had risen to about $64 a share. The company's shares were on their way to $130 in the fall of 2015. Today, the price is just north of $57 as a bear market mauls industry shares.

Jakafi is approved to treat myelofibrosis, and Incyte expects the drug will reap more than $800 million in revenue from the treatment this year. 

"The hypothesis to evaluate the therapeutic utility of JAK inhibition in patients with solid tumors and high levels of systemic inflammation was initially supported by a subgroup analysis of the randomized, double-blind Phase 2 RECAP study, which suggested a survival benefit in patients with high levels of CRP. As a result, we and the broader scientific community believed further study in pancreatic cancer and other solid tumors with evidence of systemic inflammation was warranted. Unfortunately, the larger studies did not confirm this hypothesis," said Rich Levy, Incyte's chief drug development officer.

Cancer and its elimination- $57 M.We do have believers

Indubidibly there is a connection with the proposed Cytokine Cycle and its Pathophysiologic Consequence and what Pat is funding here. I will repost it soon 

Billionaire entrepreneur Patrick Soon-Shiong's NantCell raised $57.3 million in equity to fund its work on treatments that use the immune system to fight cancer, becoming one of the most well-funded companies in its founder's constellation of biotech endeavors.

The round, which sold shares to 125 investors, follows a $100 million fundraise disclosed in September and a $75 million equity sale over the summer. Like most of Soon-Shiong's many biotech ventures, NantCell has provided little detail on its specific goals, and the company didn't respond to a request for comment Monday.

Launched early last year, NantCell is an arm of Soon-Shiong's NantWorks umbrella that is developing immuno-oncology therapies. The company's first move was paying an undisclosed sum for the rights to Amgen's ($AMGN) ganitumab, a once-failed antibody that NantCell believes can be repurposed against cancer. In March, the company widened its pipeline by trading $110 million in cash and equity for the rights to some immunotherapies from Sorrento Therapeutics ($SRNE), a frequent Soon-Shiong collaborator. And it has remained quiet ever since.

NantCell, one of about a dozen under the NantWorks name, does business alongside NantiBody, a joint venture with Sorrento; NantPharma, at work on a next-generation version of Celgene's ($CELG) Abraxane; NantBioScience, developing nanoparticle cancer treatments; NantKwest ($NK), an immuno-oncology company that raised more than $200 million in a July IPO; and NantHealth, a tech firm offering what Soon-Shiong calls "the Google of genome mapping."

                               JAK Inhibition

Jakafi has failed to help patients in a late-stage study for pancreatic cancer, and Incyte feels that it now has all the data it needs to prove that a JAK1 inhibitor is the wrong way to go in solid tumors.

Just ahead of its annual numbers release, Incyte reported today that it is slamming the brakes on a range of studies for Jakafi as well as the experimental INCB39110, another JAK1. Already halted on one colon cancer trial failure, Incyte is ending the Phase III pancreatic cancer study, a separate midstage trial in colorectal cancer, a Phase II for breast and lung cancers and a dose-ranging trial for INCB39110 in pancreatic cancer.

Shares of Wilmington, DE-based Incyte ($INCY) plunged 23% on the news of the setback.

Incyte, though, still believes that the drug's impact on the tumor microenvironment, a key target in oncology, is worth studying in combination studies using Merck's checkpoint inhibitor Keytruda, as well as its in-house IDO1 inhibitor and PI3k drug. INCB39110 plus osimertinib, AstraZeneca's next-generation EGFR inhibitor, will also stay in the pipeline.

Back in the summer of 2013, evidence of some success using Jakafi against pancreatic cancer spurred a 33% spike in the biotech's share price, encouraging CEO Hervé Hoppenot to tell reporters some months later that the company's shares were undervalued. At the time the company's shares had risen to about $64 a share. The company's shares were on their way to $130 in the fall of 2015. Today, the price is just north of $57 as a bear market mauls industry shares.

Jakafi is approved to treat myelofibrosis, and Incyte expects the drug will reap more than $800 million in revenue from the treatment this year. 

"The hypothesis to evaluate the therapeutic utility of JAK inhibition in patients with solid tumors and high levels of systemic inflammation was initially supported by a subgroup analysis of the randomized, double-blind Phase 2 RECAP study, which suggested a survival benefit in patients with high levels of CRP. As a result, we and the broader scientific community believed further study in pancreatic cancer and other solid tumors with evidence of systemic inflammation was warranted. Unfortunately, the larger studies did not confirm this hypothesis," said Rich Levy, Incyte's chief drug development officer.

 

Chronic Lymphocytic Leukemia - Finally a response to technology

About 40 years ago Alonzo Peters MD.  Peters' Productions and Advanced Medical Informatic Education predicted cures for cancer, MS , DM, arthritis and other debilitating diseases. Since that time we have not dropped back from holding our Cytokine Cycle : A Model of Inflammation

out to all as the normal physiology of the Inflammatory Process. Any disease is an aberration of the aforementioned.


Today in the email from the NEJM and MD Anderson writers as primary contributors this was lifted with quite significant results.

THIS IS A NORMAL BLOOD SMEAR (above)

THIS IS A BLOOD SMEAR REVEALING chronic lymphocytic Leukemia(immediately above)

Original Article

Ibrutinib as Initial Therapy for Patients with Chronic Lymphocytic Leukemia

Jan A. Burger, M.D., Ph.D., Alessandra Tedeschi, M.D., Paul M. Barr, M.D., Tadeusz Robak, M.D., Ph.D., Carolyn Owen, M.D., Paolo Ghia, M.D., Ph.D., Osnat Bairey, M.D., Peter Hillmen, M.B., Ch.B., Ph.D., Nancy L. Bartlett, M.D., Jianyong Li, M.D., David Simpson, M.B., B.S., Sebastian Grosicki, M.D., Ph.D., Stephen Devereux, F.R.C.P., F.R.C.Path., Ph.D., Helen McCarthy, F.R.C.P., F.R.C.Path., Ph.D., Steven Coutre, M.D., Hang Quach, M.B., B.S., M.D., Gianluca Gaidano, M.D., Ph.D., Zvenyslava Maslyak, M.D., Don A. Stevens, M.D., Ann Janssens, M.D., Fritz Offner, M.D., Ph.D., Jiří Mayer, M.D., Michael O’Dwyer, M.D., Andrzej Hellmann, M.D., Ph.D., Anna Schuh, M.D., Ph.D., Tanya Siddiqi, M.D., Aaron Polliack, M.D., Constantine S. Tam, M.B., B.S., Deepali Suri, M.S., Mei Cheng, Ph.D., Fong Clow, Sc.D., Lori Styles, M.D., Danelle F. James, M.D., and Thomas J. Kipps, M.D., Ph.D. for the RESONATE-2 Investigators

N Engl J Med 2015; 373:2425-2437December 17, 2015DOI: 10.1056/NEJMoa1509388

Share:

Background

Chronic lymphocytic leukemia (CLL) primarily affects older persons who often have coexisting conditions in addition to disease-related immunosuppression and myelosuppression. We conducted an international, open-label, randomized phase 3 trial to compare two oral agents, ibrutinib and chlorambucil, in previously untreated older patients with CLL or small lymphocytic lymphoma.

Methods

We randomly assigned 269 previously untreated patients who were 65 years of age or older and had CLL or small lymphocytic lymphoma to receive ibrutinib or chlorambucil. The primary end point was progression-free survival as assessed by an independent review committee.

Results

The median age of the patients was 73 years. During a median follow-up period of 18.4 months, ibrutinib resulted in significantly longer progression-free survival than did chlorambucil (median, not reached vs. 18.9 months), with a risk of progression or death that was 84% lower with ibrutinib than that with chlorambucil (hazard ratio, 0.16; P<0.001). Ibrutinib significantly prolonged overall survival; the estimated survival rate at 24 months was 98% with ibrutinib versus 85% with chlorambucil, with a relative risk of death that was 84% lower in the ibrutinib group than in the chlorambucil group (hazard ratio, 0.16; P=0.001). The overall response rate was higher with ibrutinib than with chlorambucil (86% vs. 35%, P<0.001). The rates of sustained increases from baseline values in the hemoglobin and platelet levels were higher with ibrutinib. Adverse events of any grade that occurred in at least 20% of the patients receiving ibrutinib included diarrhea, fatigue, cough, and nausea; adverse events occurring in at least 20% of those receiving chlorambucil included nausea, fatigue, neutropenia, anemia, and vomiting. In the ibrutinib group, four patients had a grade 3 hemorrhage and one had a grade 4 hemorrhage. A total of 87% of the patients in the ibrutinib group are continuing to take ibrutinib.

Conclusions

Ibrutinib was superior to chlorambucil in previously untreated patients with CLL or small lymphocytic lymphoma, as assessed by progression-free survival, overall survival, response rate, and improvement in hematologic variables. (Funded by Pharmacyclics and others; RESONATE-2 ClinicalTrials.gov number, NCT01722487.)

Supported by Pharmacyclics, by grants (CA016672 and 5P01CA081534-14) from the National Institutes of Health, and by the MD Anderson Moon Shot Program in CLL. Dr. Burger is a Scholar of the Leukemia and Lymphoma Society.

Disclosure forms provided by the authors are available with the full text of this article at NEJM.org.

Dr. Burger reports receiving fees for serving on advisory boards from Janssen and grant support from Pharmacyclics, Gilead Sciences, and Portola Pharmaceuticals; Dr. Barr, receiving consulting fees from Pharmacyclics and AbbVie; Dr. Owen, receiving honoraria and fees for serving on advisory boards from Janssen, Gilead Sciences, Roche, and Lundbeck; Dr. Ghia, receiving fees for serving on advisory boards from AbbVie, Gilead Sciences, H3 Biomedicine, Janssen, Pharmacyclics, and Roche, consulting fees from Adaptive Biotechnologies, lecture fees from Gilead Sciences and Janssen, and grant support from Gilead Sciences, GlaxoSmithKline, and Roche; Dr. Hillmen, receiving lecture fees from Pharmacyclics; Dr. Bartlett, receiving fees for serving on advisory boards from Gilead Sciences and Seattle Genetics; Dr. Gaidano, receiving fees for serving on advisory boards from Janssen, Roche, Amgen, Novartis, GlaxoSmithKline, and Karyopharm Therapeutics, and grant support from Celgene; Dr. Siddiqi, receiving lecture fees from Pharmacyclics and Janssen; Dr. Tam, receiving honoraria from Janssen; Ms. Suri, Dr. Cheng, Dr. Clow, Dr. Styles, and Dr. James, being employees of Pharmacyclics; and Dr. Clow, Dr. Styles, and Dr. James, holding stock in AbbVie. No other potential conflict of interest relevant to this article was reported.

This article was published on December 6, 2015, at NEJM.org.

We thank all the patients who participated in this trial and their supportive families; Cathy Zhou, M.S., of Pharmacyclics, for statistical analysis support; and Maoko Naganuma Carter, M.Sc., C.M.P.P., for medical writing support in the preparation of an earlier version of the manuscript.

Source Information

From the University of Texas MD Anderson Cancer Center, Houston (J.A.B.); Azienda Ospedaliera Niguarda Cà Granda (A.T.) and Università Vita-Salute San Raffaele and IRCCS Istituto Scientifico San Raffaele (P.G.), Milan, and the Department of Translational Medicine, Amedeo Avogadro University of Eastern Piedmont, Novara (G.G.) — all in Italy; Wilmot Cancer Institute, University of Rochester, Rochester, NY (P.M.B.); Medical University of Lodz and Copernicus Memorial Hospital, Lodz (T.R.), the Department of Cancer Prevention, School of Public Health, Medical University of Silesia, Katowice (S.G.), and the Department of Hematology, University Clinical Center of Medical University of Gdansk, Gdansk (A.H.) — all in Poland; Tom Baker Cancer Centre, Calgary, AB, Canada (C.O.); Rabin Medical Center, Beilinson Hospital and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv (O.B.), and Hadassah University Hospital, Hebrew University Medical School, Jerusalem (A.P.) — both in Israel; Leeds Teaching Hospitals, St. James Institute of Oncology, Leeds (P.H.), Kings College Hospital, London (S.D.), Royal Bournemouth Hospital, Bournemouth (H.M.), and University of Oxford, Oxford (A.S.) — all in the United Kingdom; Washington University School of Medicine, St. Louis (N.L.B.); Jiangsu Province Hospital, Nanjing, China (J.L.); North Shore Hospital, Auckland, New Zealand (D. Simpson); Stanford University School of Medicine, Stanford (S.C.), City of Hope National Medical Center, Duarte (T.S.), Pharmacyclics, Sunnyvale (D. Suri, M.C., F.C., L.S., D.F.J.), and Moores Cancer Center, University of California, San Diego, San Diego (T.J.K.) — all in California; St. Vincent’s Hospital, University of Melbourne (H.Q.), and Peter MacCallum Cancer Centre and St. Vincent’s Hospital (C.S.T.), Melbourne, VIC, Australia; Institute of Blood Pathology and Transfusion Medicine, National Academy of Medical Sciences of Ukraine, Lviv, Ukraine (Z.M.); Norton Cancer Institute, Louisville, KY (D.A.S.); University Hospital Leuven, Leuven (A.J.), and University Hospital Ghent, Ghent (F.O.) — both in Belgium; Fakultní Nemocnice Brno, Brno, Czech Republic (J.M.); and University College Hospital Galway, Galway, Ireland (M.O.).

Address reprint requests to Dr. Burger at the Department of Leukemia, University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030, or at jaburger@mdanderson.org.

A complete list of the RESONATE-2 investigators is provided

TNF-alpha stimulates MMP2 which diminishes NUCLEUS PROPULSUS

subject: TNF STIMULATED INCREASEIN MMP2
object_opposite: NUCLEUS PROPULSUS
misc: tudy Design. In vitro-formed bovine nucleus pulposus (NP) tissues were used as a model for tumor necrosis factor-α (TNF-α) induced NP degeneration. Objective. To elucidate the signal transduction mechanisms regulating TNF-α induced matrix metalloproteinase (
author_year: CA Séguin/ RM Pilliar/ JA Madri/ RA Kandel/08
journal_volume_page: Spine/33 4/ 356-365

Chondrocytes and glucose Transport

Osteoarthritis and Cartilage

Volume 11, Issue 2, February 2003, Pages 92–10

Molecular characterization and partial cDNA cloning of facilitative glucose transporters expressed in human articular chondrocytes; stimulation of 2-deoxyglucose uptake by IGF-I and elevated MMP-2 secretion by glucose deprivation
subject: articular chondrocytes; stimulation of 2-deoxyglucose uptake by IGF-I and elevated MMP-2 secretion
object_opposite: glucose deprivation/chondrocyte diminution
misc: Osteoarthritis and Cartilage Volume 11, Issue 2, February 2003, Pages 92–10 Molecular characterization and partial cDNA cloning of facilitative glucose transporters expressed in human articular chondrocytes; stimulation of 2-deoxyglucose uptake by IGF-I and elevated MMP-2 secretion by glucose deprivation
author_year: S Richardsona/G Neamaa/T Phillipsa/S Bella/S.D Cartera/K.H Moleyb/J.F Moleyc/S.J Vannuccid/A Mobasheria/2003
journal_volume_page: Osteoarthritis and Cartilage Volume 11/Issue 2/ Pages 92–10

S Richardson^a, 

G Neama^a, 

T Phillips^a, 

S Bell^a, 

S.D Carter^a, 

K.H Moley^b, 

J.F Moley^c, 

S.J Vannucci^d, 

A Mobasheri^a, f1

---

Abstract

Objective Recent evidence suggests that human chondrocytes express several facilitative glucose transporter (GLUT) isoforms and also that 2-deoxyglucose transport is accelerated by cytokine stimulation. The aim of the present investigation was to determine if human articular chondrocytes express any of the recently identified members of the GLUT/SLC2A gene family and to examine the effects of endocrine factors, such as insulin and IGF-I on the capacity of human chondrocytes for transporting 2-deoxyglucose.

Design/methods PCR, cloning and immunohistochemistry were employed to study the expression of GLUT/SLC2A transporters in normal human articular cartilage. The uptake of 2-deoxyglucose was examined in monolayer cultured immortalized human chondrocytes following stimulation with TNF-α, insulin and IGF-I. Levels of MMP-2 were assessed by gelatin zymography following glucose deprivation of alginate cultures.

Results Using PCR we detected transcripts for eight glucose transporter isoforms (GLUTs 1, 3, 6, 8, 9, 10, 11 and 12) and for a fructose transporter (GLUT5) in human articular cartilage. Expression of GLUT1, GLUT3 and GLUT9 proteins in normal human articular cartilage was confirmed by immunohistochemistry. The uptake of 2-deoxyglucose was dependent on time and temperature, inhibited by cytochalasin B and phloretin, and significantly accelerated in chondrocyte cultures stimulated with IGF-I. However, 2-deoxyglucose uptake was unaffected by short and long-term insulin treatment, which ruled out a functional role for insulin-sensitive GLUT4-mediated glucose transport. Furthermore, secretion of MMP-2 was
subject: articular chondrocytes; stimulation of 2-deoxyglucose uptake by IGF-I and elevated MMP-2 secretion
object_opposite: glucose deprivation
misc: Osteoarthritis and Cartilage Volume 11, Issue 2, February 2003, Pages 92–10 Molecular characterization and partial cDNA cloning of facilitative glucose transporters expressed in human articular chondrocytes; stimulation of 2-deoxyglucose uptake by IGF-I and elevated MMP-2 secretion by glucose deprivation
author_year: S Richardsona/G Neamaa/T Phillipsa/S Bella/S.D Cartera/K.H Moleyb/J.F Moleyc/S.J Vannuccid/A Mobasheria/2003
journal_volume_page: Osteoarthritis and Cartilage Volume 11/Issue 2/ Pages 92–10increased in alginate cultures deprived of glucose.

Conclusions The data supports a critical role for glucose transport and metabolism in the synthesis and degradation of cartilage. Copyright 2002 OsteoArthritis Research Society International. Published by Elsevier Science Ltd. All rights reserved.

Keywords

·        Chondrocyte, Cartilage, Glucose transport, GLUT, IGF-I, Insulin, MMP-2.

MMP2 involved in Ischemic reperfusion injury and Troponin diminution

Catching upon my catching up this was uncovered. Notice that only AMIE entry included journal vol and page due to incomplete copy.

subject: Ischemia-Reperfusion Injury I/R/MMP2 MMP2/Matrix Metalloproteinase-2 target
object_opposite: Myosin light chain troponin diminishes
misc: A New Intracellular Target for MMP2/Matrix Metalloproteinase-2 richard.schulz@ualberta.ca
author_year: Grzegorz Sawicki PhD*/Hernando Leon, MD*/Jolanta Sawicka/MSc;Meltem Sariahmetoglu, PhD/ Costas J. Schulze, MD/Paul G. Scott, PhD/Danuta Szczesna-Cordary, PhD; Richard Schulz, PhD/2004
journal_volume_page: Circulation/112/554

Actual article appeared in circulation as abstract

Degradation of Myosin Light Chain in Isolated Rat Hearts Subjected to Ischemia-Reperfusion Injury

A New Intracellular Target for Matrix Metalloproteinase-2

1.      Grzegorz Sawicki, PhD*; 

2.      Hernando Leon, MD*; 

3.      Jolanta Sawicka, MSc;

4.      Meltem Sariahmetoglu, PhD; 

5.      Costas J. Schulze, MD; 

6.      Paul G. Scott, PhD;

7.      Danuta Szczesna-Cordary, PhD; 

8.      Richard Schulz, PhD

+Author Affiliations

1.      From the Departments of Pharmacology (G.S., J.S., M.S., C.J.S., R.S.), Pediatrics (H.L., R.S.), and Biochemistry (P.G.S.), Cardiovascular Research Group, University of Alberta, Edmonton, Alberta, Canada, and Department of Molecular and Cellular Pharmacology (D.S.-C.), University of Miami School of Medicine, Miami, Fla.

1.      Correspondence to Dr Richard Schulz, Cardiovascular Research Group, 4-62 Heritage Medical Research Centre, University of Alberta, Edmonton, Alberta, Canada T6G 2S2. E-mail richard.schulz@ualberta.ca

Abstract

Background— Matrix metalloproteinase-2 (MMP-2) contributes to cardiac dysfunction resulting from ischemia-reperfusion (I/R) injury. MMP-2 not only remodels the extracellular matrix but also acts intracellularly in I/R by degrading troponin I. Whether other intracellular targets exist for MMP-2 during I/R is unknown.

Methods and Results— Isolated rat hearts were subjected to 20 minutes of ischemia and 30 minutes of reperfusion. The impaired recovery of mechanical function of the heart was attenuated by the MMP inhibitors o-phenanthroline or doxycycline. Quantitative 2D electrophoresis of homogenates of aerobically perfused hearts (control) or those subjected to I/R injury (in the presence or absence of MMP inhibitors) showed 3 low-molecular-weight proteins with levels that were significantly increased upon I/R injury and normalized to control levels by MMP inhibitors. Mass spectrometry analysis identified all 3 proteins as fragments of myosin light chain 1, which possesses theoretical cleavage recognition sequences for MMP-2 and is rapidly degraded by it in vitro. The association of MMP-2 with the thick myofilament in fractions prepared from I/R hearts was observed with immunogold electron microscopy, gelatin zymography for MMP-2 activity, and immunoprecipitation. MMP-2 was found to cleave myosin light chain 1 between tyrosine 189 and glutamine 190 at the C terminus.

Conclusions— Our results demonstrate that myosin light chain 1 is another novel substrate for MMP-2 in the cardiomyocyte and that its degradation may contribute to contractile dysfunction resulting from I/R injury to the heart.

Key Words:

subject: Ischemia-Reperfusion Injury I/R/MMP2 MMP2/Matrix Metalloproteinase-2 target
object_opposite: Myosin light chain troponin diminishes
misc: A New Intracellular Target for MMP2/Matrix Metalloproteinase-2 richard.schulz@ualberta.ca
author_year: Grzegorz Sawicki PhD*/Hernando Leon, MD*/Jolanta Sawicka/MSc;Meltem Sariahmetoglu, PhD/ Costas J. Schulze, MD/Paul G. Scott, PhD/Danuta Szczesna-Cordary, PhD; Richard Schulz, PhD/2004
journal_volume_page: Circulation/112/554