Evaluation and Management of Dyslipidemia in Patients Treated with Lorlatinib
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Comparative Efficacy and Safety of Lorlatinib and Alectinib for ALK
cancers Systematic Review Comparative Efficacy and Safety of Lorlatinib and Alectinib for ALK-Rearrangement Positive Advanced Non-Small Cell Lung Cancer in Asian and Non-Asian Patients: A Systematic Review and Network Meta-Analysis Koichi Ando 1,2,* , Ryo Manabe 1, Yasunari Kishino 1, Sojiro Kusumoto 1, Toshimitsu Yamaoka 3 , Akihiko Tanaka 1, Tohru Ohmori 1,4 and Hironori Sagara 1 1 Division of Respiratory Medicine and Allergology, Department of Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8666, Japan; [email protected] (R.M.); [email protected] (Y.K.); [email protected] (S.K.); [email protected] (A.T.); [email protected] (T.O.); [email protected] (H.S.) 2 Division of Internal Medicine, Showa University Dental Hospital Medical Clinic, Senzoku Campus, Showa University, 2-1-1 Kita-senzoku, Ohta-ku, Tokyo 145-8515, Japan 3 Advanced Cancer Translational Research Institute, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan; [email protected] 4 Department of Medicine, Division of Respiratory Medicine, Tokyo Metropolitan Health and Hospitals Corporation, Ebara Hospital, 4-5-10 Higashiyukigaya, Ohta-ku, Tokyo 145-0065, Japan * Correspondence: [email protected]; Tel.: +81-3-3784-8532 Citation: Ando, K.; Manabe, R.; Kishino, Y.; Kusumoto, S.; Yamaoka, Simple Summary: The treatment of anaplastic lymphoma kinase (ALK) rearrangement-positive T.; Tanaka, A.; Ohmori, T.; Sagara, H. (ALK-p) advanced non-small cell lung cancer (NSCLC) remains a challenge. -
Genetic Testing for Familial Hypercholesterolemia AHS – M2137
Corporate Medical Policy Genetic Testing for Familial Hypercholesterolemia AHS – M2137 File Name: genetic_testing_for_familial_hypercholesterolemia Origination: 01/01/2019 Last CAP Review: 07/2021 Next CAP Review: 07/2022 Last Review: 07/2021 Description of Procedure or Service Definitions Familial hypercholesterolemia (FH) is a genetic condition that results in premature atherosclerotic cardiovascular disease due to lifelong exposure to elevated low-density lipoprotein cholesterol (LDL-C) levels (Sturm et al., 2018). FH encompasses multiple clinical phenotypes associated with distinct molecular etiologies. The most common is an autosomal dominant disorder caused by mutations in one of three genes, low-density lipoprotein receptor (LDLR), apolipoprotein B-100 (APOB), and proprotein convertase subtilisin-like kexin type 9 (PCSK9) (Ahmad et al., 2016; Goldberg et al., 2011). Rare autosomal recessive disease results from mutation in low-density lipoprotein receptor adaptor protein (LDLRAP) (Garcia et al., 2001). Related Policies Cardiovascular Disease Risk Assessment AHS – G2050 ***Note: This Medical Policy is complex and technical. For questions concerning the technical language and/or specific clinical indications for its use, please consult your physician. Policy BCBSNC will provide coverage for genetic testing for familial hypercholesterolemia when it is determined the medical criteria or reimbursement guidelines below are met. Benefits Application This medical policy relates only to the services or supplies described herein. Please refer to the Member's Benefit Booklet for availability of benefits. Member's benefits may vary according to benefit design; therefore member benefit language should be reviewed before applying the terms of this medical policy. When Genetic Testing for Familial Hypercholesterolemia is covered 1. Genetic testing to establish a molecular diagnosis of Familial Hypercholesterolemia is considered medically necessary when BOTH of the following criteria are met: A. -
Lipodystrophy Due to Adipose Tissue Specific Insulin Receptor
Page 1 of 50 Diabetes Lipodystrophy Due to Adipose Tissue Specific Insulin Receptor Knockout Results in Progressive NAFLD Samir Softic1,2,#, Jeremie Boucher1,3,#, Marie H. Solheim1,4, Shiho Fujisaka1, Max-Felix Haering1, Erica P. Homan1, Jonathon Winnay1, Antonio R. Perez-Atayde5, and C. Ronald Kahn1. 1 Section on Integrative Physiology and Metabolism, Joslin Diabetes Center and Department of Medicine, Harvard Medical School, Boston, MA 2 Division of Gastroenterology, Hepatology and Nutrition, Boston Children’s Hospital, Boston, MA 3 Cardiovascular and Metabolic Diseases iMed, AstraZeneca R&D, 431 83 Mölndal, Sweden (current address) 4 KG Jebsen Center for Diabetes Research, Department of Clinical Science, University of Bergen, Bergen, Norway 5 Department of Pathology, Boston Children’s Hospital, and Harvard Medical School, Boston, MA # These authors contributed equally to this work. Corresponding author: C. Ronald Kahn, MD Joslin Diabetes Center One Joslin Place Boston, MA 02215 Phone: (617)732-2635 Fax:(617)732-2487 E-mail: [email protected] Keywords: Insulin receptors, IGF-1 receptors, lipodystrophy, diabetes, dyslipidemia, fatty liver, liver tumor, NAFLD, NASH. Running title: Lipodystrophic mice develop progressive NAFLD 1 Diabetes Publish Ahead of Print, published online May 10, 2016 Diabetes Page 2 of 50 SUMMARY Ectopic lipid accumulation in the liver is an almost universal feature of human and rodent models of generalized lipodystrophy and also is a common feature of type 2 diabetes, obesity and metabolic syndrome. Here we explore the progression of fatty liver disease using a mouse model of lipodystrophy created by a fat-specific knockout of the insulin receptor (F-IRKO) or both IR and insulin-like growth factor-1 receptor (F- IR/IGF1RKO). -
Pathophysiology of Adipocyte Defects and Dyslipidemia in HIV Lipodystrophy: New Evidence from Metabolic and Molecular Studies
American Journal of Infectious Diseases 2 (3): 167-172, 2006 ISSN 1553-6203 © 2006 Science Publications Pathophysiology of Adipocyte Defects and Dyslipidemia in HIV Lipodystrophy: New Evidence from Metabolic and Molecular Studies 1,6Ashok Balasubramanyam, 1,6Rajagopal V. Sekhar, 2,3Farook Jahoor 4Henry J. Pownall and 5Dorothy Lewis 1Translational Metabolism Unit, Division of Diabetes, Endocrinology and Metabolism, 2Department of Pediatrics, 3Children’s Nutrition Research Center 4Section of Atherosclerosis and Lipoprotein Metabolism, 5Department of Immunology Baylor College of Medicine; 6Endocrine Service, Ben Taub General Hospital, Houston, Texas Abstract: Despite a burgeoning mass of descriptive information regarding the epidemiology, clinical features, body composition changes, hormonal alterations and dyslipidemic patterns in patients with HIV lipodystrophy syndrome (HLS), the specific biochemical pathways that are dysregulated in the condition and the molecular mechanisms that lead to their dysfunction, remain relatively unexplored. In this paper, we review studies that detail the metabolic basis of the dyslipidemia - specifically, the hypertriglyceridemia - that is the serologic hallmark of HLS and present new data relevant to mechanisms of dyslipidemia in the postprandial state. We also describe preliminary experiments showing that in addition to the well-known effects of highly-active antiretroviral drugs, the functional disruption of adipocytes and preadipocytes by factors intrinsic to HIV-infected immunocytes may play a role in the pathogenesis of HLS. Key words: Triglycerides, cholesterol, lipoprotein lipase, lipolysis, lymphocyte INTRODUCTION Metabolic basis of HLS - studies in the fasting and fed state: Whole body kinetic studies have Characteristics of dyslipidemia and its relationship demonstrated defects in specific lipid metabolic [19-21] to lipodystrophy: A characteristic dyslipidemic pattern pathways in HLS patients in both the fasting and observed in the majority of patients with HLS is fed (25) states. -
Newer-Generation EGFR Inhibitors in Lung Cancer: How Are They Best Used?
cancers Review Newer-Generation EGFR Inhibitors in Lung Cancer: How Are They Best Used? Tri Le 1 and David E. Gerber 1,2,3,* 1 Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390-8852, USA; [email protected] 2 Department of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, TX 75390-8852, USA 3 Division of Hematology-Oncology, Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75390-8852, USA * Correspondence: [email protected]; Tel.: +1-214-648-4180; Fax: +1-214-648-1955 Received: 15 January 2019; Accepted: 4 March 2019; Published: 15 March 2019 Abstract: The FLAURA trial established osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), as a viable first-line therapy in non-small cell lung cancer (NSCLC) with sensitizing EGFR mutations, namely exon 19 deletion and L858R. In this phase 3 randomized, controlled, double-blind trial of treatment-naïve patients with EGFR mutant NSCLC, osimertinib was compared to standard-of-care EGFR TKIs (i.e., erlotinib or gefinitib) in the first-line setting. Osimertinib demonstrated improvement in median progression-free survival (18.9 months vs. 10.2 months; hazard ratio 0.46; 95% CI, 0.37 to 0.57; p < 0.001) and a more favorable toxicity profile due to its lower affinity for wild-type EGFR. Furthermore, similar to later-generation anaplastic lymphoma kinase (ALK) inhibitors, osimertinib has improved efficacy against brain metastases. Despite this impressive effect, the optimal sequencing of osimertinib, whether in the first line or as subsequent therapy after the failure of earlier-generation EGFR TKIs, is not clear. -
ALK Tyrosine Kinase Inhibitors, 5.01.538
PHARMACY POLICY – 5.01.538 ALK Tyrosine Kinase Inhibitors Effective Date: June 1, 2021 RELATED MEDICAL POLICIES: Last Revised: May 20, 2021 None Replaces: N/A Select a hyperlink below to be directed to that section. POLICY CRITERIA | CODING | RELATED INFORMATION EVIDENCE REVIEW | REFERENCES | HISTORY ∞ Clicking this icon returns you to the hyperlinks menu above. Introduction The anaplastic lymphoma kinase (ALK) gene provides instructions for making a specific kind of protein called ALK receptor tyrosine kinase. This protein helps cells communicate. When this gene is damaged, cell growth can get stuck in the “on” position and cells grow uncontrollably. Changes to the ALK gene can lead to non-small-cell lung cancer. Tyrosine kinase inhibitors block specific enzymes, essentially working to turn the cell growth to the “off” position. ALK tyrosine kinase inhibitors specifically targets cancers caused by changes to the ALK gene. This policy describes when this specific form of chemotherapy may be considered medically necessary. Note: The Introduction section is for your general knowledge and is not to be taken as policy coverage criteria. The rest of the policy uses specific words and concepts familiar to medical professionals. It is intended for providers. A provider can be a person, such as a doctor, nurse, psychologist, or dentist. A provider also can be a place where medical care is given, like a hospital, clinic, or lab. This policy informs them about when a service may be covered. Policy Coverage Criteria Drug Medical Necessity Alecensa® (alectinib) Alecensa® (alectinib) may be considered medically necessary for the treatment of adult patients with advanced or Drug Medical Necessity metastatic non-small cell lung cancer (NSCLC) that is anaplastic lymphoma kinase (ALK)-positive. -
Lipoprotein Lipase: a General Review Moacir Couto De Andrade Júnior1,2*
Review Article iMedPub Journals Insights in Enzyme Research 2018 www.imedpub.com Vol.2 No.1:3 ISSN 2573-4466 DOI: 10.21767/2573-4466.100013 Lipoprotein Lipase: A General Review Moacir Couto de Andrade Júnior1,2* 1Post-Graduation Department, Nilton Lins University, Manaus, Amazonas, Brazil 2Department of Food Technology, Instituto Nacional de Pesquisas da Amazônia (INPA), Manaus, Amazonas, Brazil *Corresponding author: MC Andrade Jr, Post-Graduation Department, Nilton Lins University, Manaus, Amazonas, Brazil, Tel: +55 (92) 3633-8028; E-mail: [email protected] Rec date: March 07, 2018; Acc date: April 10, 2018; Pub date: April 17, 2018 Copyright: © 2018 Andrade Jr MC. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Citation: Andrade Jr MC (2018) Lipoprotein Lipase: A General Review. Insights Enzyme Res Vol.2 No.1:3 Abstract Lipoprotein Lipase: Historical Hallmarks, Enzymatic Activity, Characterization, and Carbohydrates (e.g., glucose) and lipids (e.g., free fatty acids or FFAs) are the most important sources of energy Present Relevance in Human for most organisms, including humans. Lipoprotein lipase (LPL) is an extracellular enzyme (EC 3.1.1.34) that is Pathophysiology and Therapeutics essential in lipoprotein metabolism. LPL is a glycoprotein that is synthesized and secreted in several tissues (e.g., Macheboeuf, in 1929, first described chemical procedures adipose tissue, skeletal muscle, cardiac muscle, and for the isolation of a plasma protein fraction that was very rich macrophages). At the luminal surface of the vascular in lipids but readily soluble in water, such as a lipoprotein [1]. -
Sequential ALK Inhibitors Can Select for Lorlatinib-Resistant Compound ALK Mutations in ALK-Positive Lung Cancer
Published OnlineFirst April 12, 2018; DOI: 10.1158/2159-8290.CD-17-1256 RESEARCH ARTICLE Sequential ALK Inhibitors Can Select for Lorlatinib-Resistant Compound ALK Mutations in ALK-Positive Lung Cancer Satoshi Yoda1,2, Jessica J. Lin1,2, Michael S. Lawrence1,2,3, Benjamin J. Burke4, Luc Friboulet5, Adam Langenbucher1,2,3, Leila Dardaei1,2, Kylie Prutisto-Chang1, Ibiayi Dagogo-Jack1,2, Sergei Timofeevski4, Harper Hubbeling1,2, Justin F. Gainor1,2, Lorin A. Ferris1,2, Amanda K. Riley1, Krystina E. Kattermann1, Daria Timonina1, Rebecca S. Heist1,2, A. John Iafrate6, Cyril H. Benes1,2, Jochen K. Lennerz6, Mari Mino-Kenudson6, Jeffrey A. Engelman7, Ted W. Johnson4, Aaron N. Hata1,2, and Alice T. Shaw1,2 Downloaded from cancerdiscovery.aacrjournals.org on September 30, 2021. © 2018 American Association for Cancer Research. Published OnlineFirst April 12, 2018; DOI: 10.1158/2159-8290.CD-17-1256 ABSTRACT The cornerstone of treatment for advanced ALK-positive lung cancer is sequential therapy with increasingly potent and selective ALK inhibitors. The third-generation ALK inhibitor lorlatinib has demonstrated clinical activity in patients who failed previous ALK inhibi- tors. To define the spectrum ofALK mutations that confer lorlatinib resistance, we performed accel- erated mutagenesis screening of Ba/F3 cells expressing EML4–ALK. Under comparable conditions, N-ethyl-N-nitrosourea (ENU) mutagenesis generated numerous crizotinib-resistant but no lorlatinib- resistant clones harboring single ALK mutations. In similar screens with EML4–ALK containing single ALK resistance mutations, numerous lorlatinib-resistant clones emerged harboring compound ALK mutations. To determine the clinical relevance of these mutations, we analyzed repeat biopsies from lorlatinib-resistant patients. -
Other Types of Primary Hyperlipoproteinemia
82 Journal of Atherosclerosis and Thrombosis Vol.21, No.2 Committee Report 10 Other Types of Primary Hyperlipoproteinemia (Hyperlipidemia) Executive Summary of the Japan Atherosclerosis Society (JAS) Guidelines for the Diagnosis and Prevention of Atherosclerotic Cardiovascular Diseases in Japan ― 2012 Version Tamio Teramoto, Jun Sasaki, Shun Ishibashi, Sadatoshi Birou, Hiroyuki Daida, Seitaro Dohi, Genshi Egusa, Takafumi Hiro, Kazuhiko Hirobe, Mami Iida, Shinji Kihara, Makoto Kinoshita, Chizuko Maruyama, Takao Ohta, Tomonori Okamura, Shizuya Yamashita, Masayuki Yokode and Koutaro Yokote Committee for Epidemiology and Clinical Management of Atherosclerosis 1. Primary Hyperlipoproteinemias (Hyperlipidemias) enhanced hepatic apolipoprotein (apo) B-100 synthe- Other Than Familial Hypercholesterolemia sis, decreased LPL activity, increased very-low-density There are various types of primary hyperlipopro- lipoprotein (VLDL) secretion from the liver and the teinemias (hyperlipidemias) other than familial hyper- accumulation of visceral fat as factors for the develop- cholesterolemia (FH). These types are clinically ment of symptoms and has been reported to be related important and classified according to their associated to abnormalities of the LPL and APOC-Ⅱ genes or pathophysiology and genetic abnormalities (Table 1)1). APOA-Ⅰ/C-Ⅲ/A-Ⅳ gene cluster. However, none of Familial lipoprotein lipase (LPL) deficiency manifests these findings have been proven to be definitive. It has as severe hyperchylomicronemia and may present with also been suggested that FCHL is caused by a poly- eruptive cutaneous xanthomas or acute pancreatitis, genic background that tends to induce hyperlipopro- although it does not necessarily accompany atheroscle- teinemia due to environmental factors, such as over- rotic cardiovascular disease (CVD). On the other nutrition and a low level of physical activity. -
Spotlight on Lorlatinib and Its Potential in the Treatment of NSCLC: the Evidence to Date
Journal name: OncoTargets and Therapy Article Designation: Review Year: 2018 Volume: 11 OncoTargets and Therapy Dovepress Running head verso: Akamine et al Running head recto: Spotlight on lorlatinib in the treatment of NSCLC open access to scientific and medical research DOI: 165511 Open Access Full Text Article REVIEW Spotlight on lorlatinib and its potential in the treatment of NSCLC: the evidence to date Takaki Akamine1 Abstract: The identification of anaplastic lymphoma kinase (ALK), an oncogenetic driver Gouji Toyokawa1 mutation, in lung cancer has paved the way for a new era in the treatment of non-small cell Tetsuzo Tagawa1 lung cancer (NSCLC). Targeting ALK using tyrosine kinase inhibitors (TKI) has dramatically Takashi Seto2 improved the prognosis of patients with ALK-rearranged NSCLC. However, most patients relapse on ALK-TKI therapy within a few years because of acquired resistance. One mechanism 1Department of Surgery and Science, Graduate School of Medical Sciences, of acquiring resistance is a second mutation on the ALK gene, and the representative mutation Kyushu University, Higashi-ku, is L1996M in the gatekeeper residue. In particular, the solvent-front ALK G1202R mutation is 2 Fukuoka, Japan; Department of the common cause of resistance against first- and second-generation ALK-TKIs. Another major Thoracic Oncology, National Kyushu Cancer Center, Minami-ku, Fukuoka, concern regarding ALK-TKI is metastasis to the central nervous system, commonly observed Japan in patients relapsing after ALK-TKI therapy. The next-generation ALK inhibitor lorlatinib (PF-06463922) has therefore been developed to inhibit resistant ALK mutations, including ALK For personal use only. G1202R, and to penetrate the blood–brain barrier. -
Sequential ALK Inhibitors Can Select for Lorlatinib-Resistant Compound ALK Mutations in ALK
Author Manuscript Published OnlineFirst on April 12, 2018; DOI: 10.1158/2159-8290.CD-17-1256 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Sequential ALK Inhibitors Can Select for Lorlatinib-Resistant Compound ALK Mutations in ALK- Positive Lung Cancer Satoshi Yoda1,2, Jessica J. Lin1,2, Michael S. Lawrence1,2,3, Benjamin J. Burke4, Luc Friboulet5, Adam Langenbucher1,2,3, Leila Dardaei1,2, Kylie Prutisto-Chang1, Ibiayi Dagogo-Jack1,2, Sergei Timofeevski4, Harper Hubbeling1,2, Justin F. Gainor1,2, Lorin A. Ferris1,2, Amanda K. Riley1, Krystina E. Kattermann1, Daria Timonina1, Rebecca S. Heist1,2, A. John Iafrate6, Cyril H. Benes1,2, Jochen K. Lennerz6, Mari Mino- Kenudson6, Jeffrey A. Engelman7, Ted W. Johnson4, Aaron N. Hata1,2*‡, and Alice T. Shaw1,2*‡ 1Massachusetts General Hospital Cancer Center, Charlestown, MA, USA; 2Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; 3Broad Institute of MIT and Harvard, Cambridge, MA, USA; 4Pfizer Worldwide Research and Development, La Jolla, CA, USA; 5Gustave Roussy Cancer Campus, Université Paris Saclay, INSERM U981, Paris, France; 6Cancer Center and Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA 7Novartis Institutes for BioMedical Research, Cambridge, MA, USA * These authors contributed equally to this work Running Title: Compound ALK Mutations Mediate Resistance to Lorlatinib ‡To whom correspondence should be addressed: Alice T. Shaw, MD PhD, Massachusetts General Hospital, 32 Fruit Street, Boston, MA 02114, 617-643- 0563 (p)/617-726-0453 (f), email: [email protected] 1 Downloaded from cancerdiscovery.aacrjournals.org on September 26, 2021. -
Familial Partial Lipodystrophy
Familial Partial Lipodystrophy Purvisha Patel; Ralph Starkey, MD; Michele Maroon, MD The lipodystrophies are rare disorders character- ized by insulin resistance and the absence or loss of body fat. The 4 subtypes of lipodystrophy are characterized by onset and distribution. Partial lipodystrophy is rare, with loss of fat from the extremities and excess fat accumulation in the face and neck; recognizing this phenotype and subsequent referral for endocrinologic care may improve outcome and reduce mortality. ipodystrophies are rare disorders characterized by insulin resistance and the absence or L loss of body fat.1 Classification of the 4 main subtypes of lipodystrophy is based on onset (congenital/familial vs acquired/sporadic) and dis- Figure not available online tribution (total/generalized vs partial). Congenital total lipodystrophy (also known as Berardinelli syndrome, Seip syndrome) is a rare autosomal- recessive disorder marked by an almost complete lack of adipose tissue from birth. Familial partial lipodystrophy (also known as Kobberling-Dunnigan syndrome) involves loss of subcutaneous fat from the extremities and accumulation of excess fat in the face and neck and to a lesser extent in the hands and feet. Acquired total lipodystrophy (also known as lipoatrophy, Lawrence-Seip syndrome) presents with generalized loss of fat beginning in childhood. Acquired partial lipodystrophy (also known as progressive lipodystrophy, partial lipoat- Figure 1. Accentuation of fat pads in the face and neck. rophy, Barraquer-Simons syndrome) is character- ized by loss of fat only from the upper extremities, face, and trunk.2 tional uterine bleeding (gravida 2, para 1, AB 1) Case Report necessitating total hysterectomy. On physical A 39-year-old white woman presented with the examination, accentuation of fat pads in the face complaint of thickened brown skin on the neck and and neck (Figure 1), central obesity, and prominent medial thighs.