Biological processes are all ultimately how chemical processes react with their surroundings. The more detail that is known about a process, the greater our ability to modify it. Myopia is a complex interplay of many factors that result in an eyeball being too long for the focal plane of light entering the eye. Why this happens will ultimately be understood as the interplay of many molecular processes and the study of the very basic parts of this process will eventually allow us to greatly modify, if not control, myopia.

These references are mostly, but not exclusively, related to the lower levels of juvenile myopia. More references can be found by searching for your own articles using the PubMed (National Library of Medicine) database. Just enter some terms such as "myopia gene". There were 629 such articles listed on 04 October 2011.

MyopiaPrevention.org comment: Subtitled Myopia Control with Atropine 0.01% Eyedrops. From the conclusions: "Over 5 years, atropine 0.01% eyedrops were more effective in slowing myopia progression with less visual side effects compared with higher doses of atropine."

Read the commentary by Jeffrey Cooper: Practice Update. Eye Care. Expert Comment. August 25, 2015. "This study completes a series of clinical trials demonstrating the efficacy of atropine in slowing the progression of myopia and makes a strong case for clinical use of atropine in young patients."

MyopiaPrevention.org comment: The data is now five years old, but it shows that atropine use increased over the years while the concentration of the drop used decreased. In 2007, approximately 50% of children diagnosed with myopia were prescribed atropine, 40% of those getting .1% atropine. Among 9-10 year olds with myopia, 60% were prescribed atropine. Over the seven year period, atropine use increased 34%.

MyopiaPrevention.org comment: This ATOM2 followup of the ATOM1 study sought to determine if concentrations weaker than the previously studied 1% would have a similar effect. A dose as low as .01% was shown to slow myopia clinically at the same rate as 1% with "negligible effect on accommodation and pupil size, and no effect on near visual acuity." There were no reports of allergic conjunctivitis or dermatitis. This is a significant finding that could change how myopia is treated.

MyopiaPrevention.org comment: The abstract talks about the gene mutation identified in a specific population: "Bedouin Israeli consanguineous kindred." In other words, a very small, specific population. Such studies allow researchers to more easily determine the actions of a specific gene. Further research is then needed to determine if this action is somehow impaired in myopic individuals who do not have the specific mutation.

MyopiaPrevention.org comment: A retrospective study of controlled clinical trials. Atropine slowed myopic progression by .773D/yr compared to placebo. Effects of .5% and 1% were similar.

MyopiaPrevention.org comment: While atropine (a muscarinic antagonist) has been shown to reduce myopic progression, the specific receptor that mediates the effect has not been identified. This study indicates that "muscarinic antagonists prevent myopia progression through an M4-receptor mediated mechanism, most likely located in the retina."

This is important in that, if proven true, it would permit the development of a more targeted drug for myopia control than the more broad acting atropine.

MyopiaPrevention.org comment: This study of 22 subjects aged 13 to 25 found that myopes had slightly lower levels of Vitamin D in their blood compared to non-myopes when adjusted for age and diet, but the results were questioned because the study did not find that outdoor time was related to myopia.

MyopiaPrevention.org comment: A comprehensive review of the drugs used to study myopia progression involving various receptor targets within the eye. Various models for myopia progression are discussed. "...new bioengineering approaches for drug delivery" are called for.

MyopiaPrevention.org comment: Not yet read. The abstract states that "The findings that have resulted from this study have not only provided greater insight into the role of genes and other factors involved in myopia but have also gone some way to uncovering the aetiology of other refractive errors."

MyopiaPrevention.org comment: This is a study that looked at varying the dosage of atropine based on the season, with the idea of increasing the dose when the sun exposure is the least. It was found to be effective and tolerable to the students.

MyopiaPrevention.org comment: Insulin-like growth factor-1 (IGF-1) "may play a role in control of eye growth" and this study found a "genetic association between IGF-1 and high-grade myopia."

MyopiaPrevention.org comment: The study shows the type of work needed to identify a genetic component to myopia progression. A single gene was studied and was found to be associated with both hyperopia and myopia. No attempt is made to identify how the gene might create its influence.

MyopiaPrevention.org comment: Just like the title says. This is different than has been found in other populations.

MyopiaPrevention.org comment: In simplified terms, glucose levels in the body are regulated by insulin (lowers glucose) and glucagon (raises glucose). Chick eyes were studied for the effect of these two hormones and their ability to control ocular elongation and choroidal thickness, both responsible for emetropization and myopic development. The relationship is complicated. "the simplest view of how glucagon and insulin might control emmetropization would be that insulin stimulates the eye to elongate and the choroid to thin, thus acting like a negative lens, whereas glucagon does the reverse, slowing the elongation and causing the choroid to thicken, thus acting like a positive lens. We conclude the situation is considerably more complex." It appears that this more simplistic action is maintained if the eye is compensating for defocus during which time the eye is less responsive to the drug that would be expected to slow the process in either direction.

MyopiaPrevention.org comment: Pirenzepine was shown to slow myopia to .58 diopters over two years vs. .99 diopters for the placebo group, thus cutting the progression approximately in half. An editorial in the same edition (How should we try to affect myopic progression?) by Sherwin J. Isenberg notes that although atropine and pirenzepine have the best results "in properly conducted clinical trials" for myopia control, the former is an "off-label" use and the later is not available in the United States.

MyopiaPrevention.org comment: "The experiments reported here demonstrate that both unselective blocking of potassium channels and selective inhibition of the sodium-potassium-chloride symporter can produce dramatic interference with refractive compensation to optically induced blur." "The action of bumetanide appears to combine a defocus-sensitve inhibition of refractive compensation under conditions that would normally lead to myopia"

MyopiaPrevention.org comment: This adenosine antagonist (in tablet form) was tested in a study of 68 children of average age 11 for three years. The first year half the students received the tablets, the second year all students were given the choice of once a day or twice a day tablets and the third year all medication was stopped. The authors conclude that 7-mx is efficient in retarding myopia, but I don't see that from their results and study design.

MyopiaPrevention.org comment: Paired box gene 6 (PAX6) showed no association with myopia. COL2A1 (a collagen gene) was indicated as possibly associated with myopia.

MyopiaPrevention.org comment: In the chick eye, the perception of blur does not drive emmetropization but rather the energy at high spatial frequencies in an image, leading them to conclude that amacrine cells within the retina may be sufficient to drive emmetropization.

MyopiaPrevention.org comment: The title says it all.

MyopiaPrevention.org comment: Melatonin is a hormone that "transmits daily and seasonal timing information to a variety of tissues in essentially all vertebrate species." Application of systemic melatonin altered the growth of various ocular tissues where receptors have been identified. Further study is called for to elicit more specific data.

MyopiaPrevention.org comment: A pdf of the slides presented at a lecture for ARVO's (Association for Research in Vision and Ophthalmology) symposium. A discussion of the biochemical signals controlling growth that are operating within the retina.

MyopiaPrevention.org comment: Abstract in Polish translated into English on Pubmed.com. The abstract is perhaps most interesting for the listing of potential chemicals for myopia prevention.

MyopiaPrevention.org comment: Glucagon, a chemical messenger in the body, was investigated to see whether it is involved with signaling the eye to change its growth in response to plus lenses. It was shown to thicken the choroid and may contribute to myopia prevention by reducing sclera growth.

MyopiaPrevention.org comment: "That the combination of apomorphine and atropine were not additive suggests that combining dopaminergic and muscarinic agents is not a useful strategy for improving the efficacy of these antimyopia drug treatments."

MyopiaPrevention.org comment: A study of genes within a region previously identified as associated with high myopia. No significant gene was found. Includes a good summary of the incidence of eye problems associated with increased myopia in the section "Ocular Morbidity" including such facts as the lifetime risk of retinal detachment is 9.3% for those with myopia over 5.00 D. A necessary read for anyone thinking that identifying the genetic component of myopia should be easy.

MyopiaPrevention.org comment: Pirenzepine appeared to be safe to use in children but the study did not attempt to determine if it was effective in myopia prevention.

MyopiaPrevention.org comment: 331 children aged 6-12 studied over two years showed that myopia progressed 1.20 diopters in the control (placebo drops) group and .25 diopters in the group given 1% atropine drops daily. Results for axial elongation (another measure of myopia progression) were similar.

MyopiaPrevention.org comment: A summary of many of the issues in myopia research.

MyopiaPrevention.org comment: The concern is that long term atropine use might cause either toxic problems or lead to increased light damage to the eye due to atropine dilating pupils. This study did multifocal electroretinograms (mfERG) to determine if such damage was detectable for those who had used atropine for two years. The results showed slight changes of unknown significance in the atropine group. The author states "The clinical implications of these findings need to be further explored."

MyopiaPrevention.org comment: A review of the molecular techniques being used to study myopia.

MyopiaPrevention.org comment: Pirenzepine (a selective muscarinic antagonist) studied in 353 Asian children ages 6-12. 2% drops twice a day (progressed -.47 D), once a day (progressed -.70 D) and placebo(progressed -.84 D), thus showing a 43% drop in myopic progression for 2% pirenzepine drops given twice a day. Side effects included follicles and papillae (bumps on the inner lids) that were stated to be usually symptom free with overall "minimal anti-muscarinic safety issues."

MyopiaPrevention.org comment: An extensive review of the pharmacology of myopia presented at the 9th International Myopia Conference. You must be able to read .ppt files. From Dr. Wildsoet's web site.

MyopiaPrevention.org comment: Three groups (total 188 students age 6-13): Atropine + multifocal glasses, multifocal glasses, and single vision glasses. Followed for 18 months. Progression was least for atropine+multifocals (.40 D), and more for multifocals (1.19 D) and single vision lenses (1.40 D). Although the two glasses group did differ from each other, it was not felt the difference was strong enough to say multifocals were better at prevention than single vision glasses.

MyopiaPrevention.org comment: Amacrine cells within the retina "respond differentially" depending on whether the eye is myopic or hyperopic and thus may be important in emmetropization.

MyopiaPrevention.org comment: 168 children, age 6-13 were treated with either of .5%, .25% or .1% atropine drops nightly for up to two years. Myopic progression rates were .04, .45 and .47 Diopters/year respectively compared to a control of 1.06 Diopters/year. The .5% was the most effective.

MyopiaPrevention.org comment: A study of 214 students in Olmsted County, Minnesota (USA) received atropine for various lengths of time, from 18 weeks to 11.5 years. Photophobia and blurred vision were frequently reported, but the author did not classify those as "serious side effects". The atropine group had very little myopic change (.05 units/year) vs the "no-drug" group (.36 units/year). The article has a fairly extensive discussion of atropine in various myopia control studies and background data on myopia in general. Forty five pages.

The same article appears as Kennedy RH, Dyer JA, Kennedy MA, Parulkar S, Kurland LT, Herman DC, McIntire D, Jacobs D, Luepker RV.(2000) Reducing the progression of myopia with atropine: a long term cohort study of Olmsted County students. (ABSTRACT) Binocul Vis Strabismus Q. 2000;15(3 Suppl):281-304.

MyopiaPrevention.org comment: Injected atropine in chick eyes dramatically slowed myopic progression but did not reduce accommodation. Atropine eye drops would not stop myopic progression by affecting accommodation, further proof that accommodation or reading does not by itself cause myopia.

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Myopia Medications and Genetics - MYOPIA * Prevention

INTRODUCTION

Squamous cell carcinogenesis in the mucosa of the head and neck involves the progressive accumulation of a large series of genetic abnormalities in genes regulating cell cycle progression, mitogenic and differentiative signaling pathways, angiogenesis, and cell death. This mutagenic progression, called multistep carcinogenesis, parallels the genetic model of colorectal carcinogenesis [1,2]. (See "Molecular genetics of colorectal cancer".)

Evidence for a mutational progression in tumorigenesis of head and neck squamous cell carcinoma (HNSCC) first derived from cytogenetic studies that demonstrated nonrandom clonal losses, duplications, and rearrangements of chromosome segments in head and neck tumors [3-5]. Within many of these regions of recurring chromosomal abnormality, candidate oncogenes or tumor suppressors have since been identified, some of which appear to play critical roles in carcinogenic transformation. Subsequent detailed progression models for carcinogenesis of the head and neck have been based upon mutational models and differential gene expression [6,7]. More recently, we have a better understanding of the mutational landscape in HNSCC from newer sequencing technologies [8-10].

Identification of some of the critical genetic events leading to head and neck cancer has clarified the molecular basis for epidemiologic observations regarding risk factors (eg, tobacco), identified previously unknown risk factors (eg, human papillomavirus infection), and is yielding information that may be critical for risk stratification. (See "Epidemiology and risk factors for head and neck cancer" and "Human papillomavirus associated head and neck cancer".)

In addition, these studies have unveiled a new series of targets for chemotherapeutic and chemopreventive intervention, which ultimately may result in more rational and successful therapies for this disease. (See "Chemoprevention and screening in oral dysplasia and squamous cell head and neck cancer".)

FIELD CANCERIZATION

The term field cancerization was first used to describe observations from microscopic examination of 738 lip, oral cavity, and pharyngeal carcinomas [11]. The grossly normal epithelium adjacent to the cancer in this study frequently contained dysplasia, carcinoma in situ, or invasive carcinoma, as though the entire mucosal field had been damaged and preconditioned by a carcinogen.

Literature review current through: Mar 2016. | This topic last updated: Tue Nov 24 00:00:00 GMT 2015.

The rest is here:
Head and neck squamous cell carcinogenesis: Molecular and ...

Abstract

Five proteins are ejected from the bacteriophage T7 virion at the initiation of infection. The three known proteins of the internal core enter the infected cell; all three must both disaggregate from their structure in the mature virion and also almost completely unfold in order to leave the head and pass through the headtail connector. Two small proteins, the products of genes 6.7 and 7.3, also are ejected from the infecting virion. Gp6.7 and gp7.3 were not previously described as structural virion components, leading to a re-appraisal of the stoichiometry of virion proteins. Gp6.7 is found in tail-less particles and is defined as a head protein, whereas gp7.3 is localized in the tail. Gene 6.7 may be important in morphogenesis; mutants defective in this late gene yield a reduced burst of progeny. Gene 7.3 is essential for virion assembly but, although normally present, its product gp7.3 is not required in a mature particle. Particles assembled in the absence of gp7.3 contain tail fibers but fail to adsorb to cells.

The virions of bacteriophages T3 and T7 are very similar and have a fairly simple structure (Fig. 1). The icosahedral head has a diameter of 60 to 61 nm with a shell that is 2 nm thick (Stroud et al., 1981andRont et al., 1983). The outer shell is composed of two forms of the gene 10 protein, which are made via a programmed translational frameshift near the 3 end of the shorter gene 10A ( Dunn and Studier, 1983, Condreay et al., 1989, Condron et al., 1991aandCondron et al., 1991b). Inserted at one vertex is the headtail connector, composed of 12 gp8 molecules ( Carazo et al., 1986, Cerritelli and Studier, 1996, Kocsis et al., 1995andValpuesta et al., 1992). The connector has a 12-lobed wide domain inserted into the head cavity and a narrower domain that interacts with the tail ( Valpuesta et al., 1992andValpuesta et al., 2000). A channel, which is closed in mature virions, runs through the center of the connector (Donate et al., 1988). Inside the head, and attached to the headtail connector in the coaxial orientation, is a 26 nm21 nm cylindrical structure that is usually referred to as the internal core ( Serwer, 1976, Serwer et al., 1997andSteven and Trus, 1986). The core has recently been shown to exhibit 8-fold symmetry (Cerritelli et al., 2003), it consists of stacked rings and contains three distinct proteins, the products of genes 14, 15, and 16. The 40-kb genome is spooled around the internal core in six coaxial shells ( Cerritelli et al., 1997). Unlike most other tailed phages, the T7 tail is not assembled as a separate structure but forms directly on the DNA-filled head ( Studier, 1972, Serwer, 1976, Roeder and Sadowski, 1977andMatsuo-Kato et al., 1981). The stubby tail is 23 nm long, tapering from a diameter of 21 nm at the connector to 9 nm at its distal end, and is known to consist of two major proteins gp11 and gp12 ( Studier, 1972andSteven and Trus, 1986). Attached near the head proximal end of the tail are six symmetrically positioned tail fibers. Each fiber is composed of a trimer of gp17 that forms a kinked structure ( Kato et al., 1985, Kato et al., 1986andSteven et al., 1988). The N-terminal 150 residues of gp17 link the fiber to the tail, the next 117 residues fold into an -helix, forming a 16.4-nm rod that is flexibly joined to the 15.5-nm distal half fiber. The latter consists of a linear array of four globules that is thought to bind directly to the bacterial cell.

Bacteriophage T7 initiates an infection of Escherichia coli by the interaction of its tail fibers with the lipopolysaccharide (LPS) on the cell surface. Interaction of all six tail fibers with LPS would orient the phage tail perpendicular to the cell surface, conferring efficiency to subsequent stages of infection. However, the stubby T7 tail is too short to span the E. coli cell envelope and a channel needs to be made to allow the phage genome to travel from the virion into the cytoplasm. It was proposed that virion proteins are ejected into the cell, functionally endowing T7 with an extensible tail, in contrast to the well-known contractile tail of T4 and other Myoviridae ( Molineux, 2001). In testing this suggestion, we show here that five T7 proteins are ejected from the virion into the cell at the initiation of infection. Two of these proteins were not previously known to be part of the virion, an observation that prompted a re-evaluation of the protein composition of the T7 particle.

In order to determine which T7 virion proteins become irreversibly associated with the infected cell, adsorbed particles were gently eluted by extensive washing in pure water. Prior to infection, cells of the E. coli K-12 strain IJ1133 were treated with rifampicin so that phage development would be inhibited after the first 850 bp of the T7 genome had been translocated into the cell and there would be no phage gene expression ( Garca and Molineux, 1995, Garca and Molineux, 1996andStruthers-Schlinke et al., 2000). Adsorption of the T7 tail fibers to E. coli LPS occurs through electrostatic interactions ( Puck et al., 1951, Luria, 1953andTolmach, 1957), and the reduction in ionic strength during washing causes dissociation of the phage from the cell. A similar protocol was used to identify P22 proteins that are ejected into the host cell (Israel, 1977). Elution results in the removal of the majority of the major and minor forms of the T7 capsid protein gp10, the headtail connector gp8, and the tail proteins gp11, gp12, and gp17 (Fig. 2A). In contrast, the majority of the internal core proteins gp14, gp15, and gp16 remain stably associated with the cell during the elution regimen. At the initiation of infection, the internal core must therefore disaggregate in order to allow its constituent proteins to be ejected from the virion into the cell. Two small virion proteins, gp6.7 and gp7.3, are also ejected from the virion but are degraded in infected wild-type cells. The proteins can be stabilized when the multiply protease-deficient strain HM130 is infected (data not shown). It is not yet known which of degP, lon, tsp, or ptr, missing in strain HM130 ( Meerman and Georgiou, 1994), is responsible.

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Changes in bacteriophage T7 virion structure at the ...

Our Board of Directors is a group of volunteers committed to the Foundations mission to find a cure for retinitis pigmentosa, macular degeneration and related diseases of the retina. The Board includes representatives from the corporate and medical worlds, as well as individuals affected by vision loss.

Andrew Burke, Chair Partner, Stewart McKelvey Halifax, Nova Scotia

JoeGrech, Vice-Chair Vancouver, British Columbia

Rahn Dodick, Treasurer President, Dodick Landau Inc. Toronto, Ontario

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Michel Cayouette, PhD Research Unit Director, Institut de recherches cliniques de Montreal (IRCM) Research Associate Professor, University of Montreal Montreal, Quebec

David Drury General Manager, IBM Canada Ltd. Toronto, Ontario

Sherif El-Defrawy, MD, PhD, FRCSC Chief of Ophthalmology, University of Toronto Toronto, Ontario

Peter FarmerDirector, Strategic Partnerships, Rogers CommunicationsToronto, Ontario

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Peter J. Kertes, MD, FRCSC Vitreoretinal Surgeon/Ophthalmologist-in-Chief, Sunnybrook Health Sciences Centre Professor of Ophthalmology & Vision Sciences, University of Toronto Toronto, Ontario

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Michael Ovens Process Analyst, Change Management, Bank of Montreal Toronto, Ontario

Lorna L. Rosenstein General Manager, Lotus Canada(retired) Toronto, Ontario

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Raymond M. Stein, MD, FRCSC Medical Director, Bochner Eye Institute Toronto, Ontario

David D. Sweeny Director, RBC Capital Markets Toronto, Ontario

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The Foundation Fighting Blindness Scientific Advisory Board (SAB) is a group of highly qualified and committed volunteers. These scientists bring a wide range of expertise to the FFBs scientific decision-making in genetics, molecular genetics, molecular biology, biochemistry and cell biology. All are actively engaged in sight-saving research.

The SAB is responsible for evaluating research applications submitted to the FFBs annual grant competition(s).

SAB members also aid in promoting retinal disease research amongst the scientific community and support the quality and accuracy of our educational programs and materials. Rigorous review for scientific merit by the SAB ensures that dollars donated to the FFB are used to fund the most productive and promising research projects, addressing crucial questions about the causes and treatment of retinal degenerative diseases. Thanks to the guidance of our scientific advisory boards, past and present, scientists funded by the FFB have consistently accomplished their research goals and have been responsible for major research breakthroughs.

Dr. Rod Bremner, PhD (Interim Chair) Senior Investigator, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital Professor of Ophthalmology; Laboratory Medicine & Pathobiology, University of Toronto

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Dr. Sylvain Chemtob Sylvain Chemtob, MD, PhD Professor, Departments of Pediatrics, Ophthalmology and Pharmacology, University of Montreal

Dr. Brian Link Brian A. Link, PhD Associate Professor of Cell Biology, Neurobiology & Anatomy, Medical College of Wisconsin

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The Foundation Fighting Blindness Leadership

Description of Research Expertise:

I am a hematologist-oncologist with a specific research and clinical interest in plasma cell disorders and related dysproteinemias: multiple myeloma, immunoglobulin light chain (AL) amyloidosis, and Waldenstroms macroglobulinemia.

I also lead the multi-disciplinary Penn Amyloidosis Program. This is a cross-disciplinary program involving clinicians with expertise in amyloidosis from cardiology, nephrology, pathology and other disciplines.

I am involved in clinical, translational and epidemiologic research throughout the spectrum of plasma cell disorders. My primary research focus is on the myeloma precursor states: monoclonal gammopathy of undetermined significance (MGUS) and smoldering multiple myeloma (SMM). I have previously established that both multiple myeloma (Weiss Blood 2009) and AL amyloidosis (Weiss J Clin Oncol 2014) have precursor states that are detectable for many years prior to diagnosis. I have also validated biomarkers for ultra-high risk SMM (Waxman Leukemia 2014) that have contributed to changing the diagnostic criteria for multiple myeloma requiring treatment (Rajkumar Lancet Oncol 2014).

I am currently performing trials to develop and test novel biomarkers for progression in the myeloma precursor states (MGUS and SMM). I am also participating in trials of early intervention in high risk SMM.

I am also conducting trials of novel agents for AL amyloidosis and relapsed and refractory multiple myeloma.

Rajkumar SV, Dimopoulos MA, Palumbo A, Blade J, Merlini G, Mateos MV, Kumar S, Hillengass J, Kastritits E, Richardson P, Landgren O, Paiva B, Dispenzieri A, Weiss B, LeLeu X, Zweegman S, Lonial S, Rosinol L, Zamagni E, Jaganath S, Sezer O, Kristinsson SY, Caers J, Usmani SZ, Laheurta JJ, Johnsen HE, Beksac M, Cavo M, Goldschmidt H, Terpos E, Kyle RA, Anderson KC, Durie BGM, San Miguel JF: International Myeloma Working Group updated criteria for the diagnosis of multiple myeloma Lancet Oncol 15 : e538-48,2014.

Weiss BM, Hebreo J, Cordaro DV, Roschewski MJ, Baker TP, Abbott KC, Olson SW: Increased Serum Free Light Chains Precede the Presentation of Immunoglobulin Light Chain Amyloidosis J Clin Oncol 32 (25): 2699-704,2014.

Waxman AJ, Mick R, Garfall AL, Cohen A, Vogl DT, Stadtmauer EA, Weiss BM: Classifying ultra-high risk smoldering myeloma Leukemia : 2014.

Weiss BM: Multiethnic myeloma Blood 121 (16): 3062-4,2013.

Fermand JP, Bridoux F, Kyle RA, Kastritis E, Weiss BM, Cook MA, Drayson MT, Dispenzieri A, Leung N; International Kidney and Monoclonal Gammopathy Research Group.: How I treat monoclonal gammopathy of renal significance (MGRS) Blood 122 (22): 3583-90,2013.

Minter AR, Simpson H, Weiss BM, Landgren O: Bone Disease From Monoclonal Gammopathy of Undetermined Significance to Multiple Myeloma: Pathogenesis, Interventions, and Future Opportunities. Seminars in Hematology 48 (1): 55-65,2011.

Weiss BM, Minter A, Abadie J, Howard R, Ascencao J, Schechter GP, Kuehl M, Landgren O: Patterns of Monoclonal Immunoglobulins and Serum Free Light Chains Are Significantly Different in African-American Compared to Caucasian MGUS Patients. American Journal of Hematology 86 (6): 475-8,2011.

Waxman AJ, Mink PJ, Devesa SS, Anderson WF, Weiss BM, Kristinsson SY, McGlynn KA, Landgren O: Racial disparities in incidence and outcome in multiple myeloma: a population-based study. Blood 116 (25): 5501-5506,2010.

Weiss BM, Abadie J, Verma P, Howard RS, Kuehl WM: A monoclonal gammopathy precedes multiple myeloma in most patients. Blood 113 (22): 5418-5422,2009.

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Brendan M. Weiss, MD profile| PennMedicine.org