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Rudolfsson, Stina H.
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Publications (10 of 25) Show all publications
Mu, Y., Wallenius, A., Zang, G., Zhu, S., Rudolfsson, S. H., Aripaka, K., . . . Landström, M. (2024). The TβRI promotes migration and metastasis through thrombospondin 1 and ITGAV in prostate cancer cells. Oncogene
Open this publication in new window or tab >>The TβRI promotes migration and metastasis through thrombospondin 1 and ITGAV in prostate cancer cells
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2024 (English)In: Oncogene, ISSN 0950-9232, E-ISSN 1476-5594Article in journal (Refereed) Epub ahead of print
Abstract [en]

TGFβ potently modifies the extracellular matrix (ECM), which is thought to favor tumor cell invasion. However, the mechanism whereby the cancer cells employ the ECM proteins to facilitate their motility is largely unknown. In this study we used RNA-seq and proteomic analysis to examine the proteins secreted by castration-resistant prostate cancer (CRPC) cells upon TGFβ treatment and found that thrombospondin 1 (THBS1) was observed to be one of the predominant proteins. The CRISPR Cas9, or siRNA techniques was used to downregulate TGFβ type I receptor (TβRI) to interfere with TGFβ signaling in various cancer cells in vitro. The interaction of ECM proteins with the TβRI in the migratory prostate cancer cells in response to TGFβ1 was demonstrated by several different techniques to reveal that THBS1 mediates cell migration by interacting with integrin subunit alpha V (ITGAV) and TβRI. Deletion of TβRI or THBS1 in cancer cells prevented their migration and invasion. THBS1 belongs to a group of tumorigenic ECM proteins induced via TGFβ signaling in CRPC cells, and high expression of THBS1 in human prostate cancer tissues correlated with the degree of malignancy. TGFβ-induced production of THBS1 through TβRI facilitates the invasion and metastasis of CRPC cells as shown in vivo xenograft animal experiments.

Place, publisher, year, edition, pages
Springer Nature, 2024
National Category
Cell and Molecular Biology Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-230159 (URN)10.1038/s41388-024-03165-3 (DOI)001317360000001 ()2-s2.0-85204498915 (Scopus ID)
Funder
Region Västerbotten, RV 996277Region Västerbotten, RV 993591Umeå University, 982061Cancerforskningsfonden i Norrland, LP20-2236ProstatacancerförbundetSwedish Cancer Society, 23 2902 Pj 01 HSwedish Research Council, 2023-02370Familjen Erling-Perssons StiftelseCancerforskningsfonden i Norrland, LP20-2255Cancerforskningsfonden i Norrland, LP24-2369
Available from: 2024-10-02 Created: 2024-10-02 Last updated: 2024-10-02
Welén, K., Rosendal, E., Gisslén, M., Lenman, A., Freyhult, E., Fonseca Rodriguez, O., . . . Josefsson, A. (2022). A Phase 2 Trial of the Effect of Antiandrogen Therapy on COVID-19 Outcome: No Evidence of Benefit, Supported by Epidemiology and In Vitro Data. European Urology, 81(3), 285-293
Open this publication in new window or tab >>A Phase 2 Trial of the Effect of Antiandrogen Therapy on COVID-19 Outcome: No Evidence of Benefit, Supported by Epidemiology and In Vitro Data
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2022 (English)In: European Urology, ISSN 0302-2838, E-ISSN 1873-7560, Vol. 81, no 3, p. 285-293Article in journal (Refereed) Published
Abstract [en]

Background: Men are more severely affected by COVID-19. Testosterone may influence SARS-CoV-2 infection and the immune response.

Objective: To clinically, epidemiologically, and experimentally evaluate the effect of antiandrogens on SARS-CoV-2 infection.

Designs, settings, and participants: A randomized phase 2 clinical trial (COVIDENZA) enrolled 42 hospitalized COVID-19 patients before safety evaluation. We also conducted a population-based retrospective study of 7894 SARS-CoV-2–positive prostate cancer patients and an experimental study using an air-liquid interface three-dimensional culture model of primary lung cells.

Intervention: In COVIDENZA, patients were randomized 2:1 to 5 d of enzalutamide or standard of care.

Outcome measurements: The primary outcomes in COVIDENZA were the time to mechanical ventilation or discharge from hospital. The population-based study investigated risk of hospitalization, intensive care, and death from COVID-19 after androgen inhibition.

Results and limitations: Enzalutamide-treated patients required longer hospitalization (hazard ratio [HR] for discharge from hospital 0.43, 95% confidence interval [CI] 0.20–0.93) and the trial was terminated early. In the epidemiological study, no preventive effects were observed. The frail population of patients treated with androgen deprivation therapy (ADT) in combination with abiraterone acetate or enzalutamide had a higher risk of dying from COVID-19 (HR 2.51, 95% CI 1.52–4.16). In vitro data showed no effect of enzalutamide on virus replication. The epidemiological study has limitations that include residual confounders.

Conclusions: The results do not support a therapeutic effect of enzalutamide or preventive effects of bicalutamide or ADT in COVID-19. Thus, these antiandrogens should not be used for hospitalized COVID-19 patients or as prevention for COVID-19. Further research on these therapeutics in this setting are not warranted.

Patient summary: We studied whether inhibition of testosterone could diminish COVID-19 symptoms. We found no evidence of an effect in a clinical study or in epidemiological or experimental investigations. We conclude that androgen inhibition should not be used for prevention or treatment of COVID-19.

Place, publisher, year, edition, pages
Elsevier, 2022
Keywords
COVID-19, SARS-CoV-2, Antiandrogen, Randomized trial, Enzalutamide, Bicalutamide, Androgen deprivation therapy
National Category
Cancer and Oncology Public Health, Global Health, Social Medicine and Epidemiology Urology and Nephrology Infectious Medicine
Identifiers
urn:nbn:se:umu:diva-190911 (URN)10.1016/j.eururo.2021.12.013 (DOI)000809752100020 ()2-s2.0-85122412349 (Scopus ID)
Funder
Knut and Alice Wallenberg Foundation, 2020.0182ProstatacancerförbundetSwedish Cancer Society, 2017/478Swedish Cancer Society, 20 1055 PjFSwedish Heart Lung Foundation, 20200385Region Västerbotten, RV-836351Region Västerbotten, RV-939769
Available from: 2022-01-02 Created: 2022-01-02 Last updated: 2023-04-25Bibliographically approved
Halin Bergström, S., Rudolfsson, S. H., Lundholm, M., Josefsson, A., Wikström, P. & Bergh, A. (2021). High-grade tumours promote growth of other less-malignant tumours in the same prostate. Journal of Pathology, 253(4), 396-403
Open this publication in new window or tab >>High-grade tumours promote growth of other less-malignant tumours in the same prostate
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2021 (English)In: Journal of Pathology, ISSN 0022-3417, E-ISSN 1096-9896, Vol. 253, no 4, p. 396-403Article in journal (Refereed) Published
Abstract [en]

Prostate cancer is a multifocal disease, but if and how individual prostate tumours influence each other is largely unknown. We therefore explored signs of direct or indirect tumour–tumour interactions in experimental models and patient samples. Low‐metastatic AT1 and high‐metastatic MatLyLu (MLL) Dunning rat prostate cancer cells were injected into separate lobes of the ventral prostate of immunocompetent rats. AT1 tumours growing in the same prostate as MLL tumours had increased tumour size and proliferation compared to AT1 tumours growing alone. In addition, the vasculature and macrophage density surrounding the AT1 tumours were increased by MLL tumour closeness. In patient prostatectomy samples, selected to contain an index tumour [tumour with the highest grade, International Society of Urological Pathology (ISUP) grade 1, 2, 3 or 4] and a low‐grade satellite tumour (ISUP grade 1), cell proliferation in low‐grade satellite tumours gradually increased with increasing histological grade of the index tumour. The density of blood vessels and CD68+ macrophages also increased around the low‐grade satellite tumour if a high‐grade index tumour was present. This suggests that high‐grade tumours, by changing the prostate microenvironment, may increase the aggressiveness of low‐grade lesions in the organ. Future studies are needed to explore the mechanisms behind tumour–tumour interactions and their clinical importance.

Place, publisher, year, edition, pages
John Wiley & Sons, 2021
Keywords
high-grade prostate cancer, low-grade prostate cancer, angiogenesis, tumour-associated macrophages, tumour instigator, Ki67, Factor VIII, CD68, experimental rat prostate tumour model, multifocal primary prostate cancer
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-180651 (URN)10.1002/path.5604 (DOI)000611651900001 ()33330991 (PubMedID)2-s2.0-85099818415 (Scopus ID)
Funder
Swedish Cancer SocietyCancerforskningsfonden i NorrlandSwedish Research Council
Available from: 2021-02-24 Created: 2021-02-24 Last updated: 2021-07-02Bibliographically approved
Halin Bergström, S., Rudolfsson, S. H. & Bergh, A. (2016). Rat Prostate Tumor Cells Progress in the Bone Microenvironment to a Highly Aggressive Phenotype. Neoplasia, 18(3), 152-161
Open this publication in new window or tab >>Rat Prostate Tumor Cells Progress in the Bone Microenvironment to a Highly Aggressive Phenotype
2016 (English)In: Neoplasia, ISSN 1522-8002, E-ISSN 1476-5586, Vol. 18, no 3, p. 152-161Article in journal (Refereed) Published
Abstract [en]

Prostate cancer generally metastasizes to bone, and most patients have tumor cells in their bone marrow already at diagnosis. Tumor cells at the metastatic site may therefore progress in parallel with those in the primary tumor. Androgen deprivation therapy is often the first-line treatment for clinically detectable prostate cancer bone metastases. Although the treatment is effective, most metastases progress to a castration-resistant and lethal state. To examine metastatic progression in the bone microenvironment, we implanted androgen-sensitive, androgen receptor-positive, and relatively slow-growing Dunning G (G) rat prostate tumor cells into the tibial bone marrow of fully immune-competent Copenhagen rats. We show that tumor establishment in the bone marrow was reduced compared with the prostate, and whereas androgen deprivation did not affect tumor establishment or growth in the bone, this was markedly reduced in the prostate. Moreover, we found that, with time, G tumor cells in the bone microenvironment progress to a more aggressive phenotype with increased growth rate, reduced androgen sensitivity, and increased metastatic capacity. Tumor cells in the bone marrow encounter lower androgen levels and a higher degree of hypoxia than at the primary site, which may cause high selective pressures and eventually contribute to the development of a new and highly aggressive tumor cell phenotype. It is therefore important to specifically study progression in bone metastases. This tumor model could be used to increase our understanding of how tumor cells adapt in the bone microenvironment and may subsequently improve therapy strategies for prostate metastases in bone.

Place, publisher, year, edition, pages
Elsevier, 2016
National Category
Medical Bioscience
Identifiers
urn:nbn:se:umu:diva-119077 (URN)10.1016/j.neo.2016.01.007 (DOI)000372308400003 ()2-s2.0-84963972119 (Scopus ID)
Available from: 2016-04-15 Created: 2016-04-11 Last updated: 2023-03-24Bibliographically approved
Hammarsten, P., Winther, J., Rudolfsson, S. H., Häggström, J., Karalija, A., Egevad, L., . . . Fowler, C. (2014). ErbB2 Receptor Immunoreactivity in Prostate Cancer: Relationship to the Androgen Receptor, Disease Severity at Diagnosis and Disease Outcome. PLOS ONE, 9(9), Article ID e105063.
Open this publication in new window or tab >>ErbB2 Receptor Immunoreactivity in Prostate Cancer: Relationship to the Androgen Receptor, Disease Severity at Diagnosis and Disease Outcome
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2014 (English)In: PLOS ONE, E-ISSN 1932-6203, Vol. 9, no 9, article id e105063Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: ErbB2 is a member of the epidermal growth factor family of tyrosine kinases that is centrally involved in the pathogenesis of prostate cancer and several studies have reported that a high expression of this protein has prognostic value. In the present study, we have investigated whether tumour ErbB2 immunoreactivity (ErbB2-IR) has clinically useful prognostic value, i.e. that it provides additional prognostic information to that provided by routine clinical tests (Gleason score, tumour stage).

METHODOLOGY/PRINCIPAL FINDINGS: ErbB2-IR was measured in a well-characterised tissue microarray of tumour and non-malignant samples obtained at diagnosis. Additionally, mRNA levels of ErbB2-IR in the prostate were determined in the rat following manipulation of circulating androgen levels. Tumour ErbB2-IR was significantly associated with the downstream signalling molecule phosphorylated-Akt and with the cell proliferation marker Ki-67. The significant association of tumour ErbB2-IR with the Gleason score at diagnosis was lost when controlled for the association of both parameters with Ki-67. In the rat prostate, mRNA for ErbB2 was inversely associated with circulating androgen levels. There was no association between ErbB2-IR and the androgen receptor (AR)-IR in the tumours, but an interaction between the two parameters was seen with respect to their association with the tumour stage. Tumour ErbB2-IR was confirmed to be a prognostic marker for disease-specific survival, but it did not provide significant additive information to the Gleason score or to Ki-67.

CONCLUSIONS/SIGNIFICANCE: It is concluded that tumour ErbB2-IR is of limited clinical value as a prognostic marker to aid treatment decisions, but could be of pathophysiological importance in prostate cancer.

Place, publisher, year, edition, pages
Public Library Science, 2014
National Category
Immunology in the medical area Other Basic Medicine
Identifiers
urn:nbn:se:umu:diva-93295 (URN)10.1371/journal.pone.0105063 (DOI)000341774300001 ()25215939 (PubMedID)2-s2.0-84933059923 (Scopus ID)
Available from: 2014-09-16 Created: 2014-09-16 Last updated: 2023-03-24Bibliographically approved
Rudolfsson, S. (2013). Att hämma tumörtillväxt (1ed.). In: Mattias Grundström Mitz och Lena Åminne (Ed.), Cancerforskning på nya vägar: en bok från Forskningens dag 2013, Medicinska fakulteten vid Umeå universitet (pp. 69-76). Umeå: Umeå universitet
Open this publication in new window or tab >>Att hämma tumörtillväxt
2013 (Swedish)In: Cancerforskning på nya vägar: en bok från Forskningens dag 2013, Medicinska fakulteten vid Umeå universitet / [ed] Mattias Grundström Mitz och Lena Åminne, Umeå: Umeå universitet , 2013, 1, p. 69-76Chapter in book (Other (popular science, discussion, etc.))
Place, publisher, year, edition, pages
Umeå: Umeå universitet, 2013 Edition: 1
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-87786 (URN)978-91-7459-805-6 (ISBN)
Available from: 2014-04-09 Created: 2014-04-09 Last updated: 2018-06-08Bibliographically approved
Jernberg, E., Thysell, E., Bovinder Ylitalo, E., Rudolfsson, S., Crnalic, S., Widmark, A., . . . Wikström, P. (2013). Characterization of prostate cancer bone metastases according to expression levels of steroidogenic enzymes and androgen receptor splice variants. PLOS ONE, 8(11), e77407
Open this publication in new window or tab >>Characterization of prostate cancer bone metastases according to expression levels of steroidogenic enzymes and androgen receptor splice variants
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2013 (English)In: PLOS ONE, E-ISSN 1932-6203, Vol. 8, no 11, p. e77407-Article in journal (Refereed) Published
Abstract [en]

Background: Intra-tumoral steroidogenesis and constitutive androgen receptor (AR) activity have been associated withcastration-resistant prostate cancer (CRPC). This study aimed to examine if CRPC bone metastases expressed higher levels ofsteroid-converting enzymes than untreated bone metastases. Steroidogenic enzyme levels were also analyzed in relation toexpression of constitutively active AR variants (AR-Vs) and to clinical and pathological variables.

Methodology/Principal Findings: Untreated, hormone-naıve (HN, n = 9) and CRPC bone metastases samples (n = 45) wereobtained from 54 patients at metastasis surgery. Non-malignant and malignant prostate samples were acquired from 13prostatectomy specimens. Transcript and protein levels were analyzed by real-time RT-PCR, immunohistochemistry andimmunoblotting. No differences in steroidogenic enzyme levels were detected between CRPC and HN bone metastases.Significantly higher levels of SRD5A1, AKR1C2, AKR1C3, and HSD17B10 mRNA were however found in bone metastases thanin non-malignant and/or malignant prostate tissue, while the CYP11A1, CYP17A1, HSD3B2, SRD5A2, and HSD17B6 mRNAlevels in metastases were significantly lower. A sub-group of metastases expressed very high levels of AKR1C3, which wasnot due to gene amplification as examined by copy number variation assay. No association was found between AKR1C3expression and nuclear AR staining, tumor cell proliferation or patient outcome after metastases surgery. With only oneexception, high AR-V protein levels were found in bone metastases with low AKR1C3 levels, while metastases with highAKR1C3 levels primarily contained low AR-V levels, indicating distinct mechanisms behind castration-resistance in individualbone metastases.

Conclusions/Significance: Induced capacity of converting adrenal-gland derived steroids into more potent androgens wasindicated in a sub-group of PC bone metastases. This was not associated with CRPC but merely with the advanced stage ofmetastasis. Sub-groups of bone metastases could be identified according to their expression levels of AKR1C3 and AR-Vs,which might be of relevance for patient response to 2nd line androgen-deprivation therapy.

Place, publisher, year, edition, pages
Public Library of Science, 2013
Keywords
prostate cancer, bone metastases, androgen receptor splice variants, steroidogenic enzymes
National Category
Basic Medicine Cancer and Oncology
Research subject
molecular medicine (medical sciences)
Identifiers
urn:nbn:se:umu:diva-83840 (URN)10.1371/journal.pone.0077407 (DOI)000327162900006 ()24244276 (PubMedID)2-s2.0-84892421933 (Scopus ID)
Funder
Swedish Research CouncilSwedish Cancer Society
Available from: 2013-12-10 Created: 2013-12-10 Last updated: 2023-03-24Bibliographically approved
Johansson, A., Rudolfsson, S. H., Kilter, S. & Bergh, A. (2011). Targeting castration-induced tumour hypoxia enhances the acute effects of castration therapy in a rat prostate cancer model. BJU International, 107(11), 1818-1824
Open this publication in new window or tab >>Targeting castration-induced tumour hypoxia enhances the acute effects of castration therapy in a rat prostate cancer model
2011 (English)In: BJU International, ISSN 1464-4096, E-ISSN 1464-410X, Vol. 107, no 11, p. 1818-1824Article in journal (Refereed) Published
Abstract [en]

OBJECTIVE: •  To explore the effects of castration therapy, the standard treatment for advanced prostate cancer, in relation to tumour hypoxia and to elicit its importance for the short- and long-term therapeutic response.

MATERIAL AND METHODS: •  We used the androgen-sensitive rat Dunning H prostate tumour model that transiently responds to castration treatment followed by a subsequent relapse, much like the scenario in human patients. •  Tumour tissues were analysed using stereological methods in intact, 1 and 7 days after castration therapy.

RESULTS: •  Hypoxia was transiently up-regulated after castration therapy and correlated with the induction of tumour cell apoptosis. •  When castration therapy was combined with tirapazamine (TPZ), a drug that targets hypoxic cells and the vasculature, the effects on tumour cell apoptosis and tumour volume were enhanced in comparison to either castration or TPZ alone.

CONCLUSION: •  The present study suggests that castration-induced tumour hypoxia is a novel target for therapy.

Keywords
hypoxia;castration;tirapazamine;prostate;Dunning H
National Category
Cell and Molecular Biology
Research subject
Pathology
Identifiers
urn:nbn:se:umu:diva-40758 (URN)10.1111/j.1464-410X.2010.09690.x (DOI)20860653 (PubMedID)2-s2.0-79956370477 (Scopus ID)
Available from: 2011-03-09 Created: 2011-03-09 Last updated: 2023-03-23Bibliographically approved
Hammarsten, P., Karalija, A., Josefsson, A., Rudolfsson, S. H., Wikström, P., Egevad, L., . . . Bergh, A. (2010). Low levels of phosphorylated epidermal growth factor receptor in nonmalignant and malignant prostate tissue predict favorable outcome in prostate cancer patients.. Clinical Cancer Research, 16(4), 1245-1255
Open this publication in new window or tab >>Low levels of phosphorylated epidermal growth factor receptor in nonmalignant and malignant prostate tissue predict favorable outcome in prostate cancer patients.
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2010 (English)In: Clinical Cancer Research, ISSN 1078-0432, E-ISSN 1557-3265, Vol. 16, no 4, p. 1245-1255Article in journal (Refereed) Published
Abstract [en]

PURPOSE: To explore if the expression of phosphorylated epidermal growth factor receptor (pEGFR) in nonmalignant and malignant prostate tissue is a potential prognostic marker for outcome in prostate cancer patients. EXPERIMENTAL DESIGN: We used formalin-fixed tissues obtained through the transurethral resection of the prostate from 259 patients diagnosed with prostate cancer after the transurethral resection of the prostate, and patients were then followed with watchful waiting. Tissue microarrays of nonmalignant and malignant prostate tissue were stained with an antibody against pEGFR. The staining pattern was scored and related to clinicopathologic parameters and to outcome. RESULTS: Low phosphorylation of EGFR in prostate epithelial cells, both in the tumor and surprisingly also in the surrounding nonmalignant tissue, was associated with significantly longer cancer-specific survival in prostate cancer patients. This association remained significant when Gleason score and local tumor stage were added together with pEGFR to a Cox regression model. Tumor epithelial pEGFR immunoreactivity was significantly correlated to tumor cell proliferation, tumor vascular density, and nonmalignant epithelial pEGFR immunoreactivity. Patients with metastases had significantly higher immunoreactivity for tumor and nonmalignant epithelial pEGFR compared with patients without metastases. CONCLUSIONS: Low pEGFR immunoreactivity is associated with the favorable prognosis in prostate cancer patients and may provide information about which patients with Gleason score 6 and 7 tumors that will survive their disease even without treatment. Changes in the nonmalignant tissue adjacent to prostate tumors give prognostic information.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:umu:diva-32701 (URN)10.1158/1078-0432.CCR-09-0103 (DOI)000278545200018 ()20145160 (PubMedID)2-s2.0-76749091149 (Scopus ID)
Available from: 2010-03-22 Created: 2010-03-22 Last updated: 2023-03-24Bibliographically approved
Johansson, A., Rudolfsson, S., Hammarsten, P., Halin, S., Pietras, K., Jones, J., . . . Bergh, A. (2010). Mast cells are novel independent prognostic markers in prostate cancer and represent a target for therapy. American Journal of Pathology, 177(2), 1031-1041
Open this publication in new window or tab >>Mast cells are novel independent prognostic markers in prostate cancer and represent a target for therapy
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2010 (English)In: American Journal of Pathology, ISSN 0002-9440, E-ISSN 1525-2191, Vol. 177, no 2, p. 1031-1041Article in journal (Refereed) Published
Abstract [en]

Mast cells affect growth in various human tumors, but their role in prostate cancer (PC) is unclear. Here, we identify mast cells as independent prognostic markers in PC using a large cohort of untreated PC patients with a long follow-up. By analyzing mast cells in different tissue compartments, our data indicate that intratumoral and peritumoral mast cells have anti- opposed to protumor properties. Intratumoral mast cells negatively regulate angiogenesis and tumor growth, whereas peritumoral mast cells stimulate the expansion of human prostate tumors. We also observed mast cell recruitment particularly to the peritumoral compartment in men during the formation of castrate-resistant prostate tumors. In our ortothopic rat model, mast cells accumulated in the peritumoral tissue where they enhanced angiogenesis and tumor growth. In line with this, prostate mast cells expressed high levels of the angiogenic factor FGF-2. Similar to the situation in men, mast cells infiltrated rat prostate tumors that relapsed after initially effective castration treatment, concurrent with a second wave of angiogenesis and an up-regulation of FGF-2. We conclude that mast cells are novel independent prognostic markers in PC and affect tumor progression in animals and patients. In addition, peritumoral mast cells provide FGF-2 to the tumor micro environment, which may contribute to their stimulating effect on angiogenesis.

National Category
Pathobiology
Research subject
Pathology
Identifiers
urn:nbn:se:umu:diva-40761 (URN)10.2353/ajpath.2010.100070 (DOI)000280894600051 ()20616342 (PubMedID)2-s2.0-77957280758 (Scopus ID)
Available from: 2011-03-09 Created: 2011-03-09 Last updated: 2023-03-24Bibliographically approved
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