About

Zaibo Li, MD, PhD, MBA, is a professor (clinical) at The Ohio State University. The provided page does not include specific details about his research focus, background, or key contributions.

Research topics

• Medicine
• Pathology
• Computer Science
• Biology
• Internal medicine
• Computer vision
• Artificial Intelligence
• Medical physics
• Risk analysis (engineering)
• Oncology
• Medical emergency
• Data science
• Cancer research
• Family medicine
• Nuclear medicine
• Multimedia
• World Wide Web
• Radiology
• Immunology

Selected publications

• 166 Incidence, Clinicopathological Features and HER2 FISH Results of HER2 ultra-low Breast Carcinomas

  Laboratory Investigation · 2025-03-01

  articleSenior author
  PublisherDOI

• Integration of Digital Cytology in Quality Assurance Programs for Cytopathology

  Acta Cytologica · 2025-07-21 · 10 citations

  reviewOpen access

  Background: Quality assurance (QA) and quality control (QC) are fundamental to maintaining high standards in cytopathologic diagnostics. The recent adoption of digital cytology (DC) has led to transformative changes in cytopathology workflows, including primary diagnosis, telecytopathology-based consultations, and rapid on-site evaluations (ROSEs). These technological developments call for a conceptual shift and redefinition of QA and QC frameworks in the DC era. Summary: This review explores the evolving landscape of QA and QC in cytopathology, with a focus on the integration of DC into existing quality systems. We examine the role of DC as both a QC tool and a platform for implementing DC-specific QA/QC protocols. Practical applications discussed include leveraging DC for conventional QA/QC tasks, such as education and training of laboratory staff and cytopathologists, and facilitating digital proficiency testing through cloud-based platforms. Additionally, we review current international recommendations for the adoption of DC in cytopathology and propose strategies for the safe and efficient management of digital environments. Key Messages: (i) DC is reshaping the practice of cytopathology and requires updated QA/QC strategies. (ii) DC can enhance QA/QC activities through improved training, proficiency testing, and collaborative diagnostics. (iii) The development and implementation of DC-specific protocols are essential for ensuring accuracy and reliability in digital cytopathologic practice. .

  PublisherOA PDFDOI

• Decoding High-grade Endometrial Cancer: A Molecular-histologic Integration using the Cancer Genome Atlas Framework

  Journal of Clinical and Translational Pathology · 2025-07-21 · 1 citations

  articleOpen accessSenior author

  High-grade endometrial carcinoma (HGEC) is an aggressive tumor with increasing incidence and mortality. Traditional classifications, such as Bokhman’s dualistic model and the World Health Organization histopathological system, have limitations due to tumor heterogeneity and interobserver variability. This review provides a comprehensive understanding of how integrating histopathological and molecular data, particularly The Cancer Genome Atlas (TCGA) classification, advances risk stratification and personalized treatment in HGEC. It highlights current challenges and identifies future directions to improve diagnostic accuracy and patient outcomes through precision medicine.

  PublisherOA PDFDOI

• Breast Biomarker Cytology Practice in 2023: Results of a College of American Pathologists Survey

  Archives of Pathology & Laboratory Medicine · 2025-05-07 · 1 citations

  articleOpen access1st authorCorresponding

  CONTEXT.—: The College of American Pathologists (CAP) surveys provide national benchmarks of pathology practice. OBJECTIVE.—: To investigate breast biomarker cytology practice in domestic and international laboratories in 2023. DESIGN.—: We analyzed data from the CAP Breast Biomarker Cytology Practice Supplemental Questionnaire that was distributed to laboratories participating in the 2023 CAP Nongynecologic Cytopathology Education Program. RESULTS.—: Twenty-five percent (180 of 728) of responding laboratories routinely evaluated breast biomarkers in cytology specimens. Breast biomarkers evaluated in cytology specimens included estrogen receptor/progesterone receptor (98.9%; 175 of 177), human epidermal growth factor receptor 2 (HER2) (93.2%; 165 of 177), Ki-67 (48.6%; 86 of 177), programmed death ligand-1 (PD-L1) (20.9%; 37 of 177), and mismatch repair (19.8%; 35 of 177). Fine-needle aspiration was the most validated specimen type (85.3%; 133 of 156), followed by body fluids (82.1%; 128 of 156). All respondents validated cell blocks (100.0%; 165 of 165), with a few laboratories also validating cytospin slides (3.0%; 5 of 165), liquid-based slides (3.0%; 5 of 165), air-dried direct smears (2.4%; 4 of 165), and others. CytoLyt was the most used collection medium (55.4%; 87 of 157), followed by balanced salt solution (16.6%; 26 of 157), Roswell Park Memorial Institute Medium (13.4%; 21 of 157), and CytoRich Red (9.6%; 15 of 157). Almost all laboratories indicated routinely using formalin (90.4%; 151 of 167) as fixative, while a few laboratories used other types of fixative (ethanol [5.4%; 9 of 167], methanol [3.0%; 5 of 167]). Digital imaging platforms were used by only 12.9% (22 of 171) of responding laboratories. Forty-four laboratories (28.0%; 44 of 157) required cellularity adequacy for interpreting breast biomarkers on cytologic specimens. Additionally, some significant differences in breast biomarker testing practice were identified among different institution types and between domestic and international laboratories. CONCLUSIONS.—: This is the first survey from the CAP to investigate breast biomarker cytology practices. The findings reveal some differences among institution types and between domestic and international laboratories. These data provide a baseline for and support further studies and/or guidelines to promote and refine these practices.

  PublisherOA PDFDOI

• 140 Cyber-Dissect: Spatial logic reconciles gene-signatures methods in Triple Negative Breast Cancer

  Laboratory Investigation · 2025-03-01

  articleOpen access
  PublisherOA PDFDOI

• Abstract 429: Targeting translesion synthesis to sensitize ovarian cancer cells to PARP inhibitor treatment

  Cancer Research · 2025-04-21

  article

  Abstract BRCA-deficient tumor cells, characterized by defective homologous recombination (HR) repair, show high sensitivity to poly (ADP-ribose) polymerase inhibitors (PARPi). The mechanism is that PARPi blocks PARP and traps them at DNA damage sites (PARP-DNA complex), inducing replication fork stalling, leading to cancer cell death with BRCA mutation due to the accumulation of unrepaired DNA double-strand breaks. At present, PARP inhibitors have been widely used to treat ovarian cancer patients with deficient HR. However, like other chemotherapy agents, many patients acquire PARPi resistance. Replication fork protection is a key mechanism driving resistance to PARPi. Translesion synthesis (TLS) is an error-prone DNA damage tolerance pathway that can help cancer cells bypass DNA lesions and rescue replication fork stalling with Y-family DNA polymerases. Thus, we hypothesized that enhanced TLS enables BRCA-mutated ovarian cancer cells to overcome PARPi treatment via bypassing PARP-DNA complexes, and rescuing stalled replication forks, eventually leading to BRCA secondary mutations and partial restoration of HR function. To test this hypothesis, we first confirmed that PARPi can promote TLS activity by increasing the expression of monoubiquitinated PCNA in BRCA-mutated ovarian cancer cells. In addition, replication fork stalling has been observed following treatment with PARP inhibitors, as demonstrated by DNA fiber assays. Blocking TLS by knocking down REV1 exacerbates replication fork stalling, highlighting the interplay between PARPi treatment and TLS pathways. To further investigate the role of TLS polymerases, we individually knocked down TLS polymerases and evaluated their effects. Knocking down POLH (encode Polη), exacerbated Olaparib-induced replication fork stalling, irrespective of BRCA status. Functional analyses revealed that POLH knockdown sensitized BRCA-mutated cells to Olaparib but had no significant effect on BRCA wild-type cells. Next, we utilized a newly developed ChIP-based assay to assess TLS efficiency. We demonstrated that TLS inhibition through knocking down POLH or using a TLS inhibitor JH-RE-06 impairs DNA replication across Olaparib-induced PARP1-DNA complexes. Furthermore, JH-RE-06 sensitized HR-deficient ovarian cancer cell lines and patient-derived organoids to Olaparib in vitro. It also enhanced the efficacy of Olaparib in vivo, both in NSG mice bearing human BRCA1-mutated ovarian cancer cells and C57BL/6 mice with murine ovarian cancer cells harboring P53-/- and BRCA1-/- genotypes. In summary, our findings reveal that TLS facilitates replication fork recovery by enabling DNA replication across PARPi-induced PARP-DNA complexes, with Polη playing a key role. Importantly, JH-RE-06 represents a promising strategy to enhance the therapeutic sensitivity of HR-deficient ovarian cancer cells to PARP inhibitors like Olaparib. Citation Format: Na Li, Qianyun Ge, Yajing Yang, Linzhou Wang, Xiaoli Zhang, Junran Zhang, Zaibo Li, Floor Backes, Qi-En Wang. Targeting translesion synthesis to sensitize ovarian cancer cells to PARP inhibitor treatment [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 429.

  PublisherDOI

• Abstract P1-06-21: The Ral GTPases regulate the TNBC secretome to drive growth and metastasis

  Clinical Cancer Research · 2025-06-13

  article

  Abstract Breast Cancer (BC) is the most common cancer and leading cause of cancer associated mortality in women worldwide, with TNBC patients have the highest mortality compared to other subtypes. Ras-Like Protooncogene A (RalA) and Ras-Like Protooncogene B (RalB) are small GTPases that are known to regulate growth and metastasis in several cancers. Our group and others have identified the Rals as molecular drivers of TNBC, however the roles of these GTPases in BC is poorly understood. The goal of this study was to investigate the contributions of RalA and RalB in TNBC. We found that silencing RalA or RalB in the MDA-MB-468 (468) TNBC cells reduced primary tumor growth in NSG mice. To better recapitulate human disease, we utilized two genetically engineered mouse models of TNBC. First, we found in the MMTV-Cre; MMTV-PyMT spontaneous TNBC tumor model that loss of Rala significantly reduces primary tumor growth while loss of Ralb increases growth, with no changes in tumor initiation or mammary gland development. Then we tested loss of Rals in the Brca1; Trp53 mouse model, which form TNBC tumors phenotypically similar to human TNBC when given and intraductal injection of adenoviral-Cre. Here we find that loss of Ralb significantly increases primary tumor growth with no changes in tumor initiation. To understand how the Rals regulate tumorigenesis, we looked closer at the 468 tumors and cells. In the 468 model we found no differences in proliferation or apoptosis, leading us to test the tumor-microenvironment (TME) to explain the reduction in tumor growth. Using Masson’s Trichrome staining, we found increased collagen deposition in the 468 tumors upon depletion of either Ral. Staining for blood vessels using CD31 revealed depletion of RalB, and not RalA, reduced stromal and intertumoral blood vessel density. We then tested for macrophage infiltration and find a reduction of either Ral increases overall macrophage infiltration and specifically M1-like macrophages. Depletion of RalA also reduced recruitment of M2-like macrophages compared to control or RalB depleted cells. To find what factors lead to the differences in the TME, we performed a human secreted protein array on conditioned media from the 468 shRal cells and confirmed significant results via ELISAs. We found the Rals promote secretion of the angiogenic factor ANGPT1 and interleukins CXCL1-3. Western blot on intracellular protein showed no changes in expression of ANGPT1, revealing that changes in secreted protein are not due to altered expression from sh depletion. These results show that the Rals influence protein secretion that alters tumor angiogenesis and collagen dynamics to promote tumor microenvironment changes that aid TNBC growth and metastasis. Citation Format: Jonathan Spehar, Prathik Chakravarthy, Dillon Richardson, Reena Shakya, Zaibo Li, Daniel Stover, Gina Sizemore, Steven Sizemore. The Ral GTPases regulate the TNBC secretome to drive growth and metastasis [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 P1-06-21.

  PublisherDOI

• Incidence, Clinicopathologic Features, and Follow-Up Results of human epidermal growth factor receptor-2–Ultralow Breast Carcinoma

  Modern Pathology · 2025-04-22 · 6 citations

  articleSenior author
  PublisherDOI

• Endoscopic ultrasound–guided pancreatic core-needle/microforceps biopsy is a valuable diagnostic tool for pancreatic lesions: Experience from a large academic institution

  American Journal of Clinical Pathology · 2025-04-24 · 3 citations

  articleOpen access

  OBJECTIVE: Endoscopic ultrasound (EUS)-guided, fine-needle core biopsy (FNB), and through-the-needle microforceps biopsy (TTNB) are latest tools for evaluating pancreatic lesions. We aim to provide subspecialty surgical pathologists' experience with EUS-FNB/TTNB in diagnosing pancreatic lesions at a large academic center. METHODS: A 3-year review identified 101 EUS pancreatic specimens submitted for surgical pathology: 87 biopsy specimens (FNB = 58, TTNB = 29) and 14 fine-needle aspirations (FNAs). Diagnoses were compared with cytology and resection specimens when available. RESULTS: Of the 101 cases, 10 had previous EUS-FNA cytology with inconclusive diagnoses. Rebiopsy with EUS-FNB/TTNB provided definitive diagnoses in 9 cases. Thirty-five cases (18 cystic and 17 solid lesions) had concurrent surgical pathology and cytology specimens. The diagnostic yield of EUS-FNB/TTNB biopsy specimens (69%) was significantly higher than that of cytology specimens (26%, P = .0017), as was the diagnostic accuracy (P = .0012). This diagnostic advantage was statistically significant in cystic lesions (FNB/TTNB [83.3%] vs cytology [16.7%] for achieving a specific diagnosis, P = .0002) but not in solid lesions (61.5% vs 46.2%, P = .6951). Only in 1 case did cytology (adenocarcinoma) provide a more definitive diagnosis than surgical pathology (high-grade dysplasia cannot exclude adenocarcinoma). CONCLUSIONS: The EUS-FNB/TTNB methods complement EUS-FNA cytology in diagnosing pancreatic lesions, and they often outperforms concurrent cytology specimens, particularly in cystic lesions.

  PublisherOA PDFDOI

• Clinicopathologic and Whole Exome Sequencing Analyses of High-Grade Serous Carcinoma-Like Carcinoma of the Breast Reveal Unique Genetic Profile and Poor Clinical Outcome

  The American Journal of Surgical Pathology · 2025-05-23 · 2 citations

  article

  We identified 9 cases of primary high-grade serous-like carcinoma (HG-SL-Ca) of the breast that displayed the morphology of high-grade serous carcinoma of Müllerian origin. These cases could represent a new entity of breast carcinoma. This study included 9 cases of HG-SL-Ca of the breast. Extensive clinicopathologic features and outcome data were available and evaluated in 8 cases. We, for the first time, performed whole exome sequencing (WES) on 6 of these cases to identify pathogenic germline and somatic genetic mutations and conducted gene pathway enrichment analyses. Six cases were triple negative; 2 were HER2 positive, and 1 was ER+/PR+/HER2-. Eight of the 9 cases had high nuclear grade and the other 1 had intermediate nuclear grade. Six patients received chemotherapy; the patient with ER+/PR+/HER2-cancer received hormonal therapy only, and 1 patient with dementia did not receive any systemic therapy. Follow-up data showed 2 patients had distant metastasis and 1 had chest wall recurrence. Two patients died of disease, including 1 patient receiving palliative care and 1 with lung and pleural metastasis. Most of the cases were positive for GATA3 immunohistochemistry (IHC) staining and all were negative for PAX8. All except for 1 case (focally positive) were negative for WT1 nuclear stain. Aberrant p53 IHC staining patterns were observed in 6 cases. WES analyses showed 26 genes with pathogenic germline mutations and 28 genes with pathogenic somatic mutations in these cases that were in the ACR GENIE mutated gene list. Pathway analyses showed that these genes with pathogenic germline or somatic mutations were enriched in the PI3K-AKT-mTOR pathway, WNT pathways, and death receptor pathway. TP53 was recurrently mutated, containing somatic variants in 4 cases, and all these 4 cases had aberrant p53 IHC staining patterns. We, for the first time, performed WES analyses on HG-SL-Ca of the breast. The majority of HG-SL-Ca were triple negative or HER2 positive with high nuclear grade. Patients with HG-SL-Ca of the breast had a poor prognosis. Our pathway analyses showed that genes containing pathogenic germline or somatic mutations were enriched in the PI3K-AKT-mTOR pathway, WNT pathways, and death receptor pathway, which could provide potential targeted treatment options. TP53 was recurrently mutated in 4 cases and all these 4 cases had aberrant p53 IHC staining patterns.

  PublisherDOI

Recent grants

• Cancer Research Training and Education Coordination (CRTEC)

  NIH · $58.2M · 1997–2031

Frequent coauthors

• Chengquan Zhao

  University of Pittsburgh Medical Center

  206 shared

• Anil V. Parwani

  The Ohio State University

  92 shared

• Rhona J. Souers

  College of American Pathologists

  90 shared

• Diane D. Davey

  University of Central Florida

  89 shared

• Christine N. Booth

  Cleveland Clinic

  89 shared

• Kelly Goodrich

  College of American Pathologists

  85 shared

• Benjamin L. Witt

  University of Utah

  84 shared

• Daniel Kurtycz

  81 shared

Labs

• AI4PathPI

  From Pixels to Prognosis: AI in Action!

Education

• M.D.

  Peking University Health Science Center

• Ph.D.

  University of Rochester

• Other

  University of Rochester

• Other, Pathology

  University of Pittsburgh Medical Center

• Other, Cytopathology

  University of Pittsburgh Medical Center

• Other, Breast and Gynecological Pathology

  Magee Womens Hospital of Univ. of Pittsburgh Medical Center

Awards & honors

• Endowed University Pathology Services Anatomic Pathology Pro…