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Kavita Desai

Kavita Desai

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University of Pennsylvania · Rehabilitation Medicine

Active 2003–2025

h-index14
Citations1.1k
Papers7953 last 5y
Funding
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About

Kavita Desai, MD, is an Assistant Professor of Clinical Pediatrics (Oncology) at the Perelman School of Medicine at the University of Pennsylvania. She is affiliated with the Children’s Hospital of Philadelphia, working within the Department of Pediatrics, Division of Hematology-Oncology. Her educational background includes a B.S. in Neuroscience from the University of Michigan, obtained in 2007, and an M.D. from St. George's University School of Medicine, completed in 2012. Her research and clinical interests focus on pediatric neuro-oncology, with contributions to understanding the development of microRNA-defective pineoblastoma, outcomes in atypical teratoid rhabdoid tumors, and disease progression in neurofibromatosis type 1-associated optic pathway glioma. She has also co-authored chapters on brain tumors and germ cell tumors, and has presented on various topics related to pediatric hematology and oncology.

Research topics

  • Medicine
  • Cancer research
  • Biology
  • Internal medicine
  • Pharmacology

Selected publications

  • Toe Walking in a Formerly Preterm Child: Is it Just Cerebral Palsy?

    Journal of Pediatric Neurology · 2025-07-11

    articleOpen access

    Spastic diplegic cerebral palsy (CP) is common among children born preterm and is a known cause of toe walking. By contrast, pediatric tumors of the conus medullaris are rare. We report the case of a 28-month-old formerly extremely preterm male with global developmental delay who presented with toe walking, constipation, and asymmetric hypertonia of the lower extremities. Brain imaging revealed periventricular leukomalacia, ex-vacuo ventricular dilation, and cerebellar dysplasia consistent with a diagnosis of CP secondary to perinatal injury. Lumbar spine imaging obtained due to his worsening constipation and pain while walking demonstrated an intramedullary, well-circumscribed, contrast-enhancing lesion in the conus medullaris. Post-resection pathology revealed a pilocytic astrocytoma. Following surgery, the patient had improved constipation and lower extremity tone, allowing him to walk with bilateral heel strike. His symptomatic improvement supported the contribution of the tumor to his bowel dysfunction and gait abnormality. This case of comorbid CP and conus pilocytic astrocytoma in a child with toe walking supports careful consideration of possible concurrent neurologic pathologies in the setting of atypical history and physical exam findings, such as pain while walking and bowel/bladder dysfunction. A higher degree of suspicion and consideration of parental report of pain while walking is especially important in cases in which the patient’s ability to report subjective symptoms, such as pain, subtle bowel/ bladder dysfunction, and sensory changes, is limited.

  • An imbalance between proliferation and differentiation underlies the development of microRNA-defective pineoblastoma

    Genes & Development · 2025-04-16 · 3 citations

    articleOpen access

    Mutations in the microRNA processing genes DROSHA and DICER1 drive several cancers that resemble embryonic progenitors. To understand how microRNAs regulate tumorigenesis, we ablated Drosha or Dicer1 in the developing pineal gland to emulate the pathogenesis of pineoblastoma, a brain tumor that resembles undifferentiated precursors of the pineal gland. Accordingly, these mice develop pineal tumors marked by loss of microRNAs, particularly the let-7/miR-98-5p family, and derepression of microRNA target genes. Pineal tumors driven by loss of Drosha or Dicer1 mimic tumors driven by Rb1 loss, as they exhibit upregulation of S-phase genes and homeobox transcription factors that regulate pineal development. Blocking proliferation of these tumors facilitates expression of pinealocyte maturation markers, with a concomitant reduction in embryonic markers. Select embryonic markers remain elevated, however, as the microRNAs that normally repress these target genes remain absent. One such microRNA target gene is the oncofetal transcription factor Plagl2 , which regulates expression of progrowth genes, and inhibiting their signaling impairs tumor growth. Thus, we demonstrate that tumors driven by loss of microRNA processing may be therapeutically targeted by inhibiting downstream drivers of proliferation.

  • Integrative Role of Ayurveda, Yoga, Meditation, Sound and Mantra Therapy in Sickle Cell Disease (SCD) Management: Details and References

    Scholars International Journal of Traditional and Complementary Medicine · 2025-09-02

    articleOpen access

    Sickle cell disease (SCD) remains a major global health burden characterized by chronic pain, inflammation, and psychosocial stress. While pharmacological approaches like hydroxyurea offer partial relief, integrative therapies including Ayurveda based sound and mantra therapy provide supportive, culturally appropriate options. This paper reviews the evidence and principles behind the use of sound healing, mantra chanting, and music-based interventions in SCD management, highlighting their roles in pain relief, stress reduction, emotional stability, and quality of life improvement.

  • Phyto-Therapeutic Targeting of NF-κB Pathway in Inflammation-Linked Disorders

    Journal of Pharmaceutical Research International · 2025-12-13

    articleOpen access

    Inflammation is a vital biological response to injury and infection, but its persistence beyond resolution stages contributes to a range of chronic diseases, including arthritis, asthma and autoimmune disorders. The nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κΒ) pathway has emerged as a central mediator in sustaining inflammatory cascades through Pro-inflammatory cytokines, chemokines, and adhesion molecules undergo transcriptional regulation. Although conventional anti-inflammatory drugs may offer short-term relief, their long-term use is frequently limited by serious side effects and inadequate targeting of the root causes. In recent years, medicinal plants have gained attention for their potential to manage inflammation in a safer and more holistic way. This narrative review focuses on five such plants- Eclipta alba, Zingiber officinalis, Asparagus racemosus, Phyllanthus emblica and Justica adhatoda- all of which have shown notable analgesic and anti-inflammatory properties. These herbs act through various mechanisms, including suppression of pro-inflammatory cytokines, inhibition of oxidative stress and modulation of NF-κΒ pathway. Beyond these, the review also highlights other herbal agents known for influencing inflammatory responses through NF-κΒ inhibition. The article further discusses the pathogenesis of chronic inflammatory diseases, the biological role of NF-κB, and the limitations of existing treatment options. Together, this review emphasizes the growing relevance of plant-based therapies as effective and safer alternatives for inflammation-related disorders, especially those involving NF-κΒ dysregulation.

  • PD‐L1 Expression is Mediated by microRNA Processing, Wnt/β‐Catenin Signaling, and Chemotherapy in Wilms Tumor

    Pediatric Blood & Cancer · 2025-06-13 · 1 citations

    articleOpen access

    BACKGROUND: Inhibition of immune checkpoint proteins is effective in adult cancers but has shown limited efficacy in pediatric cancers. While factors regulating expression of immune checkpoint proteins such as PD-L1 are well documented in adult cancers, their regulation is poorly understood in pediatric cancers. METHODS: We analyzed Wilms tumor specimens with reverse-phase protein arrays. We validated correlations using published sequencing data, flow cytometry, and immunoblots. RESULTS: Using unsupervised clustering of protein arrays, we found that immune markers like PD-L1 are upregulated in distinct subsets of Wilms tumor, the most common pediatric kidney cancer. Specifically, chemotherapy-exposed Wilms tumor specimens exhibited higher levels of PD-L1 expression, and common chemotherapeutics upregulated PD-L1 in vitro. Furthermore, mutations in CTNNB1 and DROSHA, the two most commonly mutated genes in Wilms tumor, correlated with higher PD-L1. Activation of Wnt/β-catenin signaling and knockdown of DROSHA or DICER1 both increase PD-L1 in vitro. CONCLUSIONS: Together, our results identify clinical and biological properties regulating PD-L1 in Wilms tumor that may inform precision therapy approaches in pediatric immuno-oncology.

  • Table S5 from <i>DROSHA</i> Regulates Mesenchymal Gene Expression in Wilms Tumor

    2024-08-02

    preprintOpen access

    <p>Fusions</p>

  • Figure S4 from <i>DROSHA</i> Regulates Mesenchymal Gene Expression in Wilms Tumor

    2024-08-02

    preprintOpen access

    <p>Supplementary Figure S4. (A) TARGET tumors, by mutational class. (B,C) GSEA of mutational classes matched to transcriptional signatures in TARGET tumors; NES, normalized enrichment score.</p>

  • Table S3 from <i>DROSHA</i> Regulates Mesenchymal Gene Expression in Wilms Tumor

    2024-08-02

    preprintOpen access

    <p>WES results</p>

  • Figure S6 from <i>DROSHA</i> Regulates Mesenchymal Gene Expression in Wilms Tumor

    2024-08-02

    preprintOpen access

    <p>Supplementary Figure S6. Metabolomics of Wilms tumors were used to determine differential abundance of metabolites, expressed as log2-fold-change in tumors with microRNA processing mutations versus without such mutations, demonstrating that the antioxidant BH<sub>4</sub> is depleted in tumors with microRNA processing mutations.</p>

  • PD-L1 expression is mediated by microRNA processing, Wnt/β-catenin signaling, and chemotherapy in Wilms tumor

    bioRxiv (Cold Spring Harbor Laboratory) · 2024-12-03

    preprintOpen access1st author

    ABSTRACT Inhibition of immune checkpoint proteins is effective in adult cancers but has shown limited efficacy in pediatric cancers. While factors regulating expression of immune checkpoint proteins such as PD-L1 are well-documented in adult cancers, their regulation is poorly understood in pediatric cancers. Here, we show that PD-L1 is upregulated in distinct subsets of Wilms tumor, the most common pediatric kidney cancer. Specifically, chemotherapy-exposed Wilms tumor specimens exhibited higher levels of PD-L1 expression, and common chemotherapeutics upregulated PD-L1 in childhood cancer cell lines in vitro . Furthermore, mutations in CTNNB1 and DROSHA , the two most commonly mutated genes in Wilms tumor, correlated with higher PD-L1. Activation of Wnt/β-catenin signaling and knockdown of DROSHA or DICER1 both increase PD-L1 in vitro . Lastly, in adult cancers, DICER1 alterations are associated with immune gene expression signatures and improved survival in response to immune checkpoint inhibitors. Together, our results identify clinical and biological properties regulating PD-L1 in Wilms tumor that may inform precision therapy approaches in pediatric immuno-oncology.

Frequent coauthors

  • Kenneth Chen

    SingHealth

    46 shared
  • James F. Amatruda

    37 shared
  • Sridhar Mani

    Albert Einstein College of Medicine

    35 shared
  • Patricia D.B. Tiburcio

    33 shared
  • Lei Guo

    33 shared
  • Qinbo Zhou

    33 shared
  • Aysen Yuksel

    Children's Hospital at Westmead

    33 shared
  • Lin Xu

    33 shared

Labs

  • Kavita Desai LabPI

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