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- Månsson, Emeli, et al.
(author)
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Mammographic casting-type calcifications is not a prognostic factor in unifocal small invasive breast cancer : a population-based retrospective cohort study
- 2009
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In: Journal of Surgical Oncology. - : Wiley. - 0022-4790 .- 1096-9098. ; 100:8, s. 670-674
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Journal article (peer-reviewed)abstract
- BACKGROUND AND OBJECTIVES: The role of mammographic casting-type microcalcifications as a prognostic factor in breast cancer has been debated. We studied the relation between mammographic features and prognosis in a population-based cohort. METHODS: In 515 women with 1-15 mm invasive breast cancer mammograms were re-classified according to Tabar et al. The relation to breast cancer death was studied. RESULTS: During the follow-up (median 155 months) 44 of 515 women died from breast cancer. Twenty-nine of 515 presented with casting-type calcifications and three of these died from breast cancer. The adjusted odds ratio for breast cancer death was 1.6 (0.5-5.8) for patients presenting with casting-type calcifications and 4.8 (1.8-12.7) for crushed stone-like (pleomorphic) calcifications using stellate tumors as a reference group. CONCLUSIONS: Except for patients with crushed stone-like microcalcifications breast cancer survival was excellent, 87-95% after 15 years. Casting-type calcifications were not a statistically significant prognostic factor. Tumors with casting-type calcifications were more often of high grade, hormone receptor negative, and HER2 positive but this was not statistically significant either. However, microcalcifications may be more prevalent in tumors with extensive ductal cancer in situ (DCIS) containing multiple foci of invasive cancer and in this study we only included unifocal cancer.
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| 2. |
- Stockfelt, Marit, et al.
(author)
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Activated low-density granulocytes in peripheral and intervillous blood and neutrophil inflammation in placentas from SLE pregnancies
- 2021
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In: Lupus Science and Medicine. - : BMJ. - 2053-8790. ; 8:1
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Journal article (peer-reviewed)abstract
- Objective Women with SLE face an increased risk of adverse pregnancy outcomes compared with healthy women, but the underlying immunological mechanisms are unknown. Given the recognised association of neutrophil activation with SLE pathogenesis, we examined whether there is increased neutrophil activation and inflammation in blood and placenta in SLE relative to healthy pregnancy. Methods At delivery, peripheral blood, maternal-derived intervillous blood and placentas were collected from 12 SLE and 10 healthy control pregnancies. The proportion of low-density granulocytes (LDGs) and the activation status of LDG and normal-density granulocytes were examined with flow cytometry. The chemokines CXCL8 and CXCL1 were quantified with a cytometric bead-based assay and interferon alpha (IFNα) protein levels with a Simoa method. IFNα-stimulated maternal-derived decidual stromal cells were examined for CXCL8 gene expression with qPCR. A pathologist, blinded to the patient background, examined all placentas. Results Women with SLE had significantly higher proportions of LDG in peripheral blood compared with controls (p=0.02), and LDG in both peripheral and intervillous blood were more activated in SLE relative to healthy pregnancies (peripheral blood: p=0.002 and intervillous blood: p=0.05). There were higher levels of CXCL8 and CXCL1 in intervillous compared with peripheral blood in women with SLE (p=0.004 and p=<0.0001, respectively) but not in controls. In SLE pregnancy, IFNα was detectable in 6 out of 10 intervillous blood samples but only in one control. Stimulation with IFNα upregulated CXCL8 gene expression in decidual stromal cells from both SLE and healthy pregnancy. Histological chorioamnionitis was present in 6 out of 12 placentas from women with SLE and in 1 out of 10 controls. Conclusions In women with SLE, locally produced chemokines in the placenta are increased and may attract and activate neutrophils. This in turn could contribute to placental inflammation and dysfunction and increased risk of placenta-related pregnancy complications.
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| 3. |
- Torell, Agnes, 1993, et al.
(author)
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Low-density granulocytes are related to shorter pregnancy duration but not to interferon alpha protein blood levels in systemic lupus erythematosus.
- 2023
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In: Arthritis research & therapy. - : BMC. - 1478-6362 .- 1478-6354. ; 25
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Journal article (peer-reviewed)abstract
- An increased risk of pregnancy complications is seen in women with systemic lupus erythematosus (SLE), but the specific immunopathological drivers are still unclear. Hallmarks of SLE are granulocyte activation, type I interferon (IFN) overproduction, and autoantibodies. Here we examined whether low-density granulocytes (LDG) and granulocyte activation increase during pregnancy, and related the results to IFNα protein levels, autoantibody profile, and gestational age at birth.Repeated blood samples were collected during pregnancy in trimesters one, two, and three from 69 women with SLE and 27 healthy pregnant women (HC). Nineteen of the SLE women were also sampled late postpartum. LDG proportions and granulocyte activation (CD62L shedding) were measured by flow cytometry. Plasma IFNα protein concentrations were quantified by single molecule array (Simoa) immune assay. Clinical data were obtained from medical records.Women with SLE had higher LDG proportions and increased IFNα protein levels compared to HC throughout pregnancy, but neither LDG fractions nor IFNα levels differed during pregnancy compared to postpartum in SLE. Granulocyte activation status was higher in SLE relative to HC pregnancies, and it was increased during pregnancy compared to after pregnancy in SLE. Higher LDG proportions in SLE were associated with antiphospholipid positivity but not to IFNα protein levels. Finally, higher LDG proportions in trimester three correlated independently with lower gestational age at birth in SLE.Our results suggest that SLE pregnancy results in increased peripheral granulocyte priming, and that higher LDG proportions late in pregnancy are related to shorter pregnancy duration but not to IFNα blood levels in SLE.
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