Jeffrey C. Martin

ORCID: 0000-0001-8370-7527
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About
Contact & Profiles
Research Areas
  • Autophagy in Disease and Therapy
  • PARP inhibition in cancer therapy
  • CRISPR and Genetic Engineering
  • Microtubule and mitosis dynamics
  • Sarcoma Diagnosis and Treatment
  • DNA Repair Mechanisms
  • Cancer Genomics and Diagnostics
  • Protein Degradation and Inhibitors
  • Epigenetics and DNA Methylation
  • RNA modifications and cancer
  • Acute Myeloid Leukemia Research
  • Biochemical and Molecular Research
  • Cytomegalovirus and herpesvirus research
  • Inflammasome and immune disorders
  • Neurofibromatosis and Schwannoma Cases
  • Law, Rights, and Freedoms
  • Renal and related cancers
  • Kruppel-like factors research
  • Gastrointestinal Tumor Research and Treatment
  • PI3K/AKT/mTOR signaling in cancer
  • interferon and immune responses
  • Mitochondrial Function and Pathology
  • Cancer, Hypoxia, and Metabolism
  • Lung Cancer Treatments and Mutations
  • Neuroblastoma Research and Treatments

Roswell Park Comprehensive Cancer Center
2020-2025

Cancer Genetics (United States)
2020-2022

Hospital Universitario Son Dureta
2008

Institut Català d'Ornitologia
2008

Fundación Instituto Valenciano de Oncología
2008

Marqués de Valdecilla University Hospital
2008

Hospital Clínic de Barcelona
2008

Hospital Universitario Miguel Servet
2008

Hospital Virgen del Camino
2008

Hospital de León
2008

Abstract Triple negative breast cancer (TNBC) is one of the deadliest subtypes cancer, whose high frequency relapse often due to resistance chemotherapy. Here, we identify inosine monophosphate dehydrogenase 2 (IMPDH2) as a contributor doxorubicin resistance, in multiple TNBC models. Analysis publicly available datasets reveals elevated IMPDH2 expression associate with worse overall prognosis clinic, including lower recurrence-free survival post adjuvant/neoadjuvant therapy. Importantly,...

10.1038/s41598-024-85094-5 article EN cc-by Scientific Reports 2025-01-07

Abstract Ewing sarcoma is the second most common bone malignancy in children and adolescents. In recent years, a large body of evidence has emerged that suggests tumors harbor amounts replication stress (RS). CDC7, also known as DDK (DBF4-dependent kinase), serine/threonine kinase involved diverse array cellular functions including regulation DNA initiation activation RS response. Due to DDK’s roles during replication, coupled with fact there an increased level within tumors, we hypothesized...

10.1038/s41420-022-00877-x article EN cc-by Cell Death Discovery 2022-02-26

Abstract Triple-negative breast cancer (TNBC) is one of the most aggressive types cancer. Despite decades intense investigation, treatment options remain limited, and rapid recurrence with distant metastases remains a significant challenge. Cancer cell-intrinsic production cytokines such as type I interferons (IFN-I) known potent modulator response to therapy in many cancers, including TNBC, can influence therapeutic outcome. Here, we report that, TNBC systems, aryl hydrocarbon receptor...

10.1038/s41598-024-54732-3 article EN cc-by Scientific Reports 2024-03-08

Ewing sarcoma is an aggressive childhood cancer for which treatment options remain limited and toxic. There urgent need the identification of novel therapeutic strategies. Our group has recently shown that cells rely on S-phase kinase cell division cycle 7 (CDC7) DBF4-dependent (DDK) to maintain replication rates viability DDK inhibition causes increase in phosphorylation CDK1 a significant delay mitotic entry. Here, we expand our previous findings show inhibitor–induced entry dependent upon...

10.1158/2767-9764.crc-22-0130 article EN cc-by Cancer Research Communications 2022-06-13

Undifferentiated soft tissue sarcomas (UDSTSs) are a group of mesenchymal tumors that remain diagnostic challenge because their morphologic heterogeneity and unclear histologic origin (Peters et al., Mod Pathol 28: 575 [2015]). In this case report, we present the first multiomics molecular signature for BCOR–CCNB3 sarcoma (BCS) includes mutation analysis, gene expression, DNA methylation, micro RNA (miRNA) expression. We identify paucity additional mutations in tumor detail there is...

10.1101/mcs.a005942 article EN Molecular Case Studies 2021-11-24

Abstract Ewing sarcoma is the second most common bone malignancy in children and adolescents. Patients with upfront metastatic or recurrent disease have poor outcomes 5-year survival rates of <30%. CDC7, also known as DDK (DBF4-dependent kinase), a serine-threonine kinase that, coordination its activation subunit ASK (or DBF4), involved diverse array cellular functions including regulation DNA replication initiation stress response. Due to DDK’s roles during replication, coupled an...

10.1101/2021.11.02.466939 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2021-11-04

<div><p>Ewing sarcoma is an aggressive childhood cancer for which treatment options remain limited and toxic. There urgent need the identification of novel therapeutic strategies. Our group has recently shown that Ewing cells rely on S-phase kinase cell division cycle 7 (CDC7) DBF4-dependent (DDK) to maintain replication rates viability DDK inhibition causes increase in phosphorylation CDK1 a significant delay mitotic entry. Here, we expand our previous findings show...

10.1158/2767-9764.c.6550758 preprint EN 2023-04-04

<div><p>Ewing sarcoma is an aggressive childhood cancer for which treatment options remain limited and toxic. There urgent need the identification of novel therapeutic strategies. Our group has recently shown that Ewing cells rely on S-phase kinase cell division cycle 7 (CDC7) DBF4-dependent (DDK) to maintain replication rates viability DDK inhibition causes increase in phosphorylation CDK1 a significant delay mitotic entry. Here, we expand our previous findings show...

10.1158/2767-9764.c.6550758.v1 preprint EN 2023-04-04

<p>This figure includes supplementary data to show that CDC7 (DDK) inhibition delays mitotic entry in Ewing cells.</p>

10.1158/2767-9764.22544838 preprint EN cc-by 2023-04-04

<p>This figure includes supplementary data that shows CDC7 (DDK) inhibition increases pCDK1 (Y15) and causes a cell cycle accumulation in Ewing cells.</p>

10.1158/2767-9764.22544835 preprint EN cc-by 2023-04-04

<p>This figure includes supplementary data that shows CDK1 inhibition or nocodazole treatment inhibits mitotic entry/progression in Ewing cells.</p>

10.1158/2767-9764.22544832 preprint EN cc-by 2023-04-04

<p>This figure includes supplementary data that shows CDK1 inhibition or nocodazole treatment inhibits mitotic entry/progression in Ewing cells.</p>

10.1158/2767-9764.22544832.v1 preprint EN cc-by 2023-04-04

<p>This figure includes supplementary data that shows CDC7 (DDK) inhibition increases pCDK1 (Y15) and causes a cell cycle accumulation in Ewing cells.</p>

10.1158/2767-9764.22544835.v1 preprint EN cc-by 2023-04-04

<p>This figure includes supplementary data to show that CDC7 (DDK) inhibition delays mitotic entry in Ewing cells.</p>

10.1158/2767-9764.22544838.v1 preprint EN cc-by 2023-04-04

Abstract Ewing Sarcoma is a malignant tumor of the bone and soft tissue that primarily driven by fusion protein EWS-FLI1. With no current targeted therapy, treatment options remain limited toxic. Recent reports have shown tumors harbor large amounts transcription-associated replication stress this offers an attractive therapeutic intervention point. Our group has inhibition kinase complex DDK (CDC7-DBF4) results in apoptosis significant reduction cell viability EWS-FLI1-harboring Ewing's...

10.1158/1538-7445.am2021-2051 article EN Cancer Research 2021-07-01

10.2307/1599205 article EN The University of Chicago Law Review 1977-01-01
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