Shruthi Sriramkumar

ORCID: 0000-0003-1308-2546
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About
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Research Areas
  • Epigenetics and DNA Methylation
  • Colorectal Cancer Treatments and Studies
  • RNA modifications and cancer
  • Genetic factors in colorectal cancer
  • Ubiquitin and proteasome pathways
  • Cancer Research and Treatments
  • Cancer Immunotherapy and Biomarkers
  • Pancreatic and Hepatic Oncology Research
  • Histone Deacetylase Inhibitors Research
  • Microtubule and mitosis dynamics
  • Gastric Cancer Management and Outcomes
  • Cancer Diagnosis and Treatment
  • Biochemical and Molecular Research
  • Cancer Cells and Metastasis
  • MicroRNA in disease regulation
  • DNA Repair Mechanisms
  • Peptidase Inhibition and Analysis
  • RNA Research and Splicing
  • Cancer-related molecular mechanisms research
  • Cholangiocarcinoma and Gallbladder Cancer Studies
  • Ferroptosis and cancer prognosis
  • Cancer-related gene regulation
  • Cancer Genomics and Diagnostics
  • Cancer, Hypoxia, and Metabolism
  • PARP inhibition in cancer therapy

Saveetha University
2025

Indiana University School of Medicine
2017-2023

Indiana University
2023

Indiana University Bloomington
2017-2022

Abstract Despite the connection of secretory cells, including goblet and enteroendocrine (EEC) to distinct mucus-containing colorectal cancer histologic subtypes, their role in progression has been underexplored. Here, our analysis The Cancer Genome Atlas (TCGA) single-cell RNA-sequencing data demonstrates that EEC progenitor cells are enriched BRAF-mutant patient tumors, cell lines, patient-derived organoids. In cancer, progenitors were blocked from differentiating further by DNA...

10.1158/0008-5472.can-20-3562 article EN Cancer Research 2021-05-25

Colorectal cancer is multifaceted, with subtypes defined by genetic, histologic, and immunologic features that are potentially influenced inflammation, mutagens, and/or microbiota. cancers activating mutations in BRAF associated distinct clinical characteristics, although the pathogenesis not well understood. The Wnt-driven multiple intestinal neoplasia (MinApcΔ716/+) enterotoxigenic Bacteroides fragilis (ETBF) murine model characterized IL17-dependent, distal colon adenomas. Herein, we...

10.1158/2159-8290.cd-20-0770 article EN Cancer Discovery 2021-02-25

Abstract Background Platinum based agents—cisplatin and carboplatin in combination with taxanes are used for the treatment of ovarian cancer (OC) patients. However, majority OC patients develop recurrent, platinum resistant disease that is uniformly fatal. enriches chemoresistant aldehyde dehydrogenase (ALDH) + stem cells (OCSCs), which contribute to tumor recurrence relapse. Acquired resistance also includes metabolic reprograming switching oxidative phosphorylation (OXPHOS). Chemosensitive...

10.1186/s12967-022-03447-y article EN cc-by Journal of Translational Medicine 2022-05-31

Abstract Aberrant silencing of genes by DNA methylation contributes to cancer, yet how this process is initiated remains unclear. Using a murine model inflammation-induced tumorigenesis, we tested the hypothesis that inflammation promotes recruitment epigenetic proteins chromatin, initiating and gene in tumors. Compared with normal epithelium noninflammation-induced tumors, tumors gained at CpG islands, some which are associated putative tumor suppressor genes. Hypermethylated exhibited...

10.1158/0008-5472.can-17-0056 article EN Cancer Research 2017-05-19

Activation of the epithelial-to-mesenchymal transition (EMT) program is a critical mechanism for initiating cancer progression and migration. Colorectal cancers contain many genetic epigenetic alterations that can contribute to EMT. Mutations activating PI3K/AKT signaling pathway are observed in >40% patients with colorectal contributing increased invasion metastasis. Little known about how oncogenic pathways such as synergize chromatin modifiers activate EMT program. Lysine-specific...

10.1158/1541-7786.mcr-19-0748 article EN Molecular Cancer Research 2019-11-08

Ovarian cancer is a deadly disease attributed to late-stage detection as well recurrence and the development of chemoresistance. stem cells (OCSCs) are hypothesized be largely responsible for emergence chemoresistant tumors. Although chemotherapy may initially succeed at decreasing size number tumors, it leaves behind residual malignant OCSCs. In this study, we demonstrate that aldehyde dehydrogenase 1A1 (ALDH1A1) essential survival We identified first-in-class ALDH1A1 inhibitor, compound

10.3390/cancers14143437 article EN Cancers 2022-07-15

Tuberculosis (TB) remains a significant public health issue globally, with extra pulmonary tuberculosis (epTB) accounting for considerable number of TB cases. This study aims to improve our understanding epTB epidemiology by evaluating treatment outcomes and identifying factors associated positive negative results in patients. A retrospective was conducted from January 1, 2016, December 31, 2019. EpTB rifampicin-resistant were identified using the GeneXpert MTB/RIF assay. Logistic regression...

10.1038/s41598-025-92613-5 article EN cc-by-nc-nd Scientific Reports 2025-03-10

Ovarian cancer (OC) is a lethal gynecological malignancy with five-year survival rate of only 46%. Development resistance to platinum-based chemotherapy common cause high mortality rates among OC patients. Tumor and transcriptomic heterogeneity are drivers platinum in OC. Platinum-based enriches for ovarian stem cells (OCSCs) that chemoresistant contribute disease recurrence relapse. Studies examining the effect different treatments on subpopulations HGSOC cell lines limited. Having...

10.1371/journal.pone.0271584 article EN cc-by PLoS ONE 2022-08-03

Platinum resistance is a common occurrence in high-grade serous ovarian cancer and major cause of deaths. agents form DNA cross-links, which activate nucleotide excision repair (NER), Fanconi anemia, homologous recombination (HRR) pathways. Chromatin modifications occur the vicinity damage play an integral role response (DDR). modifiers, including polycomb repressive complex 1 (PRC1) members, chromatin structure are frequently dysregulated can potentially contribute to platinum resistance....

10.1158/1541-7786.mcr-20-0396 article EN Molecular Cancer Research 2020-08-15

Ovarian cancer is a deadly disease attributed to late-stage detection as well recurrence and development of chemoresistance. stem cells (OCSCs) are hypothesized be largely responsible for emergence chemoresistant tumors. Although chemotherapy may initially succeed at decreasing the size number tumors, it leaves behind residual malignant OCSCs. In this study, we demonstrate that Aldehyde dehydrogenase 1A1 (ALDH1A1) essential survival We identified novel ALDH1A1 inhibitor, compound 974, used...

10.20944/preprints202205.0001.v1 preprint EN 2022-05-02

Abstract Despite the connection to distinct mucus-containing colorectal cancer (CRC) histological subtypes, role of secretory cells, including goblet and enteroendocrine (EEC) in CRC progression has been underexplored. Analysis TCGA single cell RNA sequencing data demonstrates that multiple progenitor populations are enriched BRAF- mutant patient tumors lines. Enrichment EEC progenitors BRAF -mutant is maintained by DNA methylation silencing NEUROD1 , a key gene required for differentiation...

10.1101/2020.09.25.313536 preprint EN cc-by bioRxiv (Cold Spring Harbor Laboratory) 2020-09-25

Abstract Ovarian cancer is a deadly disease attributed to late-stage detection as well recurrence and development of chemoresistance. stem cells (OCSCs) are hypothesized be largely responsible for emergence chemoresistant tumors. Although chemotherapy may initially succeed at decreasing the size number tumors, it leaves behind residual malignant OCSCs. In this study, we demonstrate that Aldehyde dehydrogenase 1A1 (ALDH1A1) essential survival We identified first in class ALDH1A1 inhibitor,...

10.1101/2022.05.09.491218 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2022-05-10

Abstract Introduction: Epithelial Ovarian cancer (EOC) is one of the most fatal gynecological malignancies, with little improvement being made to early-stage diagnostics or treatment options over years. The standard care for EOC remains be platinum-based chemotherapy despite ultimate relapse which arises acquired chemoresistance. Accumulating studies show that stem-like cells (CSCs) following initial platinum contribute developed chemoresistance and metastasis. Thus, there an urgent need...

10.1158/1538-7445.ovarian23-b029 article EN Cancer Research 2024-03-04

ABSTRACT High grade serous ovarian cancer (HGSOC) is the most common and aggressive type of cancer. Platinum resistance a occurrence in HGSOC main cause tumor relapse resulting high patient mortality rates. Recurrent OC enriched aldehyde dehydrogenase (ALDH)+ stem cells (OCSCs), which are resistant to platinum agents. We demonstrated that acute treatment induced DNA damage-dependent decrease BRCA1 levels. In parallel response associated with G2/M arrest, also an increase expression NAMPT ,...

10.1101/2021.03.18.435878 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2021-03-18

Abstract Background Platinum based agents – cisplatin and carboplatin in combination with taxanes are used for the treatment of ovarian cancer (OC) patients. However, majority OC patients develop recurrent, platinum resistant disease that is uniformly fatal. Acute enriches chemoresistant aldehyde dehydrogenase (ALDH) + stem cells (OCSCs), which contribute to tumor recurrence relapse. Acquired resistance includes metabolic reprograming switching oxidative phosphorylation (OXPHOS)....

10.1101/2022.02.01.478738 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2022-02-03

<div>Abstract<p>Aberrant silencing of genes by DNA methylation contributes to cancer, yet how this process is initiated remains unclear. Using a murine model inflammation-induced tumorigenesis, we tested the hypothesis that inflammation promotes recruitment epigenetic proteins chromatin, initiating and gene in tumors. Compared with normal epithelium noninflammation-induced tumors, tumors gained at CpG islands, some which are associated putative tumor suppressor genes....

10.1158/0008-5472.c.6508926.v1 preprint EN 2023-03-31

<p>Supplementary Table S1: Mutational status of common oncogenes in CRC and STAD cell lines. Supplementary Figure Mutant PIK3CA does not regulate LSD1 expression. S2: DNase signal is generally depleted at TSS's, reduce global H3K4me2. S3: RCOR1 upregulated mutant versus WT cancers arising from non-gastrointestinal tissues, correlate with S4: KO reduces viability over time HT29 but SW480 cells. S5: Inhibiting AKT Snail protein level or kinase domain cells, the LSD1-AKT-GSK3b-Snail axis...

10.1158/1541-7786.22516900.v1 preprint EN cc-by 2023-04-03
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