Ryan T. Merrell, M.D.

Ryan T. Merrell, M.D.

Ryan T. Merrell, M.D.

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Personal Bio

Treatment Philosophy

My treatment philosophy is to be the best listener I can be in order to hear all of the medical and emotional needs of my patients. I also strive to use humor to make the patient experience more relaxed and enjoyable.

Personal Interests

My personal interests include long distance running, tennis, golf, softball, and basketball. I also enjoy reading non fiction, traveling, and going to sporting events.

Conditions & Procedures


Brain Cancer, Brain Tumor, Neurologic complications of cancer, Tumor in the Central Nervous System (Brain or Spine)

General Information




NorthShore Medical Group

Academic Rank

Clinical Assistant Professor



Board Certified


Clinical Service

Education, Training & Fellowships

Medical School

University of Alabama School of Medicine, 2005


Mayo School of Graduate Medical Education, 2006


Mayo School of Graduate Medical Education, 2009


Harvard Medical School/Massachusettts General Hospital Cancer Center/Dana Farber Cancer Inst.



NorthShore Medical Group

2650 Ridge Ave.
Kellogg Cancer Center
Evanston, IL 60201
847.570.1808 847.733.5137 fax Get Directions This location is wheelchair accessible.

NorthShore Medical Group

2180 Pfingsten Rd.
Suite 2000
Glenview, IL 60026
847.570.2570 847.657.5708 fax Get Directions This location is wheelchair accessible.

NorthShore Medical Group

2180 Pfingsten Rd.
Kellogg Cancer Center
Glenview, IL 60026
847.570.1808 847.733.5137 fax Get Directions This location is wheelchair accessible.


Commercial Plans
  • Aetna Choice POS
  • Aetna Elect Choice EPO and EPO
  • Aetna Health Network Options
  • Aetna HMO
  • Aetna Managed Choice
  • Aetna Managed Choice POS
  • Aetna Open Choice PPO
  • Aetna Open Choice PPO (Aetna HealthFund)
  • Aetna QPOS
  • Aetna Select
  • Beechstreet PPO Network
  • Blue Cross Blue Shield - PPO Products
    Not Contracted Blue Cross Blue Shield Blue Choice PPO
  • Blue Cross Blue Shield Blue Advantage
  • Blue Cross Blue Shield HMOI
  • Cigna HMO
  • Cigna LocalPlus
  • Cigna Open Access Plus (OAP)
  • Cigna Open Access Plus with CareLink (OAPC)
  • Cigna POS
  • Cigna PPO
  • Cofinity PPO (an Aetna Company)
  • Coventry Health Care Elect Choice EPO
  • Coventry Health Care First Health PPO
  • Galaxy Health PPO Network
  • Great West PPO/POS
  • Healthcare's Finest Network (HFN)
  • Humana - All Commercial Plans (including Choice Care)
  • Humana - NorthShore Complete Care
  • Humana/ChoiceCare Network PPO
  • Medicare
  • Multiplan and PHCS PPO Network (Including PHCS Savility)
  • NorthShore Employee Network
  • Preferred Plan PPO
  • Three Rivers Provider PPO Network (TRPN)
  • Tricare
  • Unicare
  • United Healthcare - All Commercial Plans
    Not Contracted United Healthcare Core
    Not Contracted United Healthcare Navigate
Exchange Plans
  • Aetna Whole Health Chicago
  • Not Contracted Blue Cross Blue Shield - PPO Products
    Not Contracted Blue Cross Blue Shield Blue Choice PPO
  • Blue Cross Blue Shield Blue Precision HMO
  • Coventry (PPO)
  • Harken Health - an Affiliate of United Healthcare
    Verify physician participation and out of pocket expenses with Harken
  • Land of Lincoln Health Traditional PPO
  • Not Contracted United Healthcare Compass
  • Illinois Department of Public Aid (IDPA)
  • Illinicare ICP
  • Community Care Partners
Medicare Advantage Plans
  • Aetna Medicare (SM) Plan (HMO)
  • Aetna Medicare (SM) Plan (PPO)
  • Blue Cross Blue Shield Medicare Advantage PPO Plan
  • Cigna-HealthSpring Advantage HMO
  • Cigna-HealthSpring Premier HMO-POS
  • Cigna-HealthSpring Primary HMO
  • Humana Gold Plus HMO
  • Humana Gold Plus PFFS
  • HumanaChoice PPO
  • United Healthcare - All Medicare Plans
Medicare Medicaid Alignment Initiative (MMAI) Plans
  • Blue Cross Blue Shield Community
  • HealthSpring
  • Humana
  • Illinicare Health Plan
  • Meridian Complete


  • The Glioma International Case-Control Study: A Report From the Genetic Epidemiology of Glioma International Consortium.

    American journal of epidemiology 2016 Jan 15

    Authors: Amirian ES, Armstrong GN, Zhou R, Lau CC, Claus EB, Barnholtz-Sloan JS, Il'yasova D, Schildkraut J, Ali-Osman F, Sadetzki S, Johansen C, Houlston RS, Jenkins RB, Lachance D, Olson SH, Bernstein JL, Merrell RT, Wrensch MR, Davis FG, Lai R, Shete S, Amos CI, Scheurer ME, Aldape K, Alafuzoff I, Brännström T, Broholm H, Collins P, Giannini C, Rosenblum M, Tihan T, Melin BS, Bondy ML
    Decades of research have established only a few etiological factors for glioma, which is a rare and highly fatal brain cancer. Common methodological challenges among glioma studies include small sample sizes, heterogeneity of tumor subtypes, and retrospective exposure assessment. Here, we briefly describe the Glioma International Case-Control (GICC) Study (recruitment, 2010-2013), a study being conducted by the Genetic Epidemiology of Glioma International Consortium that integrates data from multiple data collection sites, uses a common protocol and questionnaire, and includes biospecimen collection. To our knowledge, the GICC Study is the largest glioma study to date that includes collection of blood samples, which will allow for genetic analysis and interrogation of gene-environment interactions.
    PMID: 26656478 [PubMed - as supplied by publisher]
  • Targeted sequencing in chromosome 17q linkage region identifies familial glioma candidates in the Gliogene Consortium.

    Scientific reports 2015

    Authors: Jalali A, Amirian ES, Bainbridge MN, Armstrong GN, Liu Y, Tsavachidis S, Jhangiani SN, Plon SE, Lau CC, Claus EB, Barnholtz-Sloan JS, Il'yasova D, Schildkraut J, Ali-Osman F, Sadetzki S, Johansen C, Houlston RS, Jenkins RB, Lachance D, Olson SH, Bernstein JL, Merrell RT, Wrensch MR, Davis FG, Lai R, Shete S, Aldape K, Amos CI, Muzny DM, Gibbs RA, Melin BS, Bondy ML
    Glioma is a rare, but highly fatal, cancer that accounts for the majority of malignant primary brain tumors. Inherited predisposition to glioma has been consistently observed within non-syndromic families. Our previous studies, which involved non-parametric and parametric linkage analyses, both yielded significant linkage peaks on chromosome 17q. Here, we use data from next generation and Sanger sequencing to identify familial glioma candidate genes and variants on chromosome 17q for further investigation. We applied a filtering schema to narrow the original list of 4830 annotated variants down to 21 very rare (<0.1% frequency), non-synonymous variants. Our findings implicate the MYO19 and KIF18B genes and rare variants in SPAG9 and RUNDC1 as candidates worthy of further investigation. Burden testing and functional studies are planned.
    PMID: 25652157 [PubMed - as supplied by publisher]
  • Germline mutations in shelterin complex genes are associated with familial glioma.

    Journal of the National Cancer Institute 2015 Jan

    Authors: Bainbridge MN, Armstrong GN, Gramatges MM, Bertuch AA, Jhangiani SN, Doddapaneni H, Lewis L, Tombrello J, Tsavachidis S, Liu Y, Jalali A, Plon SE, Lau CC, Parsons DW, Claus EB, Barnholtz-Sloan J, Il'yasova D, Schildkraut J, Ali-Osman F, Sadetzki S, Johansen C, Houlston RS, Jenkins RB, Lachance D, Olson SH, Bernstein JL, Merrell RT, Wrensch MR, Walsh KM, Davis FG, Lai R, Shete S, Aldape K, Amos CI, Thompson PA, Muzny DM, Gibbs RA, Melin BS, Bondy ML, Gliogene Consortium
    Gliomas are the most common brain tumor, with several histological subtypes of various malignancy grade. The genetic contribution to familial glioma is not well understood. Using whole exome sequencing of 90 individuals from 55 families, we identified two families with mutations in POT1 (p.G95C, p.E450X), a member of the telomere shelterin complex, shared by both affected individuals in each family and predicted to impact DNA binding and TPP1 binding, respectively. Validation in a separate cohort of 264 individuals from 246 families identified an additional mutation in POT1 (p.D617Efs), also predicted to disrupt TPP1 binding. All families with POT1 mutations had affected members with oligodendroglioma, a specific subtype of glioma more sensitive to irradiation. These findings are important for understanding the origin of glioma and could have importance for the future diagnostics and treatment of glioma.
    PMID: 25482530 [PubMed - as supplied by publisher]
  • Germline rearrangements in families with strong family history of glioma and malignant melanoma, colon, and breast cancer.

    Neuro-oncology 2014 Oct

    Authors: Andersson U, Wibom C, Cederquist K, Aradottir S, Borg A, Armstrong GN, Shete S, Lau CC, Bainbridge MN, Claus EB, Barnholtz-Sloan J, Lai R, Il'yasova D, Houlston RS, Schildkraut J, Bernstein JL, Olson SH, Jenkins RB, Lachance DH, Wrensch M, Davis FG, Merrell R, Johansen C, Sadetzki S, Gliogene Consortium, Bondy ML, Melin BS
    Although familial susceptibility to glioma is known, the genetic basis for this susceptibility remains unidentified in the majority of glioma-specific families. An alternative approach to identifying such genes is to examine cancer pedigrees, which include glioma as one of several cancer phenotypes, to determine whether common chromosomal modifications might account for the familial aggregation of glioma and other cancers.
    Germline rearrangements in 146 glioma families (from the Gliogene Consortium; http://www.gliogene.org/) were examined using multiplex ligation-dependent probe amplification. These families all had at least 2 verified glioma cases and a third reported or verified glioma case in the same family or 2 glioma cases in the family with at least one family member affected with melanoma, colon, or breast cancer.The genomic areas covering TP53, CDKN2A, MLH1, and MSH2 were selected because these genes have been previously reported to be associated with cancer pedigrees known to include glioma.
    We detected a single structural rearrangement, a deletion of exons 1-6 in MSH2, in the proband of one family with 3 cases with glioma and one relative with colon cancer.
    Large deletions and duplications are rare events in familial glioma cases, even in families with a strong family history of cancers that may be involved in known cancer syndromes.
    PMID: 24723567 [PubMed - as supplied by publisher]
  • Intracranial, intra-axial metastatic giant cell tumor of bone: case report and review of literature.

    Clinical neurology and neurosurgery 2014 Feb

    Authors: Shakur SF, Bit-Ivan E, Watkin WG, Merrell RT, Farhat HI
    Glioblastoma (GBM) rarely presents as an infratentorial tumor in adults. The authors present a case of concomitant supratentorial and infratentorial GBM in an adult. A 72-year-old man presented with headache, nausea, vomiting, and lightheadedness. Initial MR images revealed enhancing masses in the right cerebellum and right posterior periventricular region. The patient underwent a suboccipital craniotomy and resection of the cerebellar lesion. Final histopathology was consistent with glioblastoma. The patient went on to receive standard radiation treatment for GBM with concurrent and adjuvant temozolomide. However, the patient experienced clinical deterioration within a few days after starting radiotherapy. He and his family decided to forego treatment and pursue palliative care. The patient expired three months after the initial diagnosis. Autopsy findings supported the diagnosis of GBM with leptomeningeal gliomatosis and involvement of the cerebrum, cerebellum, and spinal cord. The authors review the literature and propose that the pathogenesis of multiple and multicentric GBM may involve neural stem cells within the subventricular zone or could result from tumor dissemination along established CNS routes, such as white matter tracts and CSF pathways.
    PMID: 24438802 [PubMed - as supplied by publisher]
  • Description of selected characteristics of familial glioma patients - results from the Gliogene Consortium.

    European journal of cancer (Oxford, England : 1990) 2013 Apr

    Authors: Sadetzki S, Bruchim R, Oberman B, Armstrong GN, Lau CC, Claus EB, Barnholtz-Sloan JS, Il'yasova D, Schildkraut J, Johansen C, Houlston RS, Shete S, Amos CI, Bernstein JL, Olson SH, Jenkins RB, Lachance D, Vick NA, Merrell R, Wrensch M, Davis FG, McCarthy BJ, Lai R, Melin BS, Bondy ML, Gliogene Consortium
    While certain inherited syndromes (e.g. Neurofibromatosis or Li-Fraumeni) are associated with an increased risk of glioma, most familial gliomas are non-syndromic. This study describes the demographic and clinical characteristics of the largest series of non-syndromic glioma families ascertained from 14 centres in the United States (US), Europe and Israel as part of the Gliogene Consortium.
    Families with 2 or more verified gliomas were recruited between January 2007 and February 2011. Distributions of demographic characteristics and clinical variables of gliomas in the families were described based on information derived from personal questionnaires.
    The study population comprised 841 glioma patients identified in 376 families (9797 individuals). There were more cases of glioma among males, with a male to female ratio of 1.25. In most families (83%), 2 gliomas were reported, with 3 and 4 gliomas in 13% and 3% of the families, respectively. For families with 2 gliomas, 57% were among 1st-degree relatives, and 31.5% among 2nd-degree relatives. Overall, the mean (±standard deviation [SD]) diagnosis age was 49.4 (±18.7) years. In 48% of families with 2 gliomas, at least one was diagnosed at <40y, and in 12% both were diagnosed under 40y of age. Most of these families (76%) had at least one grade IV glioblastoma multiforme (GBM), and in 32% both cases were grade IV gliomas. The most common glioma subtype was GBM (55%), followed by anaplastic astrocytoma (10%) and oligodendroglioma (8%). Individuals with grades I-II were on average 17y younger than those with grades III-IV.
    Familial glioma cases are similar to sporadic cases in terms of gender distribution, age, morphology and grade. Most familial gliomas appear to comprise clusters of two cases suggesting low penetrance, and that the risk of developing additional gliomas is probably low. These results should be useful in the counselling and clinical management of individuals with a family history of glioma.
    PMID: 23290425 [PubMed - as supplied by publisher]
  • Brain tumors.

    Disease-a-month : DM 2012 Dec

    Authors: Sun X, Vengoechea J, Elston R, Chen Y, Amos CI, Armstrong G, Bernstein JL, Claus E, Davis F, Houlston RS, Il'yasova D, Jenkins RB, Johansen C, Lai R, Lau CC, Liu Y, McCarthy BJ, Olson SH, Sadetzki S, Schildkraut J, Shete S, Yu R, Vick NA, Merrell R, Wrensch M, Yang P, Melin B, Bondy ML, Barnholtz-Sloan JS, Gliogene Consortium
    We propose a 2-step model-based approach, with correction for ascertainment, to linkage analysis of a binary trait with variable age of onset and apply it to a set of multiplex pedigrees segregating for adult glioma.
    First, we fit segregation models by formulating the likelihood for a person to have a bivariate phenotype, affection status and age of onset, along with other covariates, and from these we estimate population trait allele frequencies and penetrance parameters as a function of age (N = 281 multiplex glioma pedigrees). Second, the best fitting models are used as trait models in multipoint linkage analysis (N = 74 informative multiplex glioma pedigrees). To correct for ascertainment, a prevalence constraint is used in the likelihood of the segregation models for all 281 pedigrees. Then the trait allele frequencies are reestimated for the pedigree founders of the subset of 74 pedigrees chosen for linkage analysis.
    Using the best-fitting segregation models in model-based multipoint linkage analysis, we identified 2 separate peaks on chromosome 17; the first agreed with a region identified by Shete and colleagues who used model-free affected-only linkage analysis, but with a narrowed peak: and the second agreed with a second region they found but had a larger maximum log of the odds (LOD).
    Our approach was able to narrow the linkage peak previously published for glioma.
    We provide a practical solution to model-based linkage analysis for disease affection status with variable age of onset for the kinds of pedigree data often collected for linkage analysis.
    PMID: 23149521 [PubMed - as supplied by publisher]
  • Anaplastic glioma.

    Current treatment options in neurology 2012 Aug

    Authors: Paleologos NA, Merrell RT
    The treatment of anaplastic glioma (AG) varies depending on histopathology of the tumor, molecular markers, and individual patient characteristics. Maximal surgical resection is desirable for all types of AG if technically feasible, with an acceptable level of risk, and with the goal of preserving neurologic function. As opposed to the standard treatment of glioblastoma, based on a large, randomized, phase 3 trial, there is no accepted standard treatment for AG. Anaplastic astrocytoma (AA) is most often treated with radiotherapy (RT), with or without concomitant temozolomide (TMZ) and with or without adjuvant temozolomide. Rarely is AA treated with chemotherapy alone, although different treatment modalities are being evaluated in ongoing trials. The treatment of anaplastic oligodendroglioma (AO) and anaplastic oligoastrocytoma (AOA) is influenced by the 1p/19q status, as allelic co-deletion of chromosomes 1p and 19q predicts increased sensitivity to chemotherapy and prolonged survival. In contrast to the treatment of AA, carefully selected patients with AO and AOA may be treated with chemotherapy alone. Temozolomide has largely replaced PCV (procarbazine, CCNU, vincristine) as the chemotherapeutic agent for AO and AOA, largely due to greater tolerability and less potential for toxicity. However, whether temozolomide has similar efficacy to PCV has not been fully evaluated. Patients with AO and AOA with significant residual tumor after surgery, intractable seizures, and/or non co-deleted 1p/19q status are often treated with RT with or without concomitant chemotherapy and with or without adjuvant chemotherapy. There is no standard postoperative care for anaplastic ependymoma (AE). The efficacy of upfront versus delayed RT has not been evaluated. Surgery may be indicated for patients with recurrent AG. There may be benefit on overall survival, although this has not been clearly proven. Reoperation may also provide symptomatic relief and confirm the pathology, including differentiation of radiation necrosis from recurrent tumor. Confirmation of tumor grade is often important for enrollment in clinical trials, a reasonable treatment choice for patients with recurrent tumor. Treatment of recurrent AG often depends on prior treatments. Patients who have progressed after RT alone may be treated with temozolomide or PCV. Patients treated previously with chemotherapy alone may be treated with RT at time of progression. Dose-intense temozolomide, bevacizumab alone, or bevacizumab in combination with a cytotoxic agent are other treatment options. Focused radiation such as stereotactic radiosurgery has no proven role in treating recurrent AG. A number of other treatment modalities are currently under active investigation, including targeted molecular inhibitors, immunotherapies, convection enhanced delivery, and viral gene therapies. There is no standard treatment for recurrent AE. Most patients undergo re-resection followed by RT if RT was not previously given. Chemotherapy may be given, but there is no standard chemotherapeutic regimen. Ongoing trials are evaluating the role of bevicizumab and targeted molecular agents in the treatment of AE.
    PMID: 22665140 [PubMed - as supplied by publisher]

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