About

Mili Arora, M.D. is an Associate Professor in the Department of Internal Medicine at UC Davis Health. She specializes in hematology and oncology, with clinical interests in breast cancer, endocrine cancers, and triple negative breast cancer. Dr. Arora's research focuses on improving treatments for breast cancer and developing better supportive therapies to be used adjunctively with standard treatments. She believes in high-quality, innovative, and compassionate patient care, utilizing a team-based approach that includes nurses, pharmacists, social workers, and consultants. Her clinical practice is based at the UC Davis Comprehensive Cancer Center Hematology/Oncology Clinic in Sacramento, California.

Research topics

• Oncology
• Medicine
• Internal medicine
• Surgery
• Gastroenterology
• Biology

Selected publications

• Abstract RF5-06: Pathologic complete response rates (pCR) after the novel HER2 ADC ARX788: Results from the I-SPY2.2 trial

  Clinical Cancer Research · 2026-02-17

  article

  Abstract Background I-SPY2.2 is a multicenter phase 2 platform sequential multiple assignment randomized trial (SMART) in the neoadjuvant breast cancer (BC) setting, evaluating novel regimens in Block A, followed by standard therapies in Blocks B/C if indicated. Therapy in Block B is guided by tumor Response Predictive Subtype (RPS; Wolf, Cancer Cell 2022), which integrates immune, DNA repair, and luminal gene expression signatures with HR and HER2 status, classifying BC into 6 subtypes. ARX788 is an anti-HER2 Antibody Drug Conjugate (ADC) with site-specific conjugation of the noncleavable tubulin polymerization inhibitor Amberstatin (AS269). Patients (pts) with RPS S5 (HER2+/non-Luminal) and S6 (HER2+/Luminal) were eligible for assignment to ARX788 Q3W x 4 cycles in Block A. The primary endpoint was pCR following investigational Block A or after the entire therapy sequence. Methods Pts underwent serial MRI scans during therapy. Projected responders after Block A or B could proceed to surgery early, while others continued to Blocks B/C, which included TCHPx6 or THP±AC. Efficacy of ARX788 followed by surgery was evaluated using a Bayesian covariate-adjusted model estimating pCR and compared to fixed subtype-specific thresholds. To estimate pCR rate in the context of a multi-decision treatment regimen (Blocks A/B/C), we estimated pCR using a Bayesian model that considers timing of pCR and compares rates to a subtype-specific Dynamic Control (DC) modeled from I-SPY data (N=1,818). Results From Sep 2022 to Dec 2024, 100 pts were randomized to ARX788. In sequence with chemotherapy, 63/100 pts achieved pCR, and 82/100 had RCB 0/1, all without AC. Notably, 40 pts proceeded to surgery after Block A alone; of these, 33 (82%) had RCB 0/1, avoiding prolonged conventional chemotherapy. The RPS S6 (HER2+/Luminal) subgroup had a pCR rate of 39%, compared to a 17% DC rate, exceeding the predefined probability threshold of superior pCR rate to DC. Receptor status alone did not correlate with efficacy, emphasizing the importance of molecular subtyping in treatment selection. There were no RCB-3 cases. Ocular toxicity was reported in 95% of patients (9% grade 3), and pneumonitis in 6% (2% grade 3), with no treatment related deaths. 8 pts did not complete all planned ARX788 due to adverse events. The results for ARX788 as a stand-alone therapy or sequential strategy are summarized in the Table. Conclusions The sequential combination of ARX788 with chemo/anti-HER2 therapy demonstrated high efficacy, particularly in the HER2+/Luminal subtype compared to DC, suggesting that a significant proportion of pts could avoid prolonged chemotherapy. Ongoing studies are underway to define and implement strategies to prevent treatment associated ocular toxicity. I-SPY2.2 validates the use of personalized neoadjuvant therapy guided by molecular diagnostics and response-adaptive strategies tailored to each individual patient. NCT01042379 Citation Format: P. R. Pohlmann, H. S. Rugo, C. Yau, D. Yee, A. J. Chien, N. O. Williams, A. M. Wallace, J. C. Boughey, C. Vaklavas, M. Arora, V. Borges, A. S. Clark, C. Omene, C. Isaacs, E. Stringer-Reasor, R. Nanda, C. Falkson, K. S. Albain, N. Chan, E. T. Roussos Torres, M. Rozenblit, J. Tseng, S. Bommakanti, C. Nangia, L. Brown-Swigart, G. L. Hirst, N. Pasricha, C. H. Kretzer, J. Perlmutter, A. Borowsky, W. F. Symmans, L. van ‘t Veer, N. Hylton, L. J. Esserman. Pathologic complete response rates (pCR) after the novel HER2 ADC ARX788: Results from the I-SPY2.2 trial [abstract]. In: Proceedings of the San Antonio Breast Cancer Symposium 2025; 2025 Dec 9-12; San Antonio, TX. Philadelphia (PA): AACR; Clin Cancer Res 2026;32(4 Suppl):Abstract nr RF5-06.

  PublisherDOI

• Breaking Barriers to Survivorship Clinic: Insights from Breast Cancer Providers

  International Journal of Cancer Care and Delivery · 2026-01-26

  articleSenior author
  PublisherDOI

• Adaptive cohort design and LAT1 expression scale: study protocol for a Phase 2a trial of QBS72S in breast cancer brain metastases

  BMC Cancer · 2025-08-15 · 1 citations

  articleOpen access

  BACKGROUND: Breast cancer is the most common cause of cancer death among women and frequently metastasizes to the brain. Up to 30% of patients with breast-to-brain metastases will develop leptomeningeal disease (LMD), with poor survival, rapid neurologic decline, and no durable treatment options. The novel agent QBS72S, also known as QBS10072S, is designed to leverage the high expression of L-type amino acid transporter 1 (LAT1) on breast cancer cells and the blood-brain barrier. By conjugating an amino acid analogue with a DNA alkylating moiety, QBS72S can exploit LAT1 for specific delivery into the brain and metastatic tumor cells. METHODS: We designed a single-arm, Phase 2a study to test the preliminary efficacy and safety of QBS72S for breast-to-brain metastasis in two distinct cohorts: intraparenchymal metastasis (Cohort 1; no LMD), and LMD (Cohort 2; with or without intraparenchymal metastasis). The primary endpoint is overall response rate across evaluable participants in Cohort 1. Secondary endpoints include progression-free survival, overall survival, duration of response, and treatment-related adverse events in Cohort 1. Exploratory endpoints include correlation of LAT1 expression in formalin-fixed paraffin-embedded samples with treatment response, CSF pharmacokinetics, perfusion MRI, and novel CSF-based biomarkers. DISCUSSION: Adaptive clinical trial design enables rapid enrollment and tailored endpoints for patient cohorts with baseline disparate outcomes. Our LAT1 staining protocol will allow ongoing trials in glioblastoma (NCT02977780) and future studies in brain metastases to correlate LAT1 expression to drug efficacy. Our exploratory endpoints may facilitate identification of more rapid and reliable biomarkers of LMD treatment response and resistance. TRIAL REGISTRATION: ClinicalTrials.gov NCT05305365.

  PublisherOA PDFDOI

• LBA16 Rates of pathologic complete response (pCR) after datopotamab deruxtecan (Dato) in the neoadjuvant setting: Results from the I-SPY 2.2 trial

  Annals of Oncology · 2024-09-01

  articleOpen access
  PublisherOA PDFDOI

• Breast Cancer Bone Metastases

  2024-01-01

  book-chapter1st authorCorresponding
  PublisherDOI

• Datopotamab–deruxtecan plus durvalumab in early-stage breast cancer: the sequential multiple assignment randomized I-SPY2.2 phase 2 trial

  Nature Medicine · 2024 · 38 citations

  • Medicine
  • Oncology
  • Internal medicine
  PublisherOA PDFDOI

• Rates of pathologic complete response (pCR)after neoadjuvant datopotamab deruxtecan (Dato): Results from the I-SPY2.2 trial.

  Journal of Clinical Oncology · 2024-06-05 · 5 citations

  article

  LBA509 Background: I-SPY2.2 is a multicenter phase 2 platform sequential multiple assignment randomized trial (SMART) evaluating novel experimental regimens in the neoadjuvant breast cancer setting. The novel therapy is given as first in a sequence (Block A), followed by standard chemo/targeted therapies (Block B/C) if indicated. The goal is to identify agents that lead to pCR after novel targeted agents alone, or in sequence with optimal therapy assigned based on the tumor response predictive subtype (RPS). RPS incorporates expression-based immune, DNA repair deficiency (DRD), and luminal signatures with hormone receptor (HR) and HER2 status to classify patients by subtype: S1: HR+HER2-Immune-DRD-; S2: HR-HER2-Immune-DRD-; S3: HER2-Immune+; S4: HER2-Immune-DRD+; S5: HER2+/non-Luminal; S6: HER2+/Luminal. Methods: RPS S1, S2, S3 and S4 were eligible for assignment to Dato in Block A. Patients (pts) were followed by MRI during treatment (at 3, 6 and 12 weeks after start of Blocks A and B). Predicted responders by MRI and biopsy at the end of Block A or B have the option of going to surgery early, otherwise they proceed to next treatment Block (B +/- C). Randomization to Block B includes a taxane-based regimen specific to the RPS, and options include S1: paclitaxel; S2 and S3: paclitaxel + carboplatin + pembrolizumab; S4: paclitaxel + carboplatin vs. paclitaxel + carboplatin + pembrolizumab. Patients who did not go to surgery after Block B proceeded to Block C (AC or AC + Pembrolizumab if HR-HER2-). The primary endpoint is pCR. Efficacy is evaluated within each RPS and HR+HER2- and HR-HER2- signatures. To estimate the arm's efficacy as a stand-alone therapy, we use a Bayesian covariate-adjusted model to estimate the pCR rate and compare the posterior distribution to a subtype-specific fixed threshold. This model uses pCR data when available and MRI data when pCR is not. To estimate pCR rate in the context of a multi-decision treatment regimen, we use a Bayesian model based on if and when a pCR occurred in the trial. The posterior is compared to a subtype-specific dynamic control generated from historical I-SPY data. Results: 103 pts were randomly assigned to the Dato arm between August 2022 and August 2023. All patients have proceeded beyond Block A; 33 went to surgery after Dato alone. The efficacy results for Dato as a stand-alone therapy are summarized in Table. Conclusions: Dato monotherapy was active, particularly in the HR-HER2- signature, but did not meet the pre-specified threshold for graduation in I-SPY 2.2. Clinical trial information: NCT01042379 . [Table: see text]

  PublisherDOI

• Abstract GS5-03: Evaluation of anti-PD-1 Cemiplimab plus anti-LAG-3 REGN3767 in early-stage, high-risk HER2-negative breast cancer: Results from the neoadjuvant I-SPY 2 TRIAL

  Cancer Research · 2023-03-01 · 16 citations

  article

  Abstract Background: I-SPY2 is a multicenter, phase 2 trial using response-adaptive randomization within biomarker subtypes defined by hormone-receptor (HR), HER2, and MammaPrint (MP) status to evaluate novel agents as neoadjuvant therapy for high-risk breast cancer. The primary endpoint is pathologic complete response (pCR). Cemiplimab is an anti-PD-1 inhibitor approved for the treatment of NSCLC and cutaneous basal and squamous cell CA. Lymphocyte activation gene 3 (LAG-3) binds MHC class II leading to inhibition of T-cell proliferation and activation and is often co-expressed with PD-1. REGN3767 is a fully humanized mAb that binds to LAG-3 and blocks inhibitory T-cell signaling. Concurrent blockade of LAG-3 with an anti-PD-1 may enhance efficacy of an anti-PD-1. Methods: Women with tumors ≥ 2.5cm were eligible for screening. Only HER2 negative (HER2-) patients were eligible for this treatment; HR positive (HR+) patients had to be MP high risk. Treatment included Paclitaxel 80 mg/m2 IV weekly x 12 and Cemiplimab 350 mg and REGN3767 1600 mg both given q3weeks x 4, followed by doxorubicin/cyclophosphamide (AC) every 2 weeks x 4. The control arm was weekly paclitaxel x 12 followed by AC every 2-3 weeks x 4. Cemiplimab/REGN3767 was eligible to graduate in 3 of 10 pre-defined signatures: HER2-, HR-HER2-, and HR+HER2-. The statistical methods for evaluating I-SPY 2 agents has been previously described. To adapt to changing standard of care, we constructed “dynamic controls” comprising ‘best’ alternative therapies using I-SPY 2 and external data and estimated the probability of Cemiplimab/REGN3767 being superior to the dynamic control. Response predictive subtypes (Immune+ vs Immune-) were assessed using pre-treatment gene expression data and the ImPrint signature. Results: 73 HER2- patients (40 HR+ and 33 HR-) received Cemiplimab/REGN3767 treatment. The control group included [357 patients with HER2- tumors (201 HR+ and 156 HR-) enrolled since March 2010. Cemiplimab/REGN3767 graduated in both HR-/HER2- and HR+/HER2- groups; estimated pCR rates (as of June 2022) are summarized in the table. Safety events of note for Cemiplimab/REGN3767 include hypothyroidism 30.8%, adrenal insufficiency (AI) 19.2%, hyperthyroidism 14.1%, pneumonitis 1.3%, and hepatitis 3.8%. All were G1/2 except for 6 (7.7%) G3 AI and 3 (3.8%) G3 colitis. Rash occurred in 62.8%, 9% G3 and 2 pts (2.6%) had pulmonary embolism. X% of adrenal insufficiency cases required replacement therapy. 40 patients (11 HR+ and 29 HR-) in Cemiplimab/REGN3767 were predicted Immune+; 32 (29 HR+ and 3 HR-) were predicted Immune-. In the HR+ group pCR was achieved in 10/11 (91%) patients with Immune+ subtype compared with 8/29 (28%) with Immune- subtype. Additional biomarker analyses are ongoing and will be presented at the meeting. Conclusion: The I-SPY 2 study aims to assess the probability that investigational regimens will be successful in a phase 3 neoadjuvant trial. Dual immune blockade with a LAG-3 inhibitor and anti-PD1 therapy resulted in a high predicted pCR rate both in HR-/HER2- (60%) and HR+/HER2- (37%) disease. The novel Imprint signature identified a group of HR+ patients most likely to benefit from this active regimen. Table 1: Estimated pCR rates Citation Format: Claudine Isaacs, Rita Nanda, Jo Chien, Meghna S. Trivedi, Erica Stringer-Reasor, Christos Vaklavas, Judy C. Boughey, Amy Sanford, Anne Wallace, Amy S. Clark, Alexandra Thomas, Kathy S. Albain, Laura C. Kennedy, Tara B. Sanft, Kevin Kalinsky, Hyo S. Han, Nicole Williams, Mili Arora, Anthony Elias, Carla Falkson, Smita Asare, Ruixiao Lu, Maria Pitsouni, Amy Wilson, Jane Perlmutter, Hope Rugo, Richard Schwab, W. Fraser Symmans, Nola M. Hylton, Laura Van’t Veer, Douglas Yee, Angela DeMichele, Donald Berry, Laura J. Esserman, I-SPY Investigators. Evaluation of anti-PD-1 Cemiplimab plus anti-LAG-3 REGN3767 in early-stage, high-risk HER2-negative breast cancer: Results from the neoadjuvant I-SPY 2 TRIAL [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr GS5-03.

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• Oral paclitaxel and dostarlimab with or without trastuzumab in early-stage, high-risk breast cancer: Results from the neoadjuvant ISPY 2 TRIAL.

  Journal of Clinical Oncology · 2023-06-07 · 2 citations

  article

  LBA612 Background: I-SPY2 is a multicenter, phase 2 trial using response-adaptive randomization within biomarker subtypes including MammaPrint (MP) status to evaluate novel neoadjuvant agents in high-risk breast cancer. The primary endpoint is pathologic complete response (pCR). Oral Paclitaxel and encequidar (OPE) is an oral combination of paclitaxel (P) with a p-glycoprotein pump inhibitor, encequidar. Dostarlimab (D) is an intravenous (IV) PD-1 inhibitor. Methods: Women with tumors ≥ 2.5cm and MP high risk cancers (MP1 = MP high; MP2 = MP ultra-high) were treated starting Oct 5, 2020. Treatment included OPE (Oral P 205mg/m2 + encequidar 12.9mg) on days 1-3 weekly x 12 and D 500 mg IV given q 3 weeks x 4, followed by doxorubicin/cyclophosphamide (AC) q 2-3 weeks x 4. Patients with HER2+ disease received IV weekly trastuzumab (T) during the first 12 weeks. The control arm was weekly IV P x 12 with or without trastuzumab followed by AC q 2-3 weeks x 4. OPE + D was eligible to graduate [85% chance of success in a 300-person phase 3 neoadjuvant trial with a pCR endpoint] in any of the pre-defined signatures. Results: 113 (78 HR+HER2-, 17 HR-HER2- and 18 HER2+ patients) received OPE + D +/- T. The control arm included 388 historical controls (201 HR+Her2-, 156 HR-HER2-, 31 HER2+). 77 patients (70 HR+ and 7 HR-) were MP1 and 36 patients (24 HR+ and 12 HR-) were MP2. Safety events of note for OPE + D versus IV P include increased rates of nausea (85% vs. 72%) diarrhea (77% vs. 41%). There was no significant difference in rates of neutropenia (23% vs.17%). Peripheral neuropathy (37% vs. 64%) and alopecia (59% vs. 66%) were significantly decreased. Immune related adverse events (irAEs) were lower than expected. Conclusions: Although both OPE and D have both been shown to have efficacy in other settings, combination therapy with OPE + D did not graduate in any of the predefined subtypes. In the HR+ signature where we would not expect a benefit of D, we see equal response to OPE with decreased rates of peripheral neuropathy and alopecia, which suggest this oral agent may be an attractive alternative to IV P in this subgroup and is under consideration in ISPY 2.2. We did not observe the expected improvement in pCR rates seen with PD-1 inhibitors in the HR- or MP2 subtypes (over P alone historic control). In addition, the irAEs were less than expected. Together these findings suggest interference of OPE with D. A potential mechanism of interference could be change in microbiome with the use of OPE vs. IV P, as the microbiome is known to influence the efficacy of immunotherapy. The source of interference is being investigated. Clinical trial information: NCT01042379 . [Table: see text]

  PublisherDOI

• Erratum to ‘Reply to: Drug-drug interactions between palbociclib and proton pump inhibitors may significantly affect clinical outcome of metastatic breast cancer patients’

  ESMO Open · 2022-03-17

  erratumOpen accessSenior author

  The publisher regrets that the affiliations for the authors in this article were incorrect at the time the article was published. They are correct as presented within this erratum. The publisher would like to apologise for any inconvenience caused. Reply to: Drug-drug interactions between palbociclib and proton pump inhibitors may significantly affect clinical outcome of metastatic breast cancer patientsESMO OpenVol. 7Issue 1PreviewDel Re et al. report that concomitant use of proton pump inhibitors (PPIs) has a detrimental effect on progression-free survival (PFS) in patients with metastatic breast cancer (mBC) treated with palbociclib.1 The authors describe a retrospective observational analysis of mBC patients treated with palbociclib, and they report that those who take PPIs for at least two-thirds of their treatment have a PFS of 14.0 months, compared to 37.9 months (P < 0.0001) in patients not taking PPIs.1 There are several critical considerations omitted in this analysis that call into question these findings and the resulting conclusions presented. Full-Text PDF Open Access

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Frequent coauthors

• Christos Vaklavas

  Huntsman Cancer Institute

  8 shared

• Claudine Isaacs

  8 shared

• Erica Stringer-Reasor

  8 shared

• Douglas Yee

  Masonic Cancer Center

  7 shared

• Rita Nanda

  University of Chicago

  7 shared

• Angela DeMichele

  University of Pennsylvania

  7 shared

• Judy C. Boughey

  Mayo Clinic in Arizona

  7 shared

• Carla I. Falkson

  University of Rochester Medical Center

  7 shared

Labs

• UC Davis Comprehensive Cancer Center Hematology/Oncology ClinicPI

Awards & honors

• Safeway Grant Recipient (2020)
• Placer Breast Cancer Foundation award for research/trial wor…
• Christine and Helen Landgraf Memorial Research Award recipie…
• Chief Fellow, UC Davis (2014, 2015)