Tumor- and organ-dependent infiltration by myeloid-derived suppressor cells

Younos, Ibrahim; Donkor, Moses; Hoke, Traci; Dafferner, Alicia J.; Samson, Holly; Westphal, Sherry; Talmadge, James E.

doi:10.1016/j.intimp.2011.02.021

Cited by 71 publications

(72 citation statements)

References 65 publications

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“…It was maintained as an adherent monolayer [5,6,10] by passage with DMEM containing 10% heat-inactivated fetal bovine serum and cells prepared for injection as previously described [22].…”

Section: Tumor Cell Linementioning

confidence: 99%

“…The mice were sacrificed, and the lungs, liver, thymi, BM, spleen, and tumors aseptically removed. Non-parenchymal cells (NPCs) from the tumor, liver, and lungs were isolated following collagenase-deoxyribonuclease dissociation and Ficoll-Hypaque (FH) density gradient centrifugation [5,10,23,24]. White blood cell numbers were determined with a Scil Vet ABC Hematology Analyzer (Scil, Grayslake, IL).…”

Section: Cell Isolationmentioning

confidence: 99%

“…The frequency of targeted cell subsets was determined with FlowJo software (TreeStar, Ashland, OR). For MDSC analysis, we excluded lymphocytes based on FS ×SS gated cells prior to analysis [5,10,23,24]. Trafficking and cellular proliferation were assessed based on the numbers, frequencies, and cellular divisions, based on a decimal label on CFSE-labeled cells and the average number of cells/generation.…”

Section: Flow Cytometric (Fcm) Analysismentioning

confidence: 99%

“…Tumor-associated proliferation, circulation, and organ/tumor infiltration by MPCs result in increased numbers of immunosuppressive cells [3][4][5][6][7] and poor clinical outcomes in cancer patients [6,8]. MDSCs, a subset of MPCs, have emerged as a key mediator of immunosuppression in mice [3][4][5] and humans, [6,9] can suppress T-cell numbers and function and inhibit the induction of antitumor immunity [5,[9][10][11][12]. In addition, MDSCs have been associated with a number of non-immunological functions, including angiogenesis, and tumor cell invasion and metastases [13].…”

Section: Introductionmentioning

confidence: 99%

“…In naïve mice, MPCs expand primarily in the BM; however, they can also proliferate at extramedullary sites [4,[14][15][16]. Tumor-associated EMH [5,17] is affiliated with increased numbers of MPCs in the circulation, spleen, liver and infiltration of tumors [12,17,18]. During stress, medullary MPCs mobilize into the PB, traffic through the circulation, and arrest and proliferate primarily in the spleen and liver [10,19].…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Tumor regulation of myeloid-derived suppressor cell proliferation and trafficking

Younos

Dafferner

Gülen

et al. 2012

International Immunopharmacology

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“…It was maintained as an adherent monolayer [5,6,10] by passage with DMEM containing 10% heat-inactivated fetal bovine serum and cells prepared for injection as previously described [22].…”

Section: Tumor Cell Linementioning

confidence: 99%

Section: Cell Isolationmentioning

confidence: 99%

Section: Flow Cytometric (Fcm) Analysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Tumor regulation of myeloid-derived suppressor cell proliferation and trafficking

Younos

Dafferner

Gülen

et al. 2012

International Immunopharmacology

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G‐CSF/GM‐CSF‐induced hematopoietic dysregulation in the progression of solid tumors

Liu

Hoffman

et al. 2022

FEBS Open Bio

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There are two types of abnormal hematopoiesis in solid tumor occurrence and treatment: pathological hematopoiesis, and myelosuppression induced by radiotherapy and chemotherapy. In this review we primarily focus on the abnormal pathological hematopoietic differentiation in cancer induced by tumor‐released granulocyte colony‐stimulating factor (G‐CSF) and granulocyte‐macrophage colony‐stimulating factor (GM‐CSF). As key factors in hematopoietic development, G‐CSF/GM‐CSF are well‐known facilitators of myelopoiesis and mobilization of hematopoietic stem cells (HSCs). In addition, these two cytokines can also promote or inhibit tumors, dependent on tumor type. In multiple cancer types, hematopoiesis is greatly enhanced and abnormal lineage differentiation is induced by these two cytokines. Here, dysregulated hematopoiesis induced by G‐CSF/GM‐CSF in solid tumors and its mechanism are summarized, and the prognostic value of G‐CSF/GM‐CSF‐associated dysregulated hematopoiesis for tumor metastasis is also briefly highlighted.

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A role for G‐CSF and GM‐CSF in nonmyeloid cancers

Aliper¹,

et al. 2014

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Granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) modulate progression of certain solid tumors. The G-CSF- or GM-CSF-secreting cancers, albeit not very common are, however, among the most rapidly advancing ones due to a cytokine-mediated immune suppression and angiogenesis. Similarly, de novo angiogenesis and vasculogenesis may complicate adjuvant use of recombinant G-CSF or GM-CSF thus possibly contributing to a cancer relapse. Rapid diagnostic tools to differentiate G-CSF- or GM-CSF-secreting cancers are not well developed therefore hindering efforts to individualize treatments for these patients. Given an increasing utilization of adjuvant G-/GM-CSF in cancer therapy, we aimed to summarize recent studies exploring their roles in pathophysiology of solid tumors and to provide insights into some complexities of their therapeutic applications.

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Tumor- and organ-dependent infiltration by myeloid-derived suppressor cells

Cited by 71 publications

References 65 publications

Tumor regulation of myeloid-derived suppressor cell proliferation and trafficking

Tumor regulation of myeloid-derived suppressor cell proliferation and trafficking

G‐CSF/GM‐CSF‐induced hematopoietic dysregulation in the progression of solid tumors

A role for G‐CSF and GM‐CSF in nonmyeloid cancers

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