Foetal haemoglobin-blood cells (F-cells) as a feature of embryonic tumours (blastomas)

Wolk, M; Martin, Joanne E.; Nowicki, Michał

doi:10.1038/sj.bjc.6603867

Cited by 10 publications

(7 citation statements)

References 31 publications

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“…That said, the lack of difference in LDH between groups indicates that a significant contribution of the fHbF plasma elevation in some FGR cases could arise through a mechanism of nonmarrow hematopoiesis, independent of mechanical hemolysis. That embryonic tissue itself has an intrinsic capacity for a and g globin production is a finding previously demonstrated in preeclampsia and other syndromes, and our data now supports this notion in FGR (12,43). Finding a reduction in fetal plasma hemopexin in FGR suggests that most of the circulating levels have been depleted through chaperoning fetal heme to the maternal liver.…”

Section: Elevated Fhbf In the Fetoplacental Circulation And Heme Handsupporting

confidence: 88%

Cell free hemoglobin in the fetoplacental circulation: a novel cause of fetal growth restriction?

et al. 2018

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Cell free hemoglobin impairs vascular function and blood flow in adult cardiovascular disease. In this study, we investigated the hypothesis that free fetal hemoglobin (fHbF) compromises vascular integrity and function in the fetoplacental circulation, contributing to the increased vascular resistance associated with fetal growth restriction (FGR). Women with normal and FGR pregnancies were recruited and their placentas collected freshly postpartum. FGR fetal capillaries showed evidence of erythrocyte vascular packing and extravasation. Fetal cord blood fHbF levels were higher in FGR than in normal pregnancies ( P < 0.05) and the elevation of fHbF in relation to heme oxygenase-1 suggests a failure of expected catabolic compensation, which occurs in adults. During ex vivo placental perfusion, pathophysiological fHbF concentrations significantly increased fetal-side microcirculatory resistance ( P < 0.05). fHbF sequestered NO in acute and chronic exposure models ( P < 0.001), and fHbF-primed placental endothelial cells developed a proinflammatory phenotype, demonstrated by activation of NF-κB pathway, generation of IL-1α and TNF-α (both P < 0.05), uncontrolled angiogenesis, and disruption of endothelial cell flow alignment. Elevated fHbF contributes to increased fetoplacental vascular resistance and impaired endothelial protection. This unrecognized mechanism for fetal compromise offers a novel insight into FGR as well as a potential explanation for associated poor fetal outcomes such as fetal demise and stillbirth.-Brook, A., Hoaksey, A., Gurung, R., Yoong, E. E. C., Sneyd, R., Baynes, G. C., Bischof, H., Jones, S., Higgins, L. E., Jones, C., Greenwood, S. L., Jones, R. L., Gram, M., Lang, I., Desoye, G., Myers, J., Schneider, H., Hansson, S. R., Crocker, I. P., Brownbill, P. Cell free hemoglobin in the fetoplacental circulation: a novel cause of fetal growth restriction?

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Section: Elevated Fhbf In the Fetoplacental Circulation And Heme Handsupporting

confidence: 88%

Cell free hemoglobin in the fetoplacental circulation: a novel cause of fetal growth restriction?

et al. 2018

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“…This was serologically demonstrated in lymphoma, ovarian cancer, brain cancer and other cancers by a high plasma HbF concentration independent of the whole blood concentration ( Wolk et al , 1999 ). The same was also immunohistochemically shown in colorectal tumours ( Wolk et al , 2006 ), as well as in blastomas ( Wolk et al , 2007 ), by high concentrations of HbF erythroid cells, distributed as separated clusters rather than mixed with the normal erythrocytes, in blood vessels. To investigate this trait further, we decided to examine HbF in transitional cell carcinoma (TCC) of the urinary bladder in relation to the grade and stage of the disease.…”

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confidence: 56%

Fetal haemopoiesis marking low-grade urinary bladder cancer

Wolk

Martin

2012

Br J Cancer

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Background: The immunohistochemical features of fetal haemoglobin cells and their distribution patterns in solid tumours, such as colorectal cancer and blastomas, suggest that fetal haemopoiesis may take place in these tumour tissues. These locally highly concentrated fetal haemoglobin (HbF) cells may promote tumour growth by providing a more efficient oxygen supply. Methods and results: Biomarkers of HbF were checked in transitional cell carcinoma (TCC) of the urinary bladder, assessing this as a new parameter for disease management. Fetal haemoglobin was immunohistochemically examined in tumours from 60 patients with TCC of the bladder. Fetal haemoglobin erythrocytes and erythroblasts were mainly clonally distributed in proliferating blood vessels and not mixed with normal haemoglobin erythrocytes. The proportion of such HbF blood vessels could reach more than half of the total number of vessels. There were often many HbF erythroblasts distributed in one-cell or two-cell capillaries and present as 5–15% of cells in multi-cell vessels. This suggests a local proliferation of HbF-cell progenitors. Fetal haemoglobin cells were prominently marking lower grades of tumours, as 76% ( n =21) of the patients with G1pTa were HbF+, whereas only 6.7% ( n =30) of the patients with G3pT1-pT2a were HbF+. Conclusion: Our results suggest that HbF, besides being a potential new marker for early tumour detection, might be an essential factor of early tumour development, as in fetal life. Inhibiting HbF upregulation may provide a therapeutic target for the inhibition of tumour growth.

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“…Hematopoietic cells in the TME can be differentiated by specific gene expression, as shown by Chifman et al by analyzing microarray expression datasets [90]. Regarding red blood cell hematopoiesis, the ability of cancer cells to generate blood cells positive for fetal hemoglobin (HbF) within solid tumors has been proven [91][92][93]. Fetal hemoglobin supplies the tumor with oxygen and supporting tumor growth.…”

Section: Hematopoiesis From Solid Cancer Stem Cellsmentioning

confidence: 99%

Blood and Cancer: Cancer Stem Cells as Origin of Hematopoietic Cells in Solid Tumor Microenvironments

Hassan

Seno

2020

Cells

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The concepts of hematopoiesis and the generation of blood and immune cells from hematopoietic stem cells are some steady concepts in the field of hematology. However, the knowledge of hematopoietic cells arising from solid tumor cancer stem cells is novel. In the solid tumor microenvironment, hematopoietic cells play pivotal roles in tumor growth and progression. Recent studies have reported that solid tumor cancer cells or cancer stem cells could differentiate into hematopoietic cells. Here, we discuss efforts and research that focused on the presence of hematopoietic cells in tumor microenvironments. We also discuss hematopoiesis from solid tumor cancer stem cells and clarify the notion of differentiation of solid tumor cancer stem cells into non-cancer hematopoietic stem cells.

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Foetal haemoglobin-blood cells (F-cells) as a feature of embryonic tumours (blastomas)

Cited by 10 publications

References 31 publications

Cell free hemoglobin in the fetoplacental circulation: a novel cause of fetal growth restriction?

Cell free hemoglobin in the fetoplacental circulation: a novel cause of fetal growth restriction?

Fetal haemopoiesis marking low-grade urinary bladder cancer

Blood and Cancer: Cancer Stem Cells as Origin of Hematopoietic Cells in Solid Tumor Microenvironments

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