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Lundberg, A.

Publications and source records attributed to Lundberg, A..

3 recordsLinked to original sources

Early gonadotoxic effects of cyclophosphamide on the prepubertal testis and the feasibility of reducing toxicity through combined antioxidant therapy

One Sentence SummaryEarly gonadotoxic effects of cyclophosphamide (CPA) on prepubertal testes were identified, with molecular damage detectable within 16 hours and histological changes by 32 hours, while antioxidant co-treatment showed potential for protection. CPA induces early molecular damage in prepubertal testes, with protective antioxidant effects observed within the first 16 hours, highlighting the potential for mitigating testicular toxicity without compromising anticancer efficacy. This study demonstrates that CPA-induced testicular toxicity in prepubertal mice occurs early at the transcriptional level, with antioxidants showing protective effects, underscoring the need for further research on safe and effective protective strategies. At high doses, alkylating drugs toxicity leads to testicular atrophy and spermatogonial stem cells depletion, rendering survivors of childhood cancers infertile, as a recognized late effect. We used in-vivo experimental models to identify early gonadotoxic effects induced by cyclophosphamide (CPA) on prepubertal testes and to investigate if a treatment with antioxidants could reduce that toxicity. Effects were estimated by histological evaluation and whole-transcriptome RNA-sequencing (RNA-seq) of sacrificed animals at 8 hours intervals. Sixty pre-pubertal mice were randomly assigned to 1) intraperitoneal treatment with 100 mg/Kg CPA; 2) CPA in addition to antioxidants (AO) L-Carnitine (LC 50mg/kg) and N-acetyl cysteine (NAC 50); 3) AO alone; 4) control receiving saline solution (Ctrl) (N=15 for each group). Three additional animals were used for baseline assessments. On histology, changes were evident at 32 hours post-treatment. However, RNA-seq analyses revealed that the molecular impact of CPA occurred early within the first 16 hours of exposure to the drug, and that protective effects of AO in combined CPA therapy (CPA+AO) could be achieved during that period. This study demonstrates side effects of CPA on testicular tissue in the first 48 hours on transcriptional scale. Our findings indicate that early administration of AO can mitigate CPA-induced testicular damage in-vivo and suggest that protective treatments against prepubertal testis damage could be developed. However, such protective treatment should not interfere with the desired cytotoxic effects on the malignancies, thus further research is needed to evaluate the timing and how safe administration of the protectant could be achieved for medical treatment.

pharmacology and toxicology↗

Reclassifying Cancer: Defining tumour cell cycle activity in terms of its tissue of origin in over 13,000 samples

Genomic alterations resulting in loss of control over the cell cycle is a fundamental hallmark of human malignancies. Whilst pan-cancer studies have broadly assessed tumour genomics and their impact on oncogenic pathways, analyses taking the baseline signalling levels in normal tissue into account are lacking. To this end, we aimed to reclassify the cell cycle activity of tumours in terms of their tissue of origin and determine the DNA mutations, chromosome arm-level changes and signalling pathways driving cell cycle activity. Combining normal tissue and pan-cancer data from over 13,000 samples we demonstrate that tumours of gynaecological origin show the highest levels of baseline corrected cell cycle activity, partially owing to hormonal signalling and gene expression changes. We also show that normal and tumour tissues can be separated into groups (quadrants) of low/high cell cycle activity and propose the novel hypothesis of an upper limit on these activity levels in tumours.

cancer biology↗

A pan-cancer analysis of the frequency of DNA alterations across cell cycle activity levels

BackgroundPan-cancer genomic analyses based on the magnitude of pathway activity are currently lacking. Focusing on the cell cycle, we examined the DNA mutations and chromosome arm-level aneuploidy within tumours with low, intermediate and high cell cycle activity. Patients and methodsMatching mRNA, gene mutational status, chromosomal arm-level aberrations and clinico-pathological data was assembled from pan-cancer studies of 9,515 patients with 32 different cancers. Cell cycle activity was estimated from mRNA data using the cell cycle score (CCS) signature. Barplots were used to visualise mutation and chromosomal aberration frequency within CCS subgroups. Kaplan-Meier and multivariable Cox-regression analyses were used to determine survival differences between CCS subgroups. ResultsCell cycle activity varied broadly across and within all cancers. TP53 and PIK3CA mutations were common in all CCS subgroups but with increasing frequency as cell cycle activity levels increased (P < 0.001). Mutations in BRAF and gains in 16p were less frequent CCS high tumours (P < 0.001). In Kaplan-Meier analysis, patients whose tumours were CCS Low had a longer PFI relative to intermediate or high (P < 0.001) and this significance remained in multivariable analysis (CCS intermediate: HR = 1.37; 95% CI 1.17 - 1.60, CCS high: 1.54; 1.29 - 1.84, CCS Low = Ref). ConclusionsCell cycle activity varies across and within cancers and whilst similar DNA alterations can be found at all activity levels, some notable exceptions exist. These data also demonstrate that independent prognostic information can be derived on a pan-cancer level from a simple measure of cell cycle activity.

genomics↗