About

Dr. Lea Baer is a Clinical Assistant Professor specializing in Hematology Oncology at Stony Brook Medicine. She completed her medical education at The Hebrew University Hadassah Medical School in 1999, followed by an internship at Bikur Holim Hospital in 1996. Her postgraduate training includes a residency in Internal Medicine at Stony Brook University Medical Center in 2011, a fellowship in IM-Hematology/Oncology at Columbia University Medical Center in 2014, and a residency in IM-Oncology at The Hebrew University Hadassah Medical School in 2006. Her professional focus encompasses the diagnosis and treatment of hematological malignancies and solid tumors, with a particular interest in cancer therapy-related cardiac dysfunction and heart failure. Dr. Baer has contributed to research on prevention, treatment, and guidelines for cardiac complications associated with cancer therapies. She is actively involved in clinical practice at Stony Brook's Cancer Center and other affiliated hospitals, providing care to patients with complex oncological conditions.

Research topics

• Internal medicine
• Medicine
• Oncology
• Cell biology
• Biology
• Nuclear medicine
• Surgery
• Pathology
• Bioinformatics
• Cancer research
• Biochemistry
• Endocrinology
• Chemistry
• Radiology
• Physical therapy

Selected publications

• Abstract P4-01-22: Serum Thymidine Kinase as a Biomarker for Response Beyond Progression in First-line CDK 4/6 Inhibitors: Insights from the Randomized Phase II MAINTAIN Trial

  Clinical Cancer Research · 2025-06-13

  article

  Abstract Background: There are multiple therapeutic strategies for patients (pts) with hormone receptor positive (HR+), HER2 negative (HER2-) metastatic breast cancer (MBC) following progression on a first-line cyclin-dependent kinase 4/6 inhibitor (CDK4/6i) and endocrine therapy (ET). There is an unmet need for predictive and prognostic biomarkers to identify HR+, HER2- MBC pts likely to benefit from continued CDK4/6i therapy beyond progression. Thymidine kinase (TK), an enzyme involved in DNA synthesis, represents a promising biomarker due to the association of elevated serum TK activity (sTKa) with greater tumor cell division and poorer clinical outcomes. We investigated sTKa as a potential biomarker of response to continued CDK4/6i therapy beyond progression in the MAINTAIN trial. Methods: MAINTAIN was the first randomized controlled trial to demonstrate a significant progression-free survival (PFS) benefit for HR+, HER2- MBC patients who switched ET (fulvestrant or exemestane) and received the CDK4/6i ribociclib compared to ET plus placebo after progressing on prior CDK4/6i and ET. We evaluated the association between sTKa and PFS. In this exploratory analysis, sTKa levels were analyzed from blood samples collected at baseline and cycle 2 day 1 (C2D1) by Biovica using the Divitum® TKa assay. Patients were categorized into low (<250 Divitum® unit of Activity [DuA]) and high (≥250 DuA) sTKa groups for PFS analysis. The cut-off point of 250 DuA is a clinically validated and FDA 510(k) cleared reference value for prognosis in HR+ MBC. Log-rank test and Cox regression models were used to assess the association between sTKa levels and PFS as well as calculate hazard ratios (HR) and 95% confidence intervals (CI). The database was locked on Jan 4, 2022. Results: Of the 119 MAINTAIN participants, 90 had samples available for analysis. Forty (44%) in the placebo+ET group and 50 (56%) in the ribociclib+ET group. Eighty-one pts had baseline sTKa, 73 had C2D1 sTKa, and 69 had sTKa at both timepoints. Fifty-three percent (43/81) of pts had high baseline TKa and 37% (27/73) of pts had high C2D1 TKa. Pts with low baseline sTKa exhibited a non-significant trend towards improved PFS compared to those with high baseline sTKa (median PFS [mPFS] 5.6 vs 3.0 mo; HR 0.73, 95% CI 0.45-1.18, p=0.198). In contrast, pts with low C2D1 sTKa demonstrated a statistically significant PFS benefit compared to those with high C2D1 sTKa (mPFS 5.7 vs 2.7 mo; HR 0.30, 95% CI 0.17-0.52, p<0.001). Notably, the mPFS in the ribociclib+ET group was 10.9 mo for pts with low C2D1 sTKa compared to 2.7 mo for those with high C2D1 sTKa (HR 0.15, 95% CI 0.06-0.37, p<0.001). The placebo+ET group did not show a statistically significant PFS benefit for those with low C2D1 sTKa versus high C2D1 sTKa (mPFS 4.8 vs 2.5 mo; HR 0.51, 95% CI 0.23-1.13, p=0.098). Among 69 pts evaluated for sTKa dynamics, the longest PFS was seen in 13 pts (19%) who transitioned from high baseline to low C2D1 sTKa (mPFS 8.2 mo; 95% CI 5.6-16.6). Twenty-one (30%) pts who maintained high sTka levels from baseline to C2D1 had the shortest PFS (mPFS 2.7 mo; 95% CI 2.1-3.0). Conclusions: In the phase II MAINTAIN trial, sTKa was a predictive biomarker for response to switching ET + continuing CDK4/6i in HR+, HER2- MBC pts following progression on CDK4/6i and ET. Low (<250 DuA) C2D1 sTKa levels predicted a positive treatment response, especially among those receiving ribociclib+ET. sTKa dynamics from baseline to C2D1 were prognostic, providing insights into PFS outcomes. Our analysis supports C2D1 as a critical timepoint for sTKa in assessing continued benefit of CDK4/6i and risk of progression. Further research in a larger trial evaluating sTKa dynamics and clinical outcomes is warranted. Citation Format: Ruth Sacks, Codruta Chiuzan, Melissa K. Accordino, Elizabeth Sakach, Amy Williams, Prabhjot S. Mundi, Claire Sathe, Meghna S. Trivedi, Naomi Sender, Yelena Novik, Amy Tiersten, George Raptis, Lea N. Baer, Sun Y. Oh, Amelia B. Zelnak, Kari B. Wisinski, Eleni Andreopoulou, Williams J. Gradishar, Erica Stringer-Reasor, Sonya A. Reid, Anne O'Dea, Ruth O'Regan, Katherine D. Crew, Dawn L. Hershman, Kevin Kalinsky. Serum Thymidine Kinase as a Biomarker for Response Beyond Progression in First-line CDK 4/6 Inhibitors: Insights from the Randomized Phase II MAINTAIN Trial [abstract]. In: Proceedings of the San Antonio Breast Cancer Symposium 2024; 2024 Dec 10-13; San Antonio, TX. Philadelphia (PA): AACR; Clin Cancer Res 2025;31(12 Suppl):Abstract nr P4-01-22.

  PublisherDOI

• Metastatic breast cancer through the Oncotype DX Breast Recurrence Score®: insights from a small cohort study

  Breast Cancer Research and Treatment · 2025-05-28

  article
  PublisherDOI

• Utility of Stereotactic Body Radiation Therapy in Establishing Local Control for Patients With Invasive Breast Cancer Not Undergoing Definitive Surgery

  International Journal of Radiation Oncology*Biology*Physics · 2023 · 10 citations

  • Medicine
  • Surgery
  • Nuclear medicine
  PublisherDOI

• Randomized Phase II Trial of Endocrine Therapy With or Without Ribociclib After Progression on Cyclin-Dependent Kinase 4/6 Inhibition in Hormone Receptor–Positive, Human Epidermal Growth Factor Receptor 2–Negative Metastatic Breast Cancer: MAINTAIN Trial

  Journal of Clinical Oncology · 2023 · 187 citations

  • Medicine
  • Internal medicine
  • Cancer research

  PURPOSE: Cyclin-dependent kinase 4/6 inhibitor (CDK4/6i) with endocrine therapy (ET) improves progression-free survival (PFS) and overall survival (OS) in hormone receptor-positive (HR+), human epidermal growth factor receptor 2-negative (HER2-) metastatic breast cancer (MBC). Although preclinical and clinical data demonstrate a benefit in changing ET and continuing a CDK4/6i at progression, no randomized prospective trials have evaluated this approach. METHODS: In this investigator-initiated, phase II, double-blind placebo-controlled trial in patients with HR+/HER2- MBC whose cancer progressed during ET and CDK4/6i, participants switched ET (fulvestrant or exemestane) from ET used pre-random assignment and randomly assigned 1:1 to the CDK4/6i ribociclib versus placebo. PFS was the primary end point, defined as time from random assignment to disease progression or death. Assuming a median PFS of 3.8 months with placebo, we had 80% power to detect a hazard ratio (HR) of 0.58 (corresponding to a median PFS of at least 6.5 months with ribociclib) with 120 patients randomly assigned using a one-sided log-rank test and significance level set at 2.5%. RESULTS: = .006. At 6 and 12 months, the PFS rate was 41.2% and 24.6% with ribociclib, respectively, compared with 23.9% and 7.4% with placebo. CONCLUSION: In this randomized trial, there was a significant PFS benefit for patients with HR+/HER2- MBC who switched ET and received ribociclib compared with placebo after previous CDK4/6i and different ET.

  PublisherDOI

• Biomarkers and Strain Echocardiography for the Detection of Subclinical Cardiotoxicity in Breast Cancer Patients Receiving Anthracyclines

  Journal of Personalized Medicine · 2023-12-14 · 15 citations

  articleOpen access

  The optimal surveillance and management strategies for breast cancer patients receiving anthracycline therapy are limited by our incomplete understanding of the role of biomarkers heralding the onset of cardiotoxicity. The purpose of this study was to determine whether there is a temporal correlation between cardiac biomarkers and subclinical left ventricular dysfunction in breast cancer patients receiving anthracycline chemotherapy. Thirty-one females between 46 and 55 years old with breast cancer treated with anthracycline chemotherapy were prospectively enrolled. Cardiac biomarkers were correlated with echocardiography with speckle tracking at baseline, post-anthracycline therapy, and 6 months post-anthracycline chemotherapy. Subclinical cardiotoxicity was defined as ≥ 10% reduction in global longitudinal strain (GLS). There was a relative reduction in left ventricular ejection fraction (LVEF) ≥ 10% in 5/30 (17%) and 7/27 (26%) patients post-anthracycline therapy and 6 months post-anthracycline therapy, respectively. Subclinical cardiotoxicity was noted in 8/30 (27%) and 10/26 (38%) patients post-anthracycline and 6 months post-anthracycline therapy, respectively. Baseline N-terminal pro B-type natriuretic peptide (NT-proBNP) was the strongest predictor of LVEF (ρ = −0.45; p = 0.019), with post-therapy NT-proBNP values illustrating similar predictive value (ρ = −0.40; p = 0.038). Interim changes in suppression of tumorigenicity 2 (ST2) and galectin-3 correlated with a 6-month change in LVEF (ρ = −0.48; p = 0.012 and ρ = −0.45; p = 0.018, for ST2 and galectin-3, respectively). Changes in galectin-3 from baseline to mid-therapy paralleled changes in GLS. NT-proBNP, ST2, and galectin-3 correlate with reduced LVEF among breast cancer patients receiving anthracycline therapy. Additional trials focusing on a cardiac biomarker approach may provide guidance in the early diagnosis and management of anthracycline-induced cardiotoxicity.

  PublisherOA PDFDOI

• Blood plasma derived extracellular vesicles (BEVs): particle purification liquid chromatography (PPLC) and proteomic analysis reveals BEVs as a potential minimally invasive tool for predicting response to breast cancer treatment

  Breast Cancer Research and Treatment · 2022 · 17 citations

  • Chemistry
  • Medicine
  • Oncology
  PublisherOA PDFDOI

• Sulindac Improves Stiffness and Quality of Life in Women Taking Aromatase Inhibitors for Breast Cancer

  Breast Cancer Research and Treatment · 2022 · 6 citations

  • Medicine
  • Physical therapy
  • Internal medicine
  PublisherOA PDFDOI

• A randomized, phase II trial of fulvestrant or exemestane with or without ribociclib after progression on anti-estrogen therapy plus cyclin-dependent kinase 4/6 inhibition (CDK 4/6i) in patients (pts) with unresectable or hormone receptor–positive (HR+), HER2-negative metastatic breast cancer (MBC): MAINTAIN trial.

  Journal of Clinical Oncology · 2022 · 73 citations

  • Medicine
  • Internal medicine
  • Oncology

  LBA1004 Background: CDK 4/6i has demonstrated benefit in progression free survival (PFS) and overall survival (OS) in pts with HR+, HER2- MBC when combined with endocrine therapy (ET). While observational data demonstrate a potential benefit of continuing CDK 4/6i and switching ET at progression, no prospective trials have evaluated this approach. We conducted a phase II, multi-center, randomized, trial to evaluate the efficacy of fulvestrant or exemestane +/- ribociclib in pts with HR+HER2- MBC whose cancer previously progressed on any CDK 4/6i + any ET. Methods: In this investigator-initiated, phase II, double-blind, placebo-controlled trial, men or women with measurable or non-measurable HR+/HER2- MBC whose cancer progressed during CDK 4/6i and ET were randomized 1:1 to fulvestrant or exemestane +/- ribociclib. Pts treated with prior fulvestrant received exemestane as ET in the randomization; if prior exemestane fulvestrant was the ET; if neither, fulvestrant or exemestane was per investigator discretion, though fulvestrant was encouraged. PFS was the primary endpoint, defined as time from randomization to progression of disease or death. A one-sided log-rank test with a sample size of 120 randomized and evaluable pts with a significance level alpha of 2.5%, achieves 80% power to detect an effect size (difference in PFS) of 3 months. Results: Of the 120 randomized evaluable pts, 1 pt was removed due to not taking ET along with ribociclib/placebo. All but 1 pt was female, the median age was 57.0 years, 88 pts (74%) were white, and 21 (17.6%) were Hispanic. For ET, 99 pts received fulvestrant (83%) and 20 pts exemestane (17%). In terms of prior CDK 4/6i, 100 pts previously received palbociclib (84%), 13 pribociclib (11%), 2 abemaciclib (2%), and 4 palbociclib and another CDK 4/6i (3%). There was a statistically significant PFS improvement for pts randomized to fulvestrant or exemestane + ribociclib [median: 5.33 months, 95% CI (Confidence Interval): 3.25–8.12 months] vs. placebo (median: 2.76 months, 95% CI: 2.66–3.25 months): Hazard Ratio (HR) = 0.56 (95% CI: 0.37-0.83), p = 0.004. Similar results were seen in the subset of pts treated with fulvestrant, with a median PFS for those randomized to ribociclib (5.29 months) vs. placebo (2.76 months), HR = 0.59 (95% CI: 0.38-0.91), p = 0.02. At 6 months, 42% were progression-free on the ribociclib arm vs. 24% on placebo. At 12 months, 25% were progression-free on the ribociclib arm vs. 7% on placebo. Additional endpoints will be reported, including overall response rate and safety. Conclusions: In this randomized, placebo-controlled trial, there was a significant PFS benefit for pts with HR+/HER2- MBC to switch ET and receive ribociclib after progression on CDK 4/6i. Clinical trial information: NCT02632045.

  PublisherDOI

• Abstract PS5-37: The feasibility of obtaining oncotype DX breast recurrence score® results from metastatic sites of patients with hormone receptor positive metastatic breast cancer

  Cancer Research · 2021-02-15

  article

  Abstract Background: Identifying when to start CDK4/6 inhibitors or use chemotherapy in hormone receptor positive (HR+) metastatic breast cancer (MBC) remains challenging. The 21-gene Oncotype DX Breast Recurrence Score® test is validated to predict chemotherapy benefit in early stage HR+ breast cancer but has not been studied for use in the MBC setting.Objective: To assess the feasibility of obtaining Recurrence Scores from metastatic sites after standard of care biopsy in HR+, HER2 negative patients and correlate Recurrence Score results from matched primary breast cancer when available. Methods: A total of 48 metastatic biopsies were retrieved retrospectively from the residual tissue of patients with primary HR+, HER2 negative breast cancer. This included 36 from bone and 12 from other sites [liver (7), lung (1), rectum (1), brain (1), skin (2)]. Slides were sent to Genomic Health Inc. for RNA isolation and Recurrence Score result determination using standardized protocols. Recurrence Score results were available for 18 matched primary and metastatic biopsy samples. The percent success rate for Recurrence Score result was determined for the various metastatic sites and results compared between matched primary and metastatic site. Results: Recurrence Score results were obtained in 48% of metastatic biopsies (23 of 48 samples) including bone (17), liver (4), lung (1), and skin (1). Reasons for Recurrence Score failure included insufficient RNA (17), poor quality RNA (1), failed QC (4), and other (3). The mean Recurrence Score from the 23 metastatic sites was 35 (range: 1–66). Notably, 70% (16/23) of successful metastatic biopsies yielded Recurrence Scores in the high-risk range (>25). None of the 23 metastatic biopsies gained HER2 by RT-PCR. Among the 18 paired samples, higher recurrence score results were observed in all but three of the metastatic biopsy samples with mean Recurrence Score results of 20 (range 7 to 41) for the primary and 35 (range 1-66) for the metastatic site. For paired samples, 72% of metastatic biopsies yielded Recurrence Scores >25 compared to 17% of primary sample. Primary Recurrence Scores were not predictive of metastatic scores (r2=0.052). Estrogen receptor (ER) expression status was conserved in 87% whereas progesterone receptor (PR) was lost in 69% of the metastatic lesion. Among the pairs, 5 had de novo metastatic disease. In these, the Recurrence Score was higher in the metastatic biopsy in each case compared to the matched primary (mean 36 versus 23, respectively). Among de novo cases, there was 100% concordance in ER positive and HER2 negative expression and only 60% concordance in PR expression between primary and metastatic sites. Conclusion: Using standard of care metastatic biopsy samples, a Recurrence Score result was successfully generated in 48% of samples including bone. This small series demonstrates wide variability in Recurrence Score results in metastatic disease with overall higher scores, common loss of PR, and minimal correlation to matched primary disease. Further examination of the potential significance of the Recurrence Score for treatment decisions in the metastatic setting requires additional tissue sampling during biopsy as insufficient RNA was the primary reason for failure. Citation Format: Julie Anne L Gemmill, Patricia Thompson, Rebecca Batiste, Caterina Vacchi-Suzzi, Christina Preece, Jules Cohen, Lea Baer, Carolyn Mies, Michelle Turner, Christy A Russell, Alison Stopeck. The feasibility of obtaining oncotype DX breast recurrence score® results from metastatic sites of patients with hormone receptor positive metastatic breast cancer [abstract]. In: Proceedings of the 2020 San Antonio Breast Cancer Virtual Symposium; 2020 Dec 8-11; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2021;81(4 Suppl):Abstract nr PS5-37.

  PublisherDOI

• Managing dermatologic changes of targeted cancer therapy.

  PubMed · 2020-04-29 · 1 citations

  articleSenior author

  Failure to control these dermatologic changes can lead to lower dosages of cancer agents or an interrupted course of Tx. These steps can help you to head off trouble.

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Frequent coauthors

• Javed Butler

  Baylor Medical Center at Garland

  147 shared

• Hal A. Skopicki

  146 shared

• Michelle Bloom

  New York University

  146 shared

• Alexander R. Lyon

  145 shared

• Bonnie Ky

  145 shared

• Daniela Cardinale

  European Institute of Oncology

  145 shared

• Anju Nohria

  Dana-Farber Brigham Cancer Center

  145 shared

• Carine E. Hamo

  New York University

  145 shared

Education

• M.D., Hematology and Oncology

  Stony Brook University School of Medicine

  2005

• B.S., Biology

  University of California, San Diego

  2001