Bayer Announces Recipients of the Pulmonary Hypertension Accelerated Bayer (PHAB) Awards at CHEST Annual Meeting 2019 - PRNewswire

Bayer Announces Recipients of the Pulmonary Hypertension Accelerated Bayer (PHAB) Awards at CHEST Annual Meeting 2019 - PRNewswire


Bayer Announces Recipients of the Pulmonary Hypertension Accelerated Bayer (PHAB) Awards at CHEST Annual Meeting 2019 - PRNewswire

Posted: 21 Oct 2019 05:00 AM PDT

WHIPPANY, N.J., Oct. 21, 2019 /PRNewswire/ -- Bayer today announced recipients of the inaugural Pulmonary Hypertension Accelerated Bayer (PHAB) Awards, a U.S.-based research grant program created to support clinical research in pulmonary hypertension (PH), with a focus on pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH). The recipients will receive a combined total of $1 million in grants over a two-year period, making the PHAB Awards one of the largest industry-funded grant programs focused on PAH and CTEPH in the U.S. The eight award recipients were formally announced at a ceremony during the American College of Chest Physicians (CHEST) Annual Meeting in New Orleans on Sunday, October 20, 2019.

"Supporting a new generation of researchers is imperative to ensure we continue the progress that has been made during the past decade in pulmonary hypertension and its related conditions," said Aleksandra Vlajnic, M.D., Senior Vice President & Head Medical Affairs Americas at Bayer. "Our hope is that the PHAB Awards program will encourage researchers to think creatively about solving the significant treatment and patient care challenges that remain, knowing Bayer is committed to providing the support needed to help bring those ideas to fruition. We want to congratulate all of the applicants on their winning proposals."

The recipients are:

  • Andrew J. Bryant, M.D., Assistant Professor of Medicine, University of Florida College of Medicine, Gainesville, FL will study the uncertain relationship between myeloid cells (or bone-marrow derived cells), circadian rhythm and PH and apply this knowledge to evaluate the use of existing treatments for patients with PH.
  • Francisco Contijoch, Ph.D., Assistant Professor, University of California at San Diego, San Diego, CA will study the effectiveness of different imaging modalities to determine if pre-operative, imaging-based prediction of surgical disease level could be utilized to assess risk-benefit of pulmonary thromboendarterectomy (PTE) surgery.
  • Michael Insel, M.D., Pulmonary Critical Care Fellow, University of Arizona Department of Medicine, Tucson, AZ will study the different causes of shortness of breath in patients who have suffered a pulmonary embolism using invasive cardiopulmonary exercise testing.
  • Sonia Jasuja, M.D., Fellow Physician, David Geffen School of Medicine at UCLA, Los Angeles, CA will study the use of impedance cardiography, a non-invasive technology measuring cardiac output and stroke volume, to assess risk and response to treatment in patients with PAH or CTEPH.
  • Manreet Kanwar, M.D., Associate Professor, Allegheny General Hospital, Pittsburgh, PA will study the role of medical therapy, in treating patients with chronic thromboembolic disease (CTED), who have symptoms of shortness of breath, to help understand progression between CTED and CTEPH and evaluate treatment options.
  • Lea Ann Matura, Ph.D., Associate Professor, School of Nursing, University of Pennsylvania, PA will study alternative treatments, such as Cognitive Behavioral Therapy and Bright Light Therapy, to improve symptoms of PAH, including insomnia, fatigue and physical activity levels.
  • Yogesh Reddy, M.D., M.Sc., Instructor of Medicine, Mayo Clinic, Rochester, MN will study the prevalence of atypical PAH in elderly patients, as well as their response to therapy using invasive exercise hemodynamic testing.
  • Maria Trivieri, M.D., Ph.D., Assistant Professor, Icahn School of Medicine at Mount Sinai, New York, NY will work to develop a new in-vitro way to generate human species-specific, and even patient-specific stem cells, to examine the underlying mechanisms of vascular pathogenesis to advance disease understanding, to make greater inroads in the treatment of PAH.

The PHAB Awards recipients were selected by an independent Grants Review Committee, consisting of the following eminent PH leaders:

  • William Auger, M.D., Temple University Medical Center, Philadelphia, PA
  • Raymond L. Benza, M.D., FACC, FCCP, Temple University School of Medicine, Cardiovascular Institute, Allegheny Health Network, Pittsburgh, PA
  • Hunter Champion M.D., Ph.D., Southeastern Cardiology, Columbus, GA
  • Rajan Saggar, M.D., Ronald Reagan University of California, Los Angeles Medical Center, Los Angeles, CA
  • Roxana Sulica, M.D., NYU Langone Medical Center, Beth Israel Medical Center, New York, NY
  • Aaron Waxman, M.D., Ph.D., Brigham and Women's Hospital, Pulmonary Vascular Disease Program, Boston, MA
  • Melisa Wilson, APRN, ACNP-BC, Florida Hospital Orlando, Center for Pulmonary Hypertension and Cardiovascular Disease, Orlando, FL

"I would like to thank and recognize the Grants Review Committee for their time and commitment, and the PH community in the U.S. for their overwhelming response to the inaugural PHAB Awards," said Sameer Bansilal, M.D., M.S., Medical Director, U.S. Medical Affairs at Bayer. "We look forward to an even greater response next year and encourage eligible applicants to start thinking about submitting their research proposals."

The PHAB Award eligibility, review and category criteria were modeled after the National Institutes of Health (NIH) system; entries were graded on significance, investigator(s), innovation, approach, and environment.

For more information on the PHAB Awards visit: https://www.phab-awards.com/awards/ or e-mail PHAB.awards@bayer.com.

Grants were made on the merits of the research, and research must be posted on ClinicalTrials.gov. Every effort should be made to publish or present study outcomes. If the research is not conducted the grant must be returned.

About Pulmonary Arterial Hypertension (PAH)
Pulmonary Arterial Hypertension (PAH, WHO Group 1) is defined by elevated pressure in the arteries going from the right side of the heart to the lungs. Typical symptoms of PAH include shortness of breath on exertion, fatigue, weakness, chest pain and syncope. PAH is caused by abnormalities in the walls of the pulmonary arteries.1,2

About Chronic Thromboembolic Pulmonary Hypertension (CTEPH)
Chronic Thromboembolic Pulmonary Hypertension (CTEPH, WHO Group 4) is a progressive type of pulmonary hypertension, in which it is believed that thromboembolic occlusion (organized blood clots) of pulmonary vessels gradually lead to an increased blood pressure in the pulmonary arteries, resulting in an overload of the right heart.3,4 CTEPH may evolve after prior episodes of acute pulmonary embolism, but the pathogenesis is not yet completely understood. The standard and potentially curative treatment for CTEPH is pulmonary thromboendarterectomy (PTE), a surgical procedure in which the blood vessels of the lungs are cleared of clot and scar material.5,6 However, a considerable number of patients with CTEPH (20%-40%) are not operable and in up to 35 percent of patients, the disease persists or reoccurs after PTE.7

About Bayer
Bayer is a global enterprise with core competencies in the life science fields of health care and nutrition. Its products and services are designed to benefit people by supporting efforts to overcome the major challenges presented by a growing and aging global population. At the same time, the Group aims to increase its earning power and create value through innovation and growth. Bayer is committed to the principles of sustainable development, and the Bayer brand stands for trust, reliability and quality throughout the world. In fiscal 2018, the Group employed around 117,000 people and had sales of 39.6 billion euros. Capital expenditures amounted to 2.6 billion euros, R&D expenses to 5.2 billion euros. For more information, go to www.bayer.us.

Our online press service is just a click away: www.bayer.us/en/newsroom 
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Media Contact:
David Patti, +1-973-452-6793
Bayer, U.S. Product Communications
david.patti@bayer.com

Forward-Looking Statements 
This release may contain forward-looking statements based on current assumptions and forecasts made by Bayer management. Various known and unknown risks, uncertainties and other factors could lead to material differences between the actual future results, financial situation, development or performance of the company and the estimates given here. These factors include those discussed in Bayer's public reports which are available on the Bayer website at www.bayer.com. The company assumes no liability whatsoever to update these forward-looking statements or to conform them to future events or developments.

References:
1 Galie et al. 2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Heart. 2016;37:67–119.
2American Lung Association. Pulmonary Hypertension. Accessed November 22, 2017. http://www.lung.org/lung-health-and-diseases/lung-disease-lookup/pulmonary-hypertension.
3 Piazza G and Goldhaber SZ. Chronic thromboembolic pulmonary hypertension. N Engl J Med. 2011; 364: 351-360.
4 Simonneau G et al. Updated Clinical Classification of Pulmonary Hypertension. Journal of the American College of Cardiology. 2013; 62(25):
5 D'Armini M. Diagnostic advances and opportunities in chronic thromboembolic pulmonary hypertension. Eur Respir Rev. 2015; 24: 253–262.
6 Kim et al. Chronic thromboembolic pulmonary hypertension. J Am Coll Cardiol. 2013; 62: D92-9.
7 Mathai et al. Quality of life in patients with chronic thromboembolic pulmonary hypertension. Eur Respir J. 2016 Aug; 48(2): 526–537.

SOURCE Bayer

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Beware Long-Term Effects Of Kyphoscoliosis - MedPage Today

Posted: 21 Oct 2019 08:31 AM PDT

A 61-year-old Caucasian female is admitted to the hospital in September 2018 with shortness of breath on exertion and increased fatigue during daily activities. Her symptoms, once mild, have been worsening for several years, she explains.

Medical History

The patient has severe congenital kyphoscoliosis of the thoracic spine (Figure). Attempted surgical correction when she was 10 years of age was not successful. She is New York Heart Association (NYHA) functional class IV, but has never smoked and has no history of prior drug abuse.

She explains that she first noticed becoming short of breath in mid-2015. In June 2016, to rule out a cardiac etiology, clinicians perform a transthoracic echocardiography (TTE). This identifies signs of right ventricular overload with an elevated right ventricular systolic pressure (RSVP) of 90 mm Hg.

image
Figure. Posteroanterior (PA) chest X-ray shows marked scoliosis of thoracic spine.

In July 2016, right heart catheterization confirms a diagnosis of pulmonary hypertension (PH). At that time, the patient begins long-term oxygen therapy (LTOT) concomitantly with off-label treatment with the endothelin receptor antagonist ambrisentan at 5 mg once daily (OD). She also receives supportive therapy with spironolactone 25 mg OD, torsemide 10 mg OD, and atorvastatin 20 mg OD.

At Admission

Assessments during her current admission reveal peripheral edema and mild acrocyanosis. Lung auscultation reveals bilaterally diminished breath sounds at the bases. She has mild tachycardia (92 beats per minute) and low blood pressure 100/60 mm Hg; otherwise, her vital signs are within normal range. The patient also has severe hypoxemia, with 75% peripheral oxygen saturation (SpO2).

Transthoracic echocardiography (TTE) at admission reveals:

  • Dilatation of right ventricle and left atrium
  • Tricuspid regurgitation grade I–II with tricuspid annular plane systolic excursion of 2.9 cm
  • Right ventricular systolic pressure (RVSP) of 65 mm Hg
  • Preserved ejection fraction of 65%

Chest computer tomography (CT) with intravenous contrast shows bilateral basal hypoventilation, focal atelectasis in right basal lobe, and prominent thoracic malformation. There is no evidence of pulmonary embolism. Test results for anti-nuclear antibody and extractable nuclear antigen panel are negative.

Several hours after being admitted to the hospital and receiving supplemental oxygen therapy by non-rebreathing face mask (12 L/minute), the patient's SpO2 declines to 64%.

Her blood count showed minor erythrocytosis (5.51 × 1012/L), with normal range white cell count, blood biochemistry (chem-8) findings, and serum brain natriuretic peptide (80.8 pg/mL).

Clinicians immediately discontinue treatment with ambrisentan, and initiate treatment with an inhaled prostanoid every 4 hours (iloprost 5 μg via nebulizer), complemented by supplemental oxygen via simple face mask (5 L/minute).

Pulmonary function tests reflect the CT evidence of a highly restrictive ventilation pattern with largely maintained diffusing capacity (DLCO 74% of predicted) and lung permeability (DLCO/VA 145% of predicted).

The Days Following

There is gradual improvement in the patient's condition in the days following her admission. Her SpO2 level increases to over 90% with a corresponding increase in functional capacity to NYHA class III.

By day 4 of hospitalization, the patient's 6-minute walk test (6MWT) result is 241 meters, a marked improvement from her day 2 results of 153 meters.

Because the patient is unable to afford inhaled prostanoids as a long-term therapy, she is switched back to ambrisentan.

Treatment and Outcome

On day 4, the patient is discharged in satisfactory condition, with recommendation to continue LTOT and to begin non-invasive positive pressure ventilation therapy.

Case Follow-up

A follow-up right heart catheterization performed in February 2019 revealed similar hemodynamic parameter values compared to the values obtained during the initial diagnosis in July 2016, with a slight improvement in pulmonary vascular resistance, from 6 to 5.62.

The patient remains in NYHA class III with moderate exertional dyspnea. On the repeated 6MWT, she covers 260 meters.

Discussion

Clinicians reporting their experience with a patient with kyphoscoliosis complicated by pulmonary hypertension (PH) note that their case provides insight into a long-term vasodilator therapy in this clinical context.

Given that kyphoscoliosis is encountered relatively rarely in clinical practice, and PH is often not diagnosed in a timely manner, in the absence of guidelines, they urge clinicians to direct their attention to identifying patients who might benefit from vasoactive agents in addition to ventilation/oxygenation therapy.

Respiratory complications are a common entity for restrictive chest wall diseases such as kyphoscoliosis. When such anatomical distortions are severe, patients have an increased risk of respiratory failure associated with poor clinical outcomes due to resulting malformation of the thoracic cavity.

Alveolar hypoventilation often develops due to a combination of reduced lung volume, increased thoracic muscle workload, and restriction in thoracic chest wall compliance and movements of diaphragm. As in two other alveolar hypoventilation disorders, obesity hypoventilation syndrome and obstructive sleep apnea, when hypoxia is aggravated, the resulting vasoconstrictive response increases pulmonary vascular resistance – ultimately resulting in development of pulmonary hypertension (PH).

Pulmonary hypertension is defined as an increase in mean pulmonary artery pressure ≥25 mm Hg, assessed by right heart catheterization (RHC) in the 2015 European Society of Cardiology (ESC) guidelines.

In patients with kyphoscoliosis, alveolar hypoventilation is one of the main contributors to the development of PH. This results in the condition being classified into the third of 5 groups: PH due to lung disease and/or hypoxia.

Although a single group, authors note that the pathogenic mechanism differs. PH develops either in the setting of lung disease or in a state of hypoxemia and alveolar hypoventilation with the absence of structural changes.

Therapeutic options are determined based on the condition underlying the pulmonary hypertension. Due to the relative rarity of kyphoscoliosis with concomitant PH, therapeutic regimens have remained largely unchanged, authors note.

Current treatment recommendations are limited to ventilatory support. The potential benefits of use of pulmonary arterial hypertension (PAH)-approved vasoactive medications remain largely unexplored.

Since kyphoscoliosis complicated by PH was first observed several decades ago, reports of novel therapeutic approaches remain scarce.

Analysis of 1,344 adults with PH enrolled in a recent registry found that none were affected by kyphoscoliosis. Similarly, a study of 362 children with confirmed PH noted only two with kyphoscoliosis.

As in other alveolar hypoventilative disorders, treatment focuses on improvement of oxygenation state and ventilator support. Long-term oxygen therapy (LTOT) remains central to slowing respiratory decline, although now it is rarely used on its own. Instead, combined treatment with LTOT and non-invasive ventilation has proven more effective against pulmonary vasoconstriction. While this approach is associated with improved long-term survival and exercise capacity, it remains unable to prevent the cardiopulmonary deterioration of the kyphoscoliosis patient.

There is little data on the use of vasoactive medication in patients with PH secondary to deformative thoracic diseases, case authors write. They cite two reports: in a case of PH secondary to Potts disease, in a short-term emergency setting, inhaled nitric oxide was reported to result in marked improvement of cardiopulmonary condition; and in a patient with severe kyphoscoliosis and many years of nocturnal noninvasive positive-pressure ventilation, who was just diagnosed with PH, initiation of phosphodiesterase-5 inhibitor and oxygen therapy produced clinical improvement.

Authors note the importance of addressing safety concerns when using a PAH-approved vasoactive drug in patients with PH with concomitant lung disease. Vasoactive drugs oppose hypoxic vasoconstriction in poorly ventilated lung areas, creating a ventilation-perfusion mismatch, subsequently impairing blood oxygenation. However, they add, these concerns might not be attributable to PH in kyphoscoliosis, as the analysis of lung parenchyma in these patients has shown no structural abnormalities with the exception of focal atelectasis. It can be expected that the deterioration of blood oxygenation is reduced to minimum in these cases.

In their case, authors note their initial decision to commence monotherapy with an endothelin receptor antagonist that is currently approved for treatment of pulmonary arterial hypertension (PAH), because of the extent of PH progression at the time of diagnosis.

However, clinicians note that the endothelin receptor antagonist could not be excluded as a cause for the declining state of the patient at the time of admission. As an alternative, they selected an inhaled prostanoid, based mainly on its mode of distribution. They explain that because this drug primarily accesses well-ventilated lung segments, the treatment does not interfere with hypoxic vasoconstriction and does not worsen oxygenation.

Ultimately, there was no evidence of concomitant lung disease on CT imaging or the pulmonary function test – leading case authors to conclude that ambrisentan is unlikely to have caused the patient's severe hypoxemia.

Subsequently, they deemed it safe to continue the oral vasodilator. Considering the progressive nature of PH in kyphoscoliosis, despite ventilatory and oxygen treatment, they propose that adding a vasoactive medication offers a safe means of combating cardiopulmonary decline, in a long-term setting as well as an acute setting.

Pulmonary hypertension in kyphoscoliosis is associated with a high mortality rate, which persists despite use of current management options.

To date, the use of PAH-approved drugs for kyphoscoliosis-related PH have been associated with positive outcomes and may limit progression of disease.

Given the relative rarity of kyphoscoliosis in clinical practice, and frequent delays in diagnosis of PH which inevitably seems to follow, these case authors urge clinician awareness in identifying patients – via individual evaluation – who might benefit from vasoactive agents in addition to ventilation/oxygenation therapy.

References

1. Tellermann J et al: Long-Term Response to Vasoactive Treatment in a Case of Kyphoscoliosis-Associated Pulmonary Hypertension. Am J Case Rep 2019; 20:1505-1508

2. Bergofsky EH, Turino GM, Fishman AP: Cardiorespiratory failure in kyphoscoliosis. Medicine (Baltimore), 1959; 38: 263–317

3. Turino GM, Goldring RM, Fishman AP: Cor pulmonale in musculoskeletal abnormalities of the thorax. Bull NY Acad Med, 1965; 41: 959–80

4. Krieger J, Sforza E, Apprill M et al: Pulmonary hypertension, hypoxemia, and hypercapnia in obstructive sleep apnea patients. Chest, 1989; 96(4):729–37

5. Galie N, Humbert M, Vachiery JL et al: 2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension: The Joint Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS): Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC), International Society for Heart and Lung Transplantation (ISHLT). Eur Heart J, 2016; 37: 67–119

6. Held M, Walthelm J, Baron S, Roth C, Jany B: Functional impact of pulmonary hypertension due to hypoventilation and changes under noninvasive ventilation. Eur Respir J, 2014; 43: 156–65

7. PajdziÅ„ski M, MÅ‚ynarczyk P, MiÅ‚kowska-Dymanowska J et al: Kyphoscoliosis - what can we do for respiration besides NIV? Adv Respir Med, 2017; 85(6):352–58

8. Hurdman J, Condliffe R, Elliot CA et al: ASPIRE registry: Assessing the spectrum of pulmonary hypertension identified at a referral centre. Eur Respir J, 2012; 39(4): 945–55

9. Berger RM, Beghetti M, Humpl T et al: Clinical features of paediatric pulmonary hypertension: A registry study. Lancet, 2012; 379(9815): 537–46

10. Smith IE, Laroche CM, Jamieson SA, Shneerson JM: Kyphosis secondary to tuberculosis osteomyelitis as a cause of ventilatory failure. Clinical features, mechanisms, and management. Chest, 1996; 110(4): 1105–10

11. Buyse B, Meersseman W, Demedts M: Treatment of chronic respiratory failure in kyphoscoliosis: oxygen or ventilation? Eur Respir J, 2003; 22(3):525–28

12. Okada S, Sugawara A, Yamagata S et al: Pulmonary hypertension and its response to treatment in a patient with kyphosis-related alveolar hypoventilation. Intern Med, 2017; 57(7): 1003–6

13. Hosokawa Y, Yamamoto T, Yabuno Y et al: Inhaled nitric oxide therapy for secondary pulmonary hypertension with hypertrophic obstructive cardiomyopathy and severe kyphoscoliosis. Int J Cardiol, 2012; 158: 20–21

14. Blanco I, Gimeno E, Munoz PA et al: Hemodynamic and gas exchange effects of sildenafil in patients with chronic obstructive pulmonary disease and pulmonary hypertension. Am J Respir Crit Care Med, 2010; 181(3):270–78

15. Wang L, Jin YZ, Zhao QH et al: Hemodynamic and gas exchange effects of inhaled iloprost in patients with COPD and pulmonary hypertension. Int J Chron Obstruct Pulmon Dis, 2017; 12: 3353–60

Authors had no disclosures.

2019-10-21T11:31:49-0400

Dogs With PH Live Longer After Adcirca Treatment, Study Finds - Pulmonary Hypertension News

Posted: 18 Oct 2019 05:30 AM PDT

Adcirca (tadalafil) helped to improve survival in dogs with pulmonary hypertension (PH), a new study suggests.

Knowing the underlying conditions associated with PH can lead to improved health outcomes in dogs, the study stated. The findings might also prove to be important in understanding the disease in humans.

The study, titled "Pulmonary hypertension secondary to respiratory disease and/or hypoxia in dogs: Clinical features, diagnostic testing and survival," was published in The Veterinary Journal.

Respiratory diseases and hypoxia (abnormally low levels of oxygen) can lead to PH in both dogs and humans. However, relatively little is known about how diseases of the lung affect pulmonary blood pressure in canines. And although this information could have important implications for the management of PH in veterinary medicine, it might also help in the understanding and/or treatment of human disease.

"Understanding the diseases that contribute to pulmonary hypertension can lead to more tailored therapy approaches and help identify which medications are likely to be most beneficial," Carol Reinero, PhD, professor at the College of Veterinary Medicine at the University of Missouri, and the study's co-author, said in a news release.

The researchers detail the cases of 47 dogs with PH and associated lung diseases, including conditions such as fibrosis (scarring) of the lungs, blockage of the airway, emphysema, and bronchiectasis (where inflammation in the lungs leads to a thickening of lung tissue that interferes with normal lung function).

"As many of these dogs have multiple issues, a thorough evaluation is needed to address the underlying problems causing the pulmonary hypertension," Reinero said.

Pulmonary blood pressure was estimated by performing an ultrasound of the heart — an echocardiogram.

Results showed that dogs with the highest pulmonary blood pressure (47 mmHg or greater) had significantly shorter survival times than those with lower pulmonary blood pressure.

The researchers also conducted statistical analyses to determine the factors most associated with longer survival times, and found the only factor to be whether or not the dog had been given tadalafil, an oral once-a-day pill.

Tadalafil is the active component of Adcirca, an approved PH therapy. The compound is also marketed under the brand name Cialis to treat erectile dysfunction and benign prostatic hypertrophy.

Similar to people with PH, "increased severity of PH is predictive of non-survival in dogs. Importantly, PDE5 inhibition [with Adcirca] provided a survival benefit," the researchers said.

Marisa holds an MS in Cellular and Molecular Pathology from the University of Pittsburgh, where she studied novel genetic drivers of ovarian cancer. She specializes in cancer biology, immunology, and genetics. Marisa began working with BioNews in 2018, and has written about science and health for SelfHacked and the Genetics Society of America. She also writes/composes musicals and coaches the University of Pittsburgh fencing club.
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PatrĂ­cia holds her PhD in Medical Microbiology and Infectious Diseases from the Leiden University Medical Center in Leiden, The Netherlands. She has studied Applied Biology at Universidade do Minho and was a postdoctoral research fellow at Instituto de Medicina Molecular in Lisbon, Portugal. Her work has been focused on molecular genetic traits of infectious agents such as viruses and parasites.
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Marisa holds an MS in Cellular and Molecular Pathology from the University of Pittsburgh, where she studied novel genetic drivers of ovarian cancer. She specializes in cancer biology, immunology, and genetics. Marisa began working with BioNews in 2018, and has written about science and health for SelfHacked and the Genetics Society of America. She also writes/composes musicals and coaches the University of Pittsburgh fencing club.
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