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  • 1.
    Bharadwaj, Mausumi
    et al.
    Division of Molecular Genetics & Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), NOIDA, India.
    Hussain, Showket
    Division of Molecular Genetics & Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), NOIDA, India.
    Tripathi, Richa
    Division of Molecular Genetics & Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), NOIDA, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Mehrotra, Ravi
    Division of Cytopathology, Institute of Cytology & Preventive Oncology (ICMR), NOIDA, India.
    Human Papillomavirus (HPV): Diagnosis and Treatment2014In: Animal Biotechnology: Models in Discovery and Translation / [ed] Ashish Verma & Anchal Singh, Elsevier, 2014, p. 95-120Chapter in book (Refereed)
  • 2.
    Carlsson, Jessica
    et al.
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Davidsson, Sabina
    Orebro Univ Hosp, Dept Urol, Orebro, Sweden / Univ Orebro, Sch Hlth & Med Sci, Orebro, Sweden.
    Helenius, Gisela
    Orebro Univ Hosp, Dept Lab Med, Orebro, Sweden.
    Karlsson, Mats
    Orebro Univ Hosp, Dept Lab Med, Orebro, Sweden.
    Lubovac, Zelmina
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Andren, Ove
    Orebro Univ Hosp, Dept Urol, Orebro, Sweden .
    Olsson, Björn
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Klinga-Levan, Karin
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    A miRNA expression signature that separates between normal and malignant prostate tissues2011In: Cancer Cell International, ISSN 1475-2867, E-ISSN 1475-2867, Vol. 11, p. 14-Article in journal (Refereed)
    Abstract [en]

    Background: MicroRNAs (miRNAs) constitute a class of small non-coding RNAs that post-transcriptionally regulate genes involved in several key biological processes and thus are involved in various diseases, including cancer. In this study we aimed to identify a miRNA expression signature that could be used to separate between normal and malignant prostate tissues. Results: Nine miRNAs were found to be differentially expressed (p < 0.00001). With the exception of two samples, this expression signature could be used to separate between the normal and malignant tissues. A cross-validation procedure confirmed the generality of this expression signature. We also identified 16 miRNAs that possibly could be used as a complement to current methods for grading of prostate tumor tissues. Conclusions: We found an expression signature based on nine differentially expressed miRNAs that with high accuracy (85%) could classify the normal and malignant prostate tissues in patients from the Swedish Watchful Waiting cohort. The results show that there are significant differences in miRNA expression between normal and malignant prostate tissue, indicating that these small RNA molecules might be important in the biogenesis of prostate cancer and potentially useful for clinical diagnosis of the disease.

  • 3.
    Chaudhari, Aditi
    et al.
    University of Gothenburg.
    Ejeskär, Katarina
    University of Skövde, School of Health and Education. University of Skövde, Health and Education.
    Wettergren, Yvonne
    University of Gothenburg, Sahlgrenska University Hospital/Östra.
    Kahn, Ronald
    Joslin Diabetes Center and Harvard Medical School, United States.
    Rotter Sopasakis, Victoria
    University of Gothenburg / Joslin Diabetes Center and Harvard Medical School, United states.
    Hepatic deletion of p110α and p85α results in insulin resistance despite sustained IRS1-associated phosphatidylinositol kinase activity2017In: F1000 Research, E-ISSN 2046-1402, Vol. 6, article id 1600Article in journal (Refereed)
    Abstract [en]

    Background: Class IA phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) is an integral mediator of insulin signaling. The p110 catalytic and p85 regulatory subunits of PI3K are the products of separate genes, and while they come together to make the active heterodimer, they have opposing roles in insulin signaling and action. Deletion of hepatic p110α results in an impaired insulin signal and severe insulin resistance, whereas deletion of hepatic p85α results in improved insulin sensitivity due to sustained levels of phosphatidylinositol (3,4,5)-trisphosphate. Here, we created mice with combined hepatic deletion of p110α and p85α (L-DKO) to study the impact on insulin signaling and whole body glucose homeostasis.Methods: Six-week old male flox control and L-DKO mice were studied over a period of 18 weeks, during which weight and glucose levels were monitored, and glucose tolerance tests, insulin tolerance test and pyruvate tolerance test were performed. Fasting insulin, insulin signaling mediators, PI3K activity and insulin receptor substrate (IRS)1-associated phosphatidylinositol kinase activity were examined at 10 weeks. Liver, muscle and white adipose tissue weight was recorded at 10 weeks and 25 weeks.Results: The L-DKO mice showed a blunted insulin signal downstream of PI3K, developed markedly impaired glucose tolerance, hyperinsulinemia and had decreased liver and adipose tissue weights. Surprisingly, however, these mice displayed normal hepatic glucose production, normal insulin tolerance, and intact IRS1-associated phosphatidylinositol kinase activity without compensatory upregulated signaling of other classes of PI3K.Conclusions: The data demonstrate an unexpectedly overall mild metabolic phenotype of the L-DKO mice, suggesting that lipid kinases other than PI3Ks might partially compensate for the loss of p110α/p85α by signaling through other nodes than Akt/Protein Kinase B.

  • 4.
    Hagberg, Malin
    et al.
    University of Skövde, School of Life Sciences.
    Holmén, Jonathan
    University of Skövde, School of Life Sciences.
    Olausson, Josefin
    University of Skövde, School of Life Sciences.
    Karlsson, Sandra
    University of Skövde, School of Life Sciences.
    Johansson, Viktoria
    University of Skövde, School of Life Sciences.
    Larsson, Dennis
    University of Skövde, School of Life Sciences.
    Rapid activation of JNK/SAPK in LNCaP prostate cancer cells by 1α,25-dihydroxyvitamin D3 is independent of PDIA3 (1,25-MARRS)2008In: Current Topics in Steroid Research, ISSN 0972-4788, Vol. 5, p. 17-24Article in journal (Refereed)
    Abstract [en]

    1α,25-dihydroxyvitamin D3 (1,25D3 ) is a highly potential anti-cancerous agent for prevention and treatment of prostate cancer, the most commonly diagnosed cancer type of males in western countries. A recent study by our laboratory, demonstrates that LNCaP cancer cells treated with 1,25D3, evoked dose-dependent activation of the JNK/SAPK MAPK signaling pathway within 10 minutes after hormone treatment, indicative of membrane-initiated steroid signaling (MISS) by 1,25D3. This confirms previous reports on intestinal-, chondrocyte- and osteoblast cells, where 1,25D3 operates through pharmacologically distinct nuclear-initiated mechanisms (NISS) and plasma membrane-initiated mechanisms. NISS is mediated via the vitamin D receptor (nVDR) and MISS is mediated through 1,25D3-MARRS (PDIA3, 1,25D3-membraneassociated rapid response steroid binding protein) or nVDR. The aims of the present study were to investigate the mechanisms of MISS evoked effects on alkaline phosphatase (ALP) and activation of the JNK/SAPK by 1,25D3, and the involvement of PDIA3 in 1,25D3 initiated activation of the JNK/SAPK signaling pathway. Furthermore, 1,25D3-treated LNCaP cells were transfected with siRNA against PDIA3 and phosphorylated JNK/SAPK was estimated by western analysis. Western analysis and ALP-assays demonstrated rapid activation of both JNK/SAPK as well as ALP. Silencing of PDIA3 did not affect 1,25D3 mediated activation of JNK/SAPK, suggesting that PDIA3 is not involved in the 1,25D3-initiated activation of the JNK/SAPK signaling pathway.

  • 5.
    Horning, Aaron M.
    et al.
    University of Texas Health Science Center, San Antonio, USA.
    Awe, Julius Adebayo
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre. Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Manitoba, Canada / Department of Clinical Genetics, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Wang, Chiou-Miin
    University of Texas Health Science Center, San Antonio, USA.
    Liu, Joseph
    University of Texas Health Science Center, San Antonio, USA.
    Lai, Zhao
    University of Texas Health Science Center, San Antonio, USA.
    Wang, Vickie Yao
    University of Texas Health Science Center, San Antonio, USA.
    Jadhav, Rohit R.
    University of Texas Health Science Center, San Antonio, USA.
    Louie, Anna D.
    University of Texas Health Science Center, San Antonio, USA.
    Lin, Chun-Lin
    University of Texas Health Science Center, San Antonio, USA.
    Kroczak, Tad
    University of Manitoba, Winnipeg, Manitoba, Canada.
    Chen, Yidong
    University of Texas Health Science Center, San Antonio, USA.
    Jin, Victor X.
    University of Texas Health Science Center, San Antonio, USA.
    Abboud-Werner, Sherry L.
    University of Texas Health Science Center, San Antonio, USA.
    Leach, Robin J.
    University of Texas Health Science Center, San Antonio, USA.
    Hernandez, Javior
    University of Texas Health Science Center, San Antonio, USA.
    Thompson, Ian M.
    University of Texas Health Science Center, San Antonio, USA.
    Saranchuk, Jeff
    University of Manitoba, Winnipeg, Canada.
    Drachenberg, Darrel
    University of Manitoba, Winnipeg, Canada.
    Chen, Chun-Liang
    University of Texas Health Science Center, San Antonio, USA.
    Mai, Sabine
    University of Manitoba, Winnipeg, Canada.
    Huang, Tim Hui-Ming
    University of Texas Health Science Center, San Antonio, USA.
    DNA Methylation Screening of Primary Prostate Tumors Identifies SRD5A2 and CYP11A1 as Candidate Markers for Assessing Risk of Biochemical Recurrence2015In: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 75, no 15, p. 1790-1801Article in journal (Refereed)
    Abstract [en]

    BACKGROUND. Altered DNA methylation in CpG islands of gene promoters has been implicated in prostate cancer (PCa) progression and can be used to predict disease outcome. In this study, we determine whether methylation changes of androgen biosynthesis pathway (ABP)-related genes in patients' plasma cell-free DNA (cfDNA) can serve as prognostic markers for biochemical recurrence (BCR). METHODS. Methyl-binding domain capture sequencing (MBDCap-seq) was used to identify differentially methylated regions (DMRs) in primary tumors of patients who subsequently developed BCR or not, respectively. Methylation pyrosequencing of candidate loci was validated in cfDNA samples of 86 PCa patients taken at and/or post-radical prostatectomy (RP) using univariate and multivariate prediction analyses. RESULTS. Putative DMRs in 13 of 30 ABP-related genes were found between tumors of BCR (n = 12) versus no evidence of disease (NED) (n = 15). In silico analysis of The Cancer Genome Atlas data confirmed increased DNA methylation of two loci-SRD5A2 and CYP11A1, which also correlated with their decreased expression, in tumors with subsequent BCR development. Their aberrant cfDNA methylation was also associated with detectable levels of PSA taken after patients' post-RP. Multivariate analysis of the change in cfDNA methylation at all of CpG sites measured along with patient's treatment history predicted if a patient will develop BCR with 77.5% overall accuracy. CONCLUSIONS. Overall, increased DNA methylation of SRD5A2 and CYP11A1 related to androgen biosynthesis functions may play a role in BCR after patients' RP. The correlation between aberrant cfDNA methylation and detectable PSA in post-RP further suggests their utility as predictive markers for PCa recurrence. (C) 2015 Wiley Periodicals, Inc.

  • 6.
    Hussain, Showket
    et al.
    Institute of Cytology & Preventive Oncology (ICMR), Noida, Uttar Pradesh, India.
    M., Yuvaraj
    Institute of Cytology & Preventive Oncology (ICMR), Noida, Uttar Pradesh, India.
    Thakur, Nisha
    Institute of Cytology & Preventive Oncology (ICMR), Noida, Uttar Pradesh, India.
    Salam, Irfana
    Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Jammu and Kashmir, India.
    Singh, Neha
    Panjab University, Chandigarh, India.
    Mir, Mohammad Muzaffar
    Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Jammu and Kashmir, India.
    Bhat, Mohammad Akbar
    Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Jammu and Kashmir, India.
    Siddiqi, Mushtaq A.
    Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Jammu and Kashmir, India.
    Das, Bhudev C.
    Dr. B.R. Ambedkar Research Centre for Biomedical Research (ACBR), University of Delhi, India.
    Bharadwaj, Mausumi
    Institute of Cytology & Preventive Oncology (ICMR), Noida, Uttar Pradesh, India.
    Association of cyclin D1 gene polymorphisms with risk of esophageal squamous cell carcinoma in Kashmir Valley: a high risk area2011In: Molecular Carcinogenesis, ISSN 0899-1987, E-ISSN 1098-2744, Vol. 50, no 7, p. 487-98Article in journal (Refereed)
    Abstract [en]

    Investigation of potential association of SNPs (G870A, rs9344; G1722C, rs678653) of cyclin D1 gene (CCND1) with susceptibility to esophageal squamous cell carcinoma (ESCC) in Kashmir valley (India). The study included 302 subjects comprising 151 ESCC cases and 151 controls. PCR-RFLP and direct sequencing were employed for genotyping. The G870A polymorphism, the individuals carrying GA + AA genotype was having 2.80-fold increased risk for development of ESCC (OR 2.8, 95% CI = 1.77-4.4; P = 0.0001) compared to GG genotype. Further a significantly higher risk was observed in individuals who consume >3 cups per day of salted tea (OR = 5.1; 95% CI = 1.6-16.7; P = 0.0016) and had smoking habits (OR = 6.3; 95% CI = 2.9-13.9; P = 0.0005). We also demonstrate for the first time in CCND1 1722 locus, the CC genotype was strongly associated with increased risk of developing ESCC (OR = 2.58; 95% CI = 1.61-4.15; P = 0.0001). In addition, the frequency of polymorphic C allele was also found to be higher in cases (OR = 1.92; 95% CI = 1.37-2.69; P = 0.0002). There appears to be an influence of CCND1 G870A/G1772C genotypes on genetic susceptibility to ESCC.

  • 7.
    Hussain, Showket
    et al.
    Division of Molecular Genetics & Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Salam, Irfana
    Department of Clinical Biochemistry, Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Jammu and Kashmir, India.
    Bandil, Kapil
    Division of Molecular Genetics & Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
    Yuvaraj, M
    Division of Molecular Genetics & Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
    Akbar Bhat, Mohammad
    Department of Cardiovascular Thoracic Surgery, Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Jammu and Kashmir, India.
    Muzaffar Mir, Mohammad
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Siddiqi, Mushtaq A.
    Department of Cardiovascular Thoracic Surgery, Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Jammu and Kashmir, India.
    Sobti, Ranbir C.
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Bharadwaj, Mausumi
    Division of Molecular Genetics & Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
    Das, Bhudev C.
    Dr. B.R. Ambedkar Centre for Biomedical Research (ACBR) University of Delhi (North Campus), Delhi, India.
    Methylation-mediated gene silencing of suppressor of cytokine signaling-1 (SOCS-1) gene in esophageal squamous cell carcinoma patients of Kashmir valley2011In: Journal of Receptor and Signal Transduction Research, ISSN 1079-9893, E-ISSN 1532-4281, Vol. 31, no 2, p. 147-56Article in journal (Refereed)
    Abstract [en]

    CONTEXT: Esophageal squamous cell carcinoma (ESCC) is a leading cause of cancer-related deaths in Jammu and Kashmir. The negative regulation of tumor suppressor gene leading to change in signaling pathway is one of the major mechanisms responsible for tumorigenic transformation.

    OBJECTIVE: In the present study, the role of silencing of suppressor of cytokine signaling-1 (SOCS-1) gene, a negative regulator of JAK/STAT pathway, was analyzed in ESCC.

    METHODS: The expression pattern of SOCS-1 gene was analyzed in esophageal tumor biopsies although normal adjacent tissues that served as controls. Reverse transcriptase polymerase chain reaction (RT-PCR), immunohistochemistry, methylation-specific PCR (MSP), and human papillomavirus (HPV) detection were performed to assess the expression pattern and promoter methylation of SOCS-1 gene including HPV status in a total of 75 surgically resected tissue specimens.

    RESULTS: Compared with the level of SOCS-1 expression in normal tissues, 53% (40/75) of the tumor tissues expressed either undetectable or reduced SOCS-1 expression (>50% loss of expression), which was significantly associated with advanced clinical stage or severe histopathological grade of the disease (P < 0.01). Aberrant promoter methylation of the SOCS-1 gene was found in 45% (34/75) of the esophageal tumor tissues, which was also found to be significantly associated with advanced stage of esophageal carcinoma (P < 0.01). The prevalence of HPV infection was found in 19% of tumor cases, whereas no HPV could be detected in any of the normal adjacent tissues.

    CONCLUSION: Transcriptional inactivation of SOCS-1 gene, primarily due to its promoter hypermethylation although HPV infection, may play an important role in esophageal carcinogenesis in Kashmir.

  • 8.
    Hussain, Showket
    et al.
    ICPO (ICMR), NOIDA, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Salam, Irfana
    Department of Clinical Biochemistry, Sher-I-Kashmir Institute of Medical Sciences, Kashmir, India.
    Bhat, Mohammad A.
    Department of Cardiovascular Thoracic Surgery, Sher-I-Kashmir Institute of Medical Sciences, Srinagar, India.
    Kakkar, Nandita
    Department of Histopathology, PGIMER, Chandigarh, India.
    Mir, Mohammad M.
    Department of Clinical Biochemistry, Sher-I-Kashmir Institute of Medical Sciences, Srinagar, India.
    Siddiqi, Mushtaq A.
    Department of Immunology and Molecular Medicine Sher-I-Kashmir Institute of Medical Sciences, Srinagar, India.
    Basir, Seemi F.
    Department of Biosciences Jamia Millia Islamia, Delhi, India.
    Bharti, Alok C.
    ICPO (ICMR), NOIDA, India.
    Bharadwaj, Mausumi
    ICPO (ICMR), NOIDA, India.
    Das, Bhudev C.
    Dr. B.R. Ambedkar Research Centre for Biomedical Research (ACBR), University of Delhi (North Campus), Delhi, India.
    Abstract 2722: Transcription factor NF-kB in esophageal squamous cell carcinoma: Alterations in activity and expression during Human Papillomavirus infection2011In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 71, no 8 Suppl, article id Abstract 2722Article in journal (Refereed)
  • 9.
    Jurcevic, Sanja
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre. Örebro universitet, Institutionen för hälsovetenskap och medicin.
    MicroRNA expression profiling in endometrial adenocarcinoma2015Doctoral thesis, comprehensive summary (Other academic)
  • 10.
    Jurcevic, Sanja
    et al.
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Klinga-Levan, Karin
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Olsson, Björn
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Ejeskär, Katarina
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Verification of microRNA expression in human endometrial adenocarcinoma2016In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 16, no 1, article id 261Article in journal (Refereed)
  • 11.
    Jurcevic, Sanja
    et al.
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Olsson, Björn
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Bioscience.
    Klinga-Levan, Karin
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Bioscience.
    MicroRNA expression in human endometrial adenocarcinoma2014In: Cancer Cell International, ISSN 1475-2867, E-ISSN 1475-2867, Vol. 14, no 1, article id 88Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: MicroRNAs are small non-coding RNAs that play crucial roles in the pathogenesis of different cancer types. The aim of this study was to identify miRNAs that are differentially expressed in endometrial adenocarcinoma compared to healthy endometrium. These miRNAs can potentially be used to develop a panel for classification and prognosis in order to better predict the progression of the disease and facilitate the choice of treatment strategy.

    METHODS: Formalin fixed paraffin embedded endometrial tissue samples were collected from the Örebro university hospital. QPCR was used to quantify the expression levels of 742 miRNAs in 30 malignant and 20 normal endometrium samples. After normalization of the qPCR data, miRNAs differing significantly in expression between normal and cancer samples were identified, and hierarchical clustering analysis was used to identify groups of miRNAs with coordinated expression profiles.

    RESULTS: In comparisons between endometrial adenocarcinoma and normal endometrium samples 138 miRNAs were found to be significantly differentially expressed (p < 0.001) among which 112 miRNAs have not been previous reported for endometrial adenocarcinoma.

    CONCLUSION: Our study shows that several miRNAs are differentially expressed in endometrial adenocarcinoma. These identified miRNA hold great potential as target for classification and prognosis of this disease. Further analysis of the differentially expressed miRNA and their target genes will help to derive new biomarkers that can be used for classification and prognosis of endometrial adenocarcinoma.

  • 12.
    Larsson, Annika
    University of Skövde, School of Health and Education. annika_bryntesson@hotmail.com.
    Att leva med bröstcancer: En litteraturbaserad studie2017Independent thesis Basic level (degree of Bachelor), 10 credits / 15 HE creditsStudent thesis
    Abstract [en]

    Background: In Sweden, more than 9000 people are diagnosed with breast cancer annually. A common experience are a loss of control and fear of the future. Furthermore, the cancer affect women's whole existence and side effects from treatment are common. With support, women are able to cope with anxiety, grief and fears that arise.

    Purpose: The aim of this litterature-based study was to examine how women with breast cancer experienced their daily life after diagnosis and treatment.

    Method: A litterature-based study with nine qualitative articles.

    Result: Three categories revealed; The uncertainty of the diagnosis; The meaning of relationships and When life gets a new meaning, and seven subcategories.

    Conclusion: Women with breast cancer were a group exposed to a greater risk of developing mental illness, where uncertainty and the need for information were unmet. The disease lead women to undergo a variety of crisis's and the need for support were important and necessary for some women in order to fight the disease. Support from healthcare and high patient-involvement facilitates and lead to a sense of control and reduced vulnerability. The disease could also cause women to experience a new meaning in life and that it became more valuable to them.

  • 13.
    Lewander, Andreas
    et al.
    Department of Oncology, Institute of Clinical and Experimental Medicine, University of Linköping, SE-581 85 Linköping, Sweden.
    Gao, Jinfang
    Department of Oncology, Institute of Clinical and Experimental Medicine, University of Linköping, SE-581 85 Linköping, Sweden.
    Adell, Gunnar
    Department of Oncology, Karolinska University Hospital, Stockholm, Sweden.
    Zhang, Hong
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Sun, Xiao-Feng
    Department of Oncology, Institute of Clinical and Experimental Medicine, University of Linköping, SE-581 85 Linköping, Sweden.
    Expression of NF-kappa B p65 phosphorylated at serine-536 in rectal cancer with or without preoperative radiotherapy2011In: Radiology and Oncology, ISSN 1318-2099, E-ISSN 1581-3207, Vol. 45, no 4, p. 279-284Article in journal (Refereed)
    Abstract [en]

    Background. In the present study, we investigated NF-kappa B p65 phosphorylated at Serine-536 (phosphor-Ser536-p65) in rectal cancer and its relationship to preoperative radiotherapy (RT), clinicopathological variables and biological factors. Patients and methods. Expression of phosphor-Ser536-p65 was examined by using immunohistochemistry in 141 primary rectal cancers, 149 normal mucosa specimens and 48 metastases in the lymph nodes, from rectal cancer patients who participated in a Swedish clinical trial of preoperative RT. Results. The expression of phosphor-Ser536-p65 in the cytoplasm increased from normal mucosa to primary tumour (p<0.0001, for both the group that did and the group that did not received RT). The expression did not further increase from primary tumour to metastasis in either group (p>0.05). Expression of phosphor-Ser536-p65 was positively related to, or tended to be related to, the expression of tumour endothelium marker 1 (TEM1, p=0.02), FXYD-3 (p=0.001), phosphatase of regenerating liver (PRL, p=0.02), p73 (p=0.048) and meningioma associated protein (MAC30, p=0.05) in the group that received RT but there were no such relationships in the group that did not received RT (p>0.05). The expression of phosphor-Ser536-p65 was not related to clinicopathological factors including survival (p>0.05). Conclusions. The increased expression of phosphor-Ser536-p65 may be involved in rectal cancer development. After RT, phosphor-Ser536-p65 seems to be positively related to the biological factors, which associated with more malignant features of tumours. However, phosphor-Ser536-p65 was not directly related to the response of RT based on recurrence and survival.

  • 14.
    Lööf, Jasmine
    et al.
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Rosell, Johan
    Department of Oncology, Linköping University Hospital, S-58185 Linköping, Sweden.
    Bratthäll, Charlotte
    Department of Oncology, Linköping University Hospital, S-58185 Linköping, Sweden.
    Doré, Siv
    Department of Pathology, Linköping University, Linköping, Sweden.
    Starkhammar, Hans
    Department of Oncology, Linköping University Hospital, S-58185 Linköping, Sweden.
    Zhang, Hong
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Sun, Xiao-Feng
    Department of Oncology, Linköping University, Linköping, Sweden.
    Impact of PINCH expression on survival in colorectal cancer patients2011In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 11, p. Artikelnr 103-Article in journal (Refereed)
    Abstract [en]

    Background: The adaptor protein PINCH is overexpressed in the stroma of several types of cancer, and is an independent prognostic marker in colorectal cancer. In this study we further investigate the relationship of PINCH and survival regarding the response to chemotherapy in colorectal cancer. Results: Paraffin-embedded tissue sections from 251 primary adenocarcinomas, 149 samples of adjacent normal mucosa, 57 samples of distant normal mucosa and 75 lymph node metastases were used for immunohistochemical staining. Stromal staining for PINCH increased from normal mucosa to primary tumour to metastasis. Strong staining in adjacent normal mucosa was related to worse survival independently of sex, age, tumour location, differentiation and stage (p = 0.044, HR, 1.60, 95% Cl, 1.01-2.52). PINCH staining at the invasive margin tended to be related to survival (p = 0.051). In poorly differentiated tumours PINCH staining at the invasive margin was related to survival independently of sex, age and stage (p = 0.013, HR, 1.90, 95% Cl, 1.14-3.16), while in better differentiated tumours it was not. In patients with weak staining, adjuvant chemotherapy was related to survival (p = 0.010, 0.013 and 0.013 in entire tumour area, invasive margin and inner tumour area, respectively), but not in patients with strong staining. However, in the multivariate analysis no such relationship was seen. Conclusions: PINCH staining in normal adjacent mucosa was related to survival. Further, PINCH staining at the tumour invasive margin was related to survival in poorly differentiated tumours but not in better differentiated tumours, indicating that the impact of PINCH on prognosis was dependent on differentiation status.

  • 15.
    Marcišauskas, Simonas
    et al.
    Division of Systems and Synthetic Biology, Department of Biology and Biological Engineering, Chalmers University of Technology, Gothenburg, Sweden.
    Ulfenborg, Benjamin
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Kristjansdottir, Björg
    Department of Obstetrics and Gynecology, Institute of Clinical Sciences, Sahlgrenska Cancer Center, University of Gothenburg, Gothenburg, Sweden.
    Waldemarson, Sofia
    Department of Immunotechnology, Lund University, Medicon Village, Lund, Sweden.
    Sundfeldt, Karin
    Department of Obstetrics and Gynecology, Institute of Clinical Sciences, Sahlgrenska Cancer Center, University of Gothenburg, Gothenburg, Sweden.
    Univariate and classification analysis reveals potential diagnostic biomarkers for early stage ovarian cancer Type 1 and Type 22019In: Journal of Proteomics, ISSN 1874-3919, E-ISSN 1876-7737, Vol. 196, p. 57-68Article in journal (Refereed)
    Abstract [en]

    Biomarkers for early detection of ovarian tumors are urgently needed. Tumors of the ovary grow within cysts and most are benign. Surgical sampling is the only way to ensure accurate diagnosis, but often leads to morbidity and loss of female hormones. The present study explored the deep proteome in well-defined sets of ovarian tumors, FIGO stage I, Type 1 (low-grade serous, mucinous, endometrioid; n = 9), Type 2 (high-grade serous; n = 9), and benign serous (n = 9) using TMT–LC–MS/MS. Data are available via ProteomeXchange with identifier PXD010939. We evaluated new bioinformatics tools in the discovery phase. This innovative selection process involved different normalizations, a combination of univariate statistics, and logistic model tree and naive Bayes tree classifiers. We identified 142 proteins by this combined approach. One biomarker panel and nine individual proteins were verified in cyst fluid and serum: transaldolase-1, fructose-bisphosphate aldolase A (ALDOA), transketolase, ceruloplasmin, mesothelin, clusterin, tenascin-XB, laminin subunit gamma-1, and mucin-16. Six of the proteins were found significant (p <.05) in cyst fluid while ALDOA was the only protein significant in serum. The biomarker panel achieved ROC AUC 0.96 and 0.57 respectively. We conclude that classification algorithms complement traditional statistical methods by selecting combinations that may be missed by standard univariate tests. Significance: In the discovery phase, we performed deep proteome analyses of well-defined histology subgroups of ovarian tumor cyst fluids, highly specified for stage and type (histology and grade). We present an original approach to selecting candidate biomarkers combining several normalization strategies, univariate statistics, and machine learning algorithms. The results from validation of selected proteins strengthen our prior proteomic and genomic data suggesting that cyst fluids are better than sera in early stage ovarian cancer diagnostics. 

  • 16.
    Saxenborn, Patricia
    University of Skövde, School of Health and Education.
    Investigating the Effect of 1,25-Dihydroxyvitamin D3 and Retinoic acid on Viability, Differentiation and Migration in NB69 and T47D cells.2016Independent thesis Basic level (degree of Bachelor), 20 credits / 30 HE creditsStudent thesis
    Abstract [en]

    Cancer is a well-known disease that many people encounter in their lifetime. There is constantly research being performed on cancer to find treatments for those types where none has been found, or even find better or more efficient treatments for those cancer types where there already is treatment available. Two types of cancer that have been studied in this thesis are neuroblastoma, which is a form of cancer that affects children and infants, and breast cancer. The 13-cis retinoic acid is presently used as treatment for neuroblastoma post-surgery and post-chemo therapy, but the treatment is quite invasive. It has been shown that 1,25-dihydroxyvitamin D3 is a good candidate for cancer treatment, and the aim of this study was to investigate whether a combination of 1,25-dihydroxyvitamin D3 and two forms of retinoic acid, all-trans and 13-cis, could cause synergistic effects on cell viability, invasion, and differentiation of the cells. The two vitamins were combined at different concentrations and ratios to make the different treatments. A proliferation assay with absorbance measurement was performed to determine cell viability, and a migration assay was performed to observe the migratory properties of the cells after treatment. The results concluded that the combined treatments had greater effect than the single treatments on cell viability in both neuroblastoma and breast cancer cells. The results showed that single treatment of 13-cis retinoic acid and combined treatments had the highest effect on invasion and differentiation on neuroblastoma cells.

  • 17.
    Singh, Neha
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Breakthrough insight into HPV infection as an emerging risk factor in prostate cancer2015In: Onkologi i Sverige, ISSN 1653-1582, no 3, p. 76-77Article in journal (Other (popular science, discussion, etc.))
  • 18.
    Singh, Neha
    et al.
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Hussain, Showket
    Division of Molecular Genetics and Biochemistry, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Bharadwaj, Mausumi
    Division of Molecular Genetics and Biochemistry, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Kakkar, Nandita
    Department of Urology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Singh, S. K.
    Department of Histopathology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Sobti, Ranbir C.
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Overexpression of signal transducer and activator of transcription (STAT-3 and STAT-5) transcription factors and alteration of suppressor of cytokine signaling (SOCS-1) protein in prostate cancer2012In: Journal of Receptor and Signal Transduction Research, ISSN 1079-9893, E-ISSN 1532-4281, Vol. 32, no 6, p. 321-7Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Prostate cancer is a leading cause of mortality in men worldwide especially in developing countries like India. The molecular mechanisms of the oncogenic signaling pathway(s) that are involved in prostate carcinogenesis play a crucial role in disease progression and persistence. There is an important role of signal transducer and activator of transcriptions (STATs) particularly STAT-3 and STAT-5 and its negative regulator suppressor of cytokine signaling-1 (SOCS-1).

    METHODS: In the present study, the expression and localization of STAT and SOCS-1 proteins in prostate cancer by immunohistochemistry in a total of 150 formalin-fixed, paraffin-embedded human prostate tissues of different grade obtained by radical prostatectomies or transurethral resection.

    RESULTS: A significantly strong STAT-3 expression pattern in 68% (65/95) prostate cancer cases as compared to 12% (5/55) in benign prostatic hyperplasia (BPH) controls (P < 0.001) was observed. Interestingly the SOCS-1 expression was found to be significantly elevated in prostate cancer cases (P < 0.001).

    CONCLUSIONS: The present study demonstrates overexpression of STAT-3 and STAT-5 proteins and a contrasting role of SOCS-1 in prostate cancer. These results suggest a critical association between altered expression of STAT-3 and STAT-5 with SOCS-1 and indicate its potential role as a negative regulator independent of JAK-STAT pathway in tumorigenic transformation of prostate tissue. The results of the present report focuses on the fundamental differences in major oncogenic signaling cascades between benign and malignant form of prostate tissue that plays a crucial role in prostate cancer biology.

  • 19.
    Singh, Neha
    et al.
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre. Department of Biotechnology, Panjab University, Chandigarh, India.
    Hussain, Showket
    Division of Molecular Oncology, Institute of Cytology and Preventive Oncology (ICMR), NOIDA, India.
    Kakkar, Nandita
    Department of Histopathology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Singh, Shrawan K.
    Department of Urology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Sobti, Ranbir C.
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Bharadwaj, Mausumi
    Division of Molecular Oncology, Institute of Cytology and Preventive Oncology (ICMR), NOIDA, India.
    Implication of high risk Human papillomavirus HR-HPV infection in prostate cancer in Indian population- A pioneering case-control analysis2015In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 5, article id 7822Article in journal (Refereed)
    Abstract [en]

    Prostate cancer is the second most common cancer with sexual history as a consistent risk factor. This is the pioneering study that evaluates the frequency of HPV infection in prostate cancer in India. Ninety five (95) histopathologically confirmed cancer and fifty five (55) BPH from Indian population were analyzed for HPV infection using a pair of consensus sequence primer followed by type specific PCRs for both high-risk and low-risk HPV types. The data demonstrate HPV infection in 41% of prostate tumor biopsies and 20% in BPH. Subsequent PCR- based HPV typing using type - specific primers revealed 32% were infected with HPV type 16 whereas 6% were found to be positive for HPV type 18, while in BPH controls only 5% of the BPH controls were infected with HPV 16 and this difference was highly significant (p = 0.0004). Significant proportion of HPV infected (74%) cases belonged to stage III and IV (p < 0.001) with a high Gleason score ≥8 (p = 0.003). The study represents for the first time the incidence of HPV infection in prostate cancer in Indian population and strengthens the hypothesis that HPV infection could be one of the co factor associated with progression of prostate cancer.

  • 20.
    Singh, Neha
    et al.
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre. Department of Biotechnology, Panjab University, Chandigarh, India.
    Hussain, Showket
    Division of Molecular Oncology, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Sharma, Upma
    Division of Molecular Genetics and Biochemistry, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Suri, Vanita
    Department of Obstetrics and Gynecology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Nijhawan, Raje
    Department of Cytology & Gynae. Pathology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Bharadwaj, Mausumi
    Division of Molecular Genetics and Biochemistry, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Sobti, R. C.
    Department of Biotechnology, Panjab University, Chandigarh, India / Vice Chancellor BBA (Central) University, Lucknow, India.
    The protective role of the -1306C>T functional polymorphism in matrix metalloproteinase-2 gene is associated with cervical cancer: implication of human papillomavirus infection2016In: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 37, no 4, p. 5295-5303Article in journal (Refereed)
  • 21.
    Singh, Neha
    et al.
    Panjab University, Chandigarh, India.
    Hussain, Showket
    Division of Molecular Genetics, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Suri, Vanita
    Department of Obstetrics and Gynaecology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Bharadwaj, Mausumi
    Division of Molecular Genetics, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Das, B. C.
    Ambedkar Centre for Biomedical Research, Delhi University, New Delhi, India.
    Sobti, R. C.
    Panjab University, Chandigarh, India.
    Abstract 2719: Aberrant expression of transcription factors STAT-3 and STAT-5 and their epigenetic control by SOCS-1 gene: The STAT signaling crosstalk in HPV coupled cervical carcinogenesis2011In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 71, no 8 Suppl, article id Abstract 2719Article in journal (Refereed)
  • 22.
    Singh, Neha
    et al.
    Department of Biotechnology, Panjab University, Chandigarh, India / Centre for Stem Cell and Tissue Engineering, Panjab University, Chandigarh, India.
    Sobti, R. C.
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Suri, Vanita
    Department of Obstetrics and Gynecology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Nijhawan, Raje
    Department of Cytology and Gynae Pathology, PGIMER, Sector-12, Chandigarh, India.
    Sharma, Shweta
    Division of Molecular Genetics and Biochemistry, Institute of Cytology and Preventive Oncology (ICMR), NOIDA, India.
    Das, B. C.
    Dr. B.R. Ambedkar Research Centre for Biomedical Research (ACBR), University of Delhi (North Campus), Delhi, 110 007, INDIA.
    Bharadwaj, Mausumi
    Division of Molecular Genetics and Biochemistry, Institute of Cytology and Preventive Oncology (ICMR), NOIDA, India.
    Hussain, Showket
    Division of Molecular Genetics and Biochemistry, Institute of Cytology and Preventive Oncology (ICMR), NOIDA, India.
    Downregulation of tumor suppressor gene PML in uterine cervical carcinogenesis: impact of human papillomavirus infection (HPV)2013In: Gynecologic Oncology, ISSN 0090-8258, E-ISSN 1095-6859, Vol. 128, no 3, p. 420-6Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: Cervical cancer is a leading gynecological cancer in Indian women and is caused due to infection with high risk human pappilloma virus (HR-HPV) 16 and 18. It has been well documented that PML (promyelocytic leukemia) enhances viral infectivity and plays a crucial role in antiviral response mechanisms. The aim of the present study was to evaluate the role of PML gene with context to HPV infection in cervical carcinogenesis.

    METHODS: The expression pattern of PML was analyzed by western blotting and immunohistochemistry in a total of 170 fresh surgically resected cervical tissue specimens comprising precancer (n=12), cancer (n=118) and normal controls (n=40) recruited from PGIMER, Chandigarh, India. HPV status was analyzed by L1 consensus PCR followed by type specific PCR for HR-HPV types 16 and 18 and low risk types 6 and 11.

    RESULTS: A significant downregulation of PML protein was observed in the majority of cervical cancer and precancer cases 68% (89/130) compared to normal controls. The loss of expression pattern of PML gene was significantly increased with severity of disease both clinically and pathologically (p<0.001). HPV infection was detected in the majority of cancer cases 96% (113/118) and in 83% (10/12) of precancer lesions whereas no infection could be detected in normal controls. Interestingly, all the 68% (89/130) cervical cancer cases that showed downregulation of PML were HPV infected (p=0.0001).

    CONCLUSION: Taken together, these observations suggest that the downregulation of PML gene and its synergism with HPV infection may play an important role and may serve as a new marker for early diagnosis and therapeutic intervention for cervical carcinogenesis.

  • 23.
    Sobti, R. C.
    et al.
    Department of Biotechnology, Panjab University, Chandigarh 160014, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, Chandigarh 160014, India.
    Hussain, Showket
    Division of Molecular Oncology, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Suri, Vanita
    Department of Obstetrics and Gynaecology, Post Graduate Institute of Medical Education and Research, Chandigarh 160014, India.
    Bharti, A. C.
    Division of Molecular Oncology, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Das, B. C.
    Division of Molecular Oncology, Institute of Cytology and Preventive Oncology (ICMR), Noida, India / Ambedkar Centre for Biomedical Research, Delhi University, Delhi, India.
    Overexpression of STAT3 in HPV-mediated cervical cancer in a north Indian population2009In: Molecular and Cellular Biochemistry, ISSN 0300-8177, E-ISSN 1573-4919, Vol. 330, no 1-2, p. 193-9Article in journal (Refereed)
    Abstract [en]

    The constitutively activated STAT family members, particularly STAT3, have been shown to possess transforming properties, and are strongly correlated with tumor development and progression. STAT3 transmits signals from many cytokines and growth factors to target genes in the nucleus through the Jak/Stat signaling pathway. HPV is the main etiological factor in the development of cervical cancer. In the current study, the expression of STAT3 was analyzed in various stages of HPV-mediated cervical carcinogenesis. Tissue biopsies from 100 patients with cervical cancer of different stages and normal tissues from patients undergoing hysterectomy were selected for studying the HPV status and STAT3 expression. HPV status of each corresponding biopsy was analyzed by PCR and typing. The mRNA expression was analyzed by reverse-transcriptase polymerase chain reaction (RT-PCR). HPV infection was detected in majority of cases: 75% (9/12) in precancer, 85% (34/40) stage I & II, and 95% (36/38) in stage III & IV of cervical cancer cases by L1 PCR. Further sub typing revealed HPV16 in 100% (9/9) of L1 positives in precancerous & 90% (63/70) in different stages of cancer. Significant level of STAT3 mRNA expression was predominantly found in cervical cancer cases as compared to normal controls (P = 0.001). We also found a significant correlation of STAT3 expression in cases infected with HPV (P = 0.001). Our results indicate a potentially interactive effect between HPV 16/18 and transcriptional activation of STAT3 gene in cervical carcinogenesis. To our knowledge, this is the first such study to be reported from India. Further investigations are needed to determine the influence of STAT3 expression on cervical carcinogenesis and its possible interaction with HPV infection status.

  • 24.
    Sobti, R. C.
    et al.
    Department of Biotechnology, Panjab University, Sector-14, Chandigarh, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, Sector-14, Chandigarh, India.
    Hussain, Showket
    Division of Molecular Genetics and Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), I-7, Sector-39, Noida, India.
    Suri, Vanita
    Department of Gynaecology and Obstetrics, PGIMER, Sector-12, Chandigarh, India.
    Nijhawan, Raje
    Department of Cytology & Gynae Pathology, PGIMER, Sector-12, Chandigarh, India.
    Bharti, A. C.
    Division of Molecular Oncology, Institute of Cytology & Preventive Oncology (ICMR), I-7, Sector-39, Noida, India.
    Bharadwaj, Mausumi
    Division of Molecular Genetics and Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), I-7, Sector-39, Noida, India.
    Das, B. C.
    Dr. B.R. Ambedkar Research Centre for Biomedical Research (ACBR), University of Delhi, (North Campus), Delhi, India.
    Aberrant promoter methylation and loss of suppressor of cytokine signalling-1 gene expression in the development of uterine cervical carcinogenesis2011In: Cellular Oncology, ISSN 2211-3428, E-ISSN 2211-3436, Vol. 34, no 6, p. 533-43Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Cervical cancer is a leading cause of cancer related deaths in women worldwide caused due to infection of high-risk human papillomaviruses. As JAK/STAT signalling pathway has been shown to play an important role during carcinogenesis, we studied the role of silencing of Suppressor of Cytokine Signalling-1 (SOCS-1) gene, a negative regulator of JAK/STAT pathway in cervical cancer.

    METHODS: The expression pattern of SOCS-1 mRNA and protein was analyzed in different stages of cervical tumor biopsies while normal cervical tissues served as controls. RT-PCR, immunohistochemistry and methylation-specific PCR (MSP) were performed to assess the expression pattern and promoter methylation of SOCS-1 gene in a total of 120 fresh surgically resected cervical tissue specimens comprising precancer (n = 12), cancer (n = 78) and normal controls (n = 30).

    RESULTS: Compared with expression of SOCS-1 in normal tissues, 64% of the tumor tissues expressed either undetectable or reduced expression. Aberrant promoter methylation of SOCS-1 was found in 61% of the cervical tumor tissues. SOCS-1 expression and methylation were significantly associated with severity of the disease (p < 0.01).

    CONCLUSION: We demonstrate for the first time the transcriptional inactivation of SOCS-1 gene due to hypermethylation and synergism with HPV infection which may play an important role in cervical carcinoma.

  • 25.
    Sobti, Ranbir C.
    et al.
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Hussain, Showket
    Division of Molecular Genetics and Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
    Suri, Vanita
    Department of Gynaecology and Obstetrics, PGIMER, Chandigarh, India.
    Bharadwaj, Mausumi
    Division of Molecular Genetics and Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
    Das, Bhudev C.
    Dr. B.R. Ambedkar Research Centre for Biomedical Research (ACBR), University of Delhi, India.
    Deregulation of STAT-5 isoforms in the development of HPV-mediated cervical carcinogenesis2010In: Journal of Receptor and Signal Transduction Research, ISSN 1079-9893, E-ISSN 1532-4281, Vol. 30, no 3, p. 178-188Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Cervical cancer is the second most common cancer and is leading cause of cancer related deaths in women worldwide. High Risk-Human papillomavirus (HPV) types play an important role in cervical carcinogenesis. Considering the important role of signal transducer and activator of transcription-5 (STAT-5), an important member of JAK/STAT family which plays a crucial role in various cancers and HPV as a key mediator in the development of cervical carcinogenesis, the purpose of the current study was to examine the possible relationship between HPV infection and expression of STAT-5 gene isoforms in cervical cancer.

    METHODS: A total of 120 fresh cervical tissue specimens comprising precancer (n = 12), cancer (n = 78) and normal controls (n = 30) were analyzed for HPV infection and expression pattern of STAT-5 mRNA (both isoforms STAT-5a and STAT-5b) and protein in different stages of cervical carcinoma biopsies by reverse-transcriptase-PCR, western blotting and immunohistochemistry.

    RESULTS: A significantly increased expression of STAT-5 was detected in most of the cervical tumors (P < 0.001), whereas it was almost undetectable in normal controls. Also the study of relative contribution of STAT-5 isoforms revealed a higher expression pattern of STAT-5b and was associated with severity of the disease. On the contrary, STAT-5a was found to be significantly downregulated in cervical tumor tissues (P < 0.001). HPV infection was found in 90% of the cervical cancer cases and was significantly associated with STAT-5 overexpression (P = 0.001).

    CONCLUSIONS: We observed for the first time the differential expression pattern of STAT-5 isoforms in cervical cancer and that STAT-5 may play an important role in the progression of HPV-mediated cervical cancer.

  • 26.
    Sobti, Ranbir Chander
    et al.
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Askari, Marjan
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Nikbakht, Mohsen
    Department of Experimental Medicine and Biotechnology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Sharma, Suresh C.
    Department of Radiotherapy and Oncology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Abitew, Abayneh Munshea
    Department of Zoology, Punjab University, Chandigarh, India.
    Genetic variants of EGFR (142285G>A) and ESR1 (2014G>A) gene polymorphisms and risk of breast cancer2012In: Molecular and Cellular Biochemistry, ISSN 0300-8177, E-ISSN 1573-4919, Vol. 369, no 1-2, p. 217-25Article in journal (Refereed)
    Abstract [en]

    Breast cancer is one of the most common cancers in women worldwide. The estrogen receptor alpha (ESR1) and epidermal growth factor receptor (EGFR) have been known to play a vital role in development and progression of breast cancer. The aim of the present study was to determine the relationship, if any, between genetic polymorphism in (ESR1) 2014G>A (T594T) and (EGFR) 142285G>A (R521K) with risk of breast cancer and the prognosis in a heterogeneous North Indian population that is known for its diverse ethnicity. A case-control study in a total of 300 individuals comprising of 150 breast cancer patients and 150 normal controls was performed. PCR-RFLP was employed for genotyping. The G/A heterozygous genotype EGFR R521K, was slightly higher in cases (56.7 %) than in controls (48.3 %) (P = 0.20). The results indicated that EGFR polymorphism does not show any significant association with breast cancer in this population. On the other hand, the mutant A/A genotype ESR1 codon 594, showed a 6.4-folds risk for breast cancer and this association was highly significant (P = 0.00) as compared to wild GG genotype, the heterozygous G/A genotype also showed a significant association with disease (P = 0.00, OR = 2.03). In addition, the frequency of A allele was also higher in cases (36 %) than in controls (19 %) and a highly significant difference was observed with wild G allele (63.3 % in cases and 6.6 % in controls). This clearly indicates that there appears to be an influence of ESR1 codon 594 genotypes on genetic susceptibility to breast cancer. Further a significantly higher risk was observed in individuals who had diabetes {OR = 3.04 (1.68-5.50), P = 0.00} and females with ESR polymorphism in pre-menopause patients that had undergone menopause above the age of 50 years {OR = 3.58 (1.86-6.90), P < 0.05}. The different ethnic backgrounds and geographical locations have complimented the present genotypic analysis and have highlighted the influence of ethnicity, race and geographic location in genetic predisposition to breast cancer.

  • 27.
    Sobti, Ranbir Chander
    et al.
    Department of Biotechnology, Panjab University, 160014 Chandigarh, India.
    Berhane, Nega
    Department of Biotechnology, University of Gondar, Gondar, Ethiopia.
    Melese, Shiferaw
    Department of Mathematics, University of Gondar, Gondar, Ethiopia.
    Mahdi, Salih Abdul
    Department of Biotechnology, Panjab University, 160014 Chandigarh, India.
    Gupta, Libsy
    Department of Biotechnology, Panjab University, 160014 Chandigarh, India.
    Thakur, Hitender
    Department of Biotechnology, Panjab University, 160014 Chandigarh, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, 160014 Chandigarh, India.
    Impact of XPD gene polymorphism on risk of prostate cancer on north Indian population2012In: Molecular and Cellular Biochemistry, ISSN 0300-8177, E-ISSN 1573-4919, Vol. 362, no 1-2, p. 263-8Article in journal (Refereed)
    Abstract [en]

    Prostate cancer is the second most diagnosed cancer in men next to skin cancer in the developed world. Risk of disease varies most prominently with age, ethnicity, family history, and diet. Genetic polymorphism of some genes has been implicated in increasing the risk. The XPD (Xeroderma pigmentosum group D) gene codes for a DNA helicase involved in transcription and nucleotide excision repair. The aim of this study is to evaluate the effect of XPD 751 Lys/Gln polymorphism on risk of prostate cancer on north Indian patients. Blood sample from 150 prostate cancer patients, 150 from Prostate Hyper Plasia and equal number of samples from healthy control groups was collected from North India. The polymerase chain reaction and restrictive fragment length polymorphism techniques were implemented. Statistically non-significant increase risk of prostate cancer was observed with patients having Gln/Gln genotype (OR 1.62, 95% CI).

  • 28.
    Sobti, Ranbir Chander
    et al.
    Department of Biotechnology, Panjab University, India.
    Kler, Rupinder
    Department of Biotechnology, Panjab University, India.
    Sharma, Yash Paul
    Department of Cardiology, PGIMER, Chandigarh 160012, India.
    Talwar, Kewal Krishan
    Department of Cardiology, PGIMER, Chandigarh 160012, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, India.
    Risk of obesity and type 2 diabetes with tumor necrosis factor-α 308G/A gene polymorphism in metabolic syndrome and coronary artery disease subjects2012In: Molecular and Cellular Biochemistry, ISSN 0300-8177, E-ISSN 1573-4919, Vol. 360, no 1-2, p. 1-7Article in journal (Refereed)
    Abstract [en]

    Tumor Necrosis Factor-alpha (TNF-α) has been implicated in the pathogenesis of insulin resistance and obesity. The increased expression of TNF-α in adipose tissue is known to induce insulin resistance, and a polymorphism at position -308 in the promoter region of TNF-α gene may lead to its increased transcription in adipocytes. The objective of this work was to determine the role of TNFα-308G/A gene polymorphism in metabolic syndrome (MetS) and coronary artery disease (CAD) with obesity and type 2 diabetes mellitus (T2DM). A total of 250 MetS and 224 CAD patients and 214 controls were studied. TNFα-308G/A polymorphism was detected from the whole blood genomic DNA using PCR-amplification refractory mutation system. The 2 × 2 contingency tables and multiple regression analysis were used for determining the association of genotypes with obesity and type 2 diabetes mellitus (T2DM) in MetS and CAD subjects. In CAD subjects with T2DM, the AG genotypes showed a very strong association (P < 0.0001; OR 0.194, 95%CI 0.103-0.365). In CAD subjects with obesity, the AA (P = 0.049; OR 2.449) and AG genotypes showed a strong association (P < 0.0001; OR 0.206). In both males and females, AG genotype and G allele (P < 0.0001) showed a strong association with T2DM. In MetS subjects with T2DM, there was a strong association with AG (P = 0.002; OR 4.483) as well as AA+AG genotypes (P = 0.002; OR 4.255). The AA and AG genotype (P = 0.001; OR 5.497) in males showed a strong 4.6- and 5.4-fold risks, respectively, with obesity. In females, only AG genotype showed a strong 4.5-fold risk with obesity (P = 0.001). In MetS subjects with obesity, the AA genotype (P = 0.043; OR 3.352) as well as AG showed a very strong association (P = 0.001; OR 5.011). The AG genotypes showed a high 3.5-fold risk with T2DM in females (P = 0.011). In CAD subjects, AG genotype showed a protective effect in both obese males and females (P < 0.0001). Heterozygous TNFα-308G/A gene variant may be an important risk factor for MetS with T2DM and obesity in both males and females, but may have a protective role in CAD subjects with obesity and T2DM. A allele may be an important risk factor for MetS and CAD with obesity as well as CAD subjects with T2DM.

  • 29.
    Ulfenborg, Benjamin
    et al.
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Jurcevic, Sanja
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Lindelöf, Angelica
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Klinga-Levan, Karin
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Olsson, Björn
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    miREC: a database of miRNAs involved in the development of endometrial cancer2015In: BMC Research Notes, ISSN 1756-0500, E-ISSN 1756-0500, Vol. 8, no 1, article id 104Article in journal (Refereed)
    Abstract [en]

    Background

    Endometrial cancer (EC) is the most frequently diagnosed gynecological malignancy and the fourth most common cancer diagnosis overall among women. As with many other forms of cancer, it has been shown that certain miRNAs are differentially expressed in EC and these miRNAs are believed to play important roles as regulators of processes involved in the development of the disease. With the rapidly growing number of studies of miRNA expression in EC, there is a need to organize the data, combine the findings from experimental studies of EC with information from various miRNA databases, and make the integrated information easily accessible for the EC research community.

    Findings

    The miREC database is an organized collection of data and information about miRNAs shown to be differentially expressed in EC. The database can be used to map connections between miRNAs and their target genes in order to identify specific miRNAs that are potentially important for the development of EC. The aim of the miREC database is to integrate all available information about miRNAs and target genes involved in the development of endometrial cancer, and to provide a comprehensive, up-to-date, and easily accessible source of knowledge regarding the role of miRNAs in the development of EC. Database URL: http://www.mirecdb.orgwebcite.

    Conclusions

    Several databases have been published that store information about all miRNA targets that have been predicted or experimentally verified to date. It would be a time-consuming task to navigate between these different data sources and literature to gather information about a specific disease, such as endometrial cancer. The miREC database is a specialized data repository that, in addition to miRNA target information, keeps track of the differential expression of genes and miRNAs potentially involved in endometrial cancer development. By providing flexible search functions it becomes easy to search for EC-associated genes and miRNAs from different starting points, such as differential expression and genomic loci (based on genomic aberrations).

  • 30.
    Wallander, Marit
    et al.
    Department of Medicine Huddinge, Karolinska Institute, Stockholm, Sweden / Geriatric Medicine, Department of Internal Medicine and Clinical Nutrition, Center for Bone Research at the Sahlgrenska Academy, University of Gothenburg, Sweden.
    Axelsson, Kristian F.
    Geriatric Medicine, Department of Internal Medicine and Clinical Nutrition, Center for Bone Research at the Sahlgrenska Academy, University of Gothenburg, Sweden / Department of Orthopaedic Surgery, Skaraborg Hospital, Skövde, Sweden.
    Lundh, Dan
    University of Skövde, School of Health and Education. University of Skövde, Health and Education.
    Lorentzon, Mattias
    Geriatric Medicine, Department of Internal Medicine and Clinical Nutrition, Center for Bone Research at the Sahlgrenska Academy, University of Gothenburg, Sweden / Geriatric Medicine, Institute of Medicine, The Sahlgrenska Academy, Sahlgrenska University Hospital, Sweden.
    Patients with prostate cancer and androgen deprivation therapy have increased risk of fractures: a study from the fractures and fall injuries in the elderly cohort (FRAILCO)2019In: Osteoporosis International, ISSN 0937-941X, E-ISSN 1433-2965, Vol. 30, no 1, p. 115-125Article in journal (Refereed)
    Abstract [en]

    Summary: Osteoporosis is a common complication of androgen deprivation therapy (ADT). In this large Swedish cohort study consisting of a total of nearly 180,000 older men, we found that those with prostate cancer and ADT have a significantly increased risk of future osteoporotic fractures. Introduction: Androgen deprivation therapy (ADT) in patients with prostate cancer is associated to increased risk of fractures. In this study, we investigated the relationship between ADT in patients with prostate cancer and the risk of incident fractures and non-skeletal fall injuries both compared to those without ADT and compared to patients without prostate cancer. Methods: We included 179,744 men (79.1 ± 7.9 years (mean ± SD)) from the Swedish registry to which national directories were linked in order to study associations regarding fractures, fall injuries, morbidity, mortality and medications. We identified 159,662 men without prostate cancer, 6954 with prostate cancer and current ADT and 13,128 men with prostate cancer without ADT. During a follow-up of approximately 270,300 patient-years, we identified 10,916 incident fractures including 4860 hip fractures. Results: In multivariable Cox regression analyses and compared to men without prostate cancer, those with prostate cancer and ADT had increased risk of any fracture (HR 95% CI 1.40 (1.28–1.53)), hip fracture (1.38 (1.20–1.58)) and MOF (1.44 (1.28–1.61)) but not of non-skeletal fall injury (1.01 (0.90–1.13)). Patients with prostate cancer without ADT did not have increased risk of any fracture (0.97 (0.90–1.05)), hip fracture (0.95 (0.84–1.07)), MOF (1.01 (0.92–1.12)) and had decreased risk of non-skeletal fall injury (0.84 (0.77–0.92)). Conclusions: Patients with prostate cancer and ADT is a fragile patient group with substantially increased risk of osteoporotic fractures both compared to patients without prostate cancer and compared to those with prostate cancer without ADT. We believe that this must be taken in consideration in all patients with prostate cancer already at the initiation of ADT. 

  • 31.
    Wengström, Y.
    et al.
    Department of Neurobiology, Care Science and Society, Division of Nursing, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden / Department of Oncology, Karolinska University Hospital, Stockholm, Sweden.
    Bolam, K. A.
    Åstrand Laboratory of Work Physiology, The Swedish School of Sport and Health Sciences, Stockholm, Sweden / School of Human Movement and Nutrition Sciences, The University of Queensland, Brisbane, Australia.
    Mijwel, S.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Sundberg, C. J.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden / Unit for Bioentrepreneurship, Karolinska Institutet, Solna, Sweden.
    Backman, M.
    Department of Neurobiology, Care Science and Society, Division of Nursing, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden / Department of Oncology, Karolinska University Hospital, Stockholm, Sweden.
    Browall, Maria
    University of Skövde, School of Health and Education. University of Skövde, Health and Education.
    Norrbom, J.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Rundqvist, H.
    Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
    Optitrain: a randomised controlled exercise trial for women with breast cancer undergoing chemotherapy2017In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 17, article id 100Article in journal (Refereed)
    Abstract [en]

    Background: Women with breast cancer undergoing chemotherapy suffer from a range of detrimental disease and treatment related side-effects. Exercise has shown to be able to counter some of these side-effects and improve physical function as well as quality of life. The primary aim of the study is to investigate and compare the effects of two different exercise regimens on the primary outcome cancer-related fatigue and the secondary outcomes muscle strength, function and structure, cardiovascular fitness, systemic inflammation, skeletal muscle gene activity, health related quality of life, pain, disease and treatment-related symptoms in women with breast cancer receiving chemotherapy. The second aim is to examine if any effects are sustained 1, 2, and 5 years following the completion of the intervention and to monitor return to work, recurrence and survival. The third aim of the study is to examine the effect of attendance and adherence rates on the effects of the exercise programme. Methods: This study is a randomised controlled trial including 240 women with breast cancer receiving chemotherapy in Stockholm, Sweden. The participants are randomly allocated to either: group 1: Aerobic training, group 2: Combined resistance and aerobic training, or group 3: usual care (control group). During the 5-year follow-up period, participants in the exercise groups will receive a physical activity prescription. Measurements for endpoints will take place at baseline, after 16 weeks (end of intervention) as well as after 1, 2 and 5 years. Discussion: This randomised controlled trial will generate substantial information regarding the effects of different types of exercise on the health of patients with breast cancer undergoing chemotherapy. We expect that dissemination of the knowledge gained from this study will contribute to developing effective long term strategies to improve the physical and psychosocial health of breast cancer survivors.

  • 32.
    Yang, Lie
    et al.
    Sichuan Univ, W China Hosp, Inst Digest Surg, Chengdu 610064, Sichuan Prov, Peoples R China / Sichuan Univ, W China Hosp, State Key Lab Biotherapy, Chengdu 610064, Sichuan Prov, Peoples R China / Linkoping Univ, Dept Oncol & Clin & Expt Med, SE-58185 Linkoping, Sweden .
    Zhang, Hong
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Zhou, Zong-Guang
    Sichuan Univ, W China Hosp, Inst Digest Surg, Chengdu 610064, Sichuan Prov, Peoples R China / Sichuan Univ, W China Hosp, State Key Lab Biotherapy, Chengdu 610064, Sichuan Prov, Peoples R China .
    Yan, Hui
    Sichuan Univ, W China Hosp, Inst Digest Surg, Chengdu 610064, Sichuan Prov, Peoples R China / Sichuan Univ, W China Hosp, State Key Lab Biotherapy, Chengdu 610064, Sichuan Prov, Peoples R China .
    Adell, Gunnar
    Karolinska Univ Hosp, Dept Oncol, Stockholm, Sweden.
    Sun, Xiao-Feng
    Sichuan Univ, W China Hosp, Inst Digest Surg, Chengdu 610064, Sichuan Prov, Peoples R China / Sichuan Univ, W China Hosp, State Key Lab Biotherapy, Chengdu 610064, Sichuan Prov, Peoples R China / Linkoping Univ, Dept Oncol & Clin & Expt Med, SE-58185 Linkoping, Sweden .
    Biological Function and Prognostic Significance of Peroxisome Proliferator-Activated Receptor delta in Rectal Cancer2011In: Clinical Cancer Research, ISSN 1078-0432, E-ISSN 1557-3265, Vol. 17, no 11, p. 3760-3770Article in journal (Refereed)
    Abstract [en]

    Purpose: To investigate the expression significance of PPAR beta/delta in relation to radiotherapy (RT), clinicopathologic, and prognostic variables of rectal cancer patients. Experimental Design: We included 141 primary rectal cancer patients who participated in a Swedish clinical trial of preoperative RT. Tissue microarray samples from the excised rectal cancers and the adjacent or distant normal mucosa and lymph node metastases were stained with PPAR delta antibody. Survival probability was computed by the Kaplan-Meier method and Cox regression model. The proliferation of colon cancer cell lines KM12C, KM12SM, and KM12L4a was assayed after PPAR delta knockdown. Results: PPAR delta was increased from adjacent or distant normal mucosa to primary cancers, whereas it decreased from primary cancers to lymph node metastases. After RT, PPAR delta was increased in normal mucosa, whereas it decreased in primary cancers and lymph node metastases. In primary cancers, the high expression of PPAR delta was related to higher frequency of stage I cases, lower lymph node metastasis rate, and low expression of Ki-67 in the unirradiated cases, and related to favorable survival in the cases either with or without RT. The proliferation of the KM12C, KM12SM, or KM12L4a cells was significantly accelerated after PPAR delta knockdown. Conclusions: RT decreases the PPAR delta expression in primary rectal cancers and lymph node metastases. PPAR delta is related to the early development of rectal cancer and inhibits the proliferation of colorectal cancer cells. Increase of PPAR delta predicts favorable survival in the rectal cancer patients either with or without preoperative RT. Clin Cancer Res; 17(11); 3760-70. (C)2011 AACR.

  • 33.
    Zhang, Hong
    et al.
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Wang, Da-Wei
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre. Department of Stomatology, The Third Hospital of Hebei Medical University, Hebei, China.
    Adell, Gunnar
    Department of Oncology, Karolinska University Hospital, Karolinska, Sweden.
    Sun, Xiao-Feng
    Division of Oncology, Department of Clinical and Experimental Medicine, Faculty of Heath Science, Linköping University, Sweden .
    WRAP53 is an independent prognostic factor in rectal cancer- a study of Swedish clinical trial of preoperative radiotherapy in rectal cancer patients2012In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 12, p. 294-Article in journal (Refereed)
    Abstract [en]

    Background: Expression of WRAP53 protein has oncogenic properties and it is up regulated in several types of tumors. Methods: We examined expression of WRAP53 protein in rectal cancers and analyzed its relationship to the response to preoperative radiotherapy and patient survival. The WRAP53 protein was examined by immunohistochemistry in normal mucosa, primary tumors and lymph node metastases from 143 rectal cancer patients participated in a Swedish clinical trial of preoperative radiotherapy. Results: Frequency of WRAP53 protein expression was increased in primary rectal cancer compared to the normal mucosa (p < 0.05). In non-radiotherapy group positive WRAP53 in primary tumors (p = 0.03, RR, 3.73, 95% CI, 1.13-11.89) or metastases (p = 0.01, RR, 4.11, 95% CI, 1.25-13.14), was associated with poor prognosis independently of stages and differentiations. In radiotherapy group, positive WRAP53 in the metastasis correlated with better survival (p = 0.04). An interaction analysis showed that the correlations of WRAP53 with the prognostic significance with and without radiotherapy in the metastasis differed (p = 0.01). In the radiotherapy group, expression of WRAP53 in metastases gave a better outcome (p = 0.02, RR, 0.32, 95% CI, 0.13-0.84), and an interaction analysis showed significance between the two groups (p = 0.01). Conclusion: WRAP53 may be a new biomarker used to predict prognosis and to select suitable patients for preoperative radiotherapy.

  • 34.
    Åberg, Malin
    et al.
    University of Skövde, School of Health and Education.
    Joelsson, Josefine
    University of Skövde, School of Health and Education.
    Kvinnliga patienters upplevelse under pågående behandling av bröstcancer.: En kvalitativ studie av bloggar2016Independent thesis Basic level (university diploma), 10 credits / 15 HE creditsStudent thesis
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