Biology subjects

Matuszewski, M.

Publications and source records attributed to Matuszewski, M..

3 recordsLinked to original sources

bioRxiv2026

Diabetes Might Shape Vasculature, Tumor Dissemination and Circulating Inflammation Marker Profiles in Prostate Cancer.

Background and objectiveChronic comorbidities like diabetes mellitus can influence cancer incidence and progression. However, their impact on pathological and molecular tumor characteristics, and dissemination, especially in prostate cancer (PCa), is not fully understood. Here, we investigated differences in the PCa molecular landscape with coexisting diabetes type 2 and its link to tumor dissemination. MethodsDAmico intermediate- or high-risk PCa patients (n=145), with type 2 diabetes or no diabetes, were analyzed for clinico-pathological features, circulating tumor cell (CTC) presence, yields and phenotypes in tumor-draining vein (TDVB) and peripheral blood (PB), primary tumor characteristics, and selected plasma biomarkers. Key findings and limitationsDiabetes type 2 was found in 20/13.8% patients and associated with more advanced clinical outcomes, i.e. pathological tumor stage (p=0.011) and lymph node involvement (p=0.020). Among patients diagnosed before age 65, diabetes and PCa showed a borderline association with shorter time-to-biochemical recurrence (p=0.032). Diabetic PCa patients had significantly higher total CTC counts in TDVB but not in PB, indicating enhanced tumor cell dissemination from primary tumor (PT). PTs from diabetic PCa patients displayed a borderline association with higher ALDH1 expression (p=0.054) and significantly lower vascular vessel density (p=0.008). Similarly, in patients under 65, PTs from diabetic PCa patients expressed genes linked to decreased angiogenesis. Plasma analyses revealed elevated GDF15 levels in PB (p<0.001), increased TRAP5 concentrations in TDVB (p=0.001), and reduced osteonectin levels in TDVB (p=0.026) in diabetic PCa patients. The studys limitation is the relatively small cohort, especially those with coexisting diabetes type 2. Conclusion and clinical implicationsDiabetes in PCa patients associates with advanced tumor stage, enhanced tumor cell dissemination, impaired vascularization, and distinct circulating biomarker alterations. Vascular alterations from diabetes, with systemic factors, especially in PCa patients under 65, may increase tumor dissemination in PCa. However, exact mechanisms need investigation in larger cohorts of patients. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=134 SRC="FIGDIR/small/720986v1_ufig1.gif" ALT="Figure 1"> View larger version (58K): org.highwire.dtl.DTLVardef@1f5047forg.highwire.dtl.DTLVardef@fa3f43org.highwire.dtl.DTLVardef@14f7765org.highwire.dtl.DTLVardef@27a12d_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

bioRxiv2023

Pauperization of Emerin from nuclear envelope drives prostate cancer cell migration and invasiveness

Micronuclei (MN) can arise from many causes, including the breakage of aberrant cytokinetic chromatin bridge. The frequent observation of MN in tumors raises the specter that they might not merely be passive elements but could instead play active roles in tumor progression. Here, we test the hypothesis that the presence of micronuclei could induce specific phenotypic and functional changes to the cell and lead to increased cancer invasive potential. With a variety of imaging and molecular methods in vitro and in clinical samples from prostate cancer (PCa) patients, we show that chromosome bridge resolution can lead to EMD accumulation and formation of EMD-rich MN. Such structure is negative for Lamin A/C and positive for LBR and Sec6{beta}. It can cause EMD pauperization from NE affecting migratory and invasive properties of a cell and can be translated to PCa patients poor prognosis.

cancer biology↗

bioRxiv2021

Comprehensive cancer-oriented biobanking resource of human samples for studies of post-zygotic genetic variation involved in cancer predisposition

The progress in translational cancer research relies on access to well-characterized samples from a representative number of patients and controls. The rationale behind our biobanking are explorations of post-zygotic pathogenic gene variants, especially in non-tumoral tissue, which might predispose to cancers. The targeted diagnoses are carcinomas of the breast (via mastectomy or breast conserving surgery), colon and rectum, prostate, and urinary bladder (via cystectomy or transurethral resection), exocrine pancreatic carcinoma as well as metastases of colorectal cancer to the liver. The choice was based on the high incidence of these cancers and/or frequent fatal outcome. We also collect age-matched normal controls. Our still ongoing collection originates from five clinical centers and after nearly 2-year cooperation reached 1711 patients and controls, yielding a total of 23226 independent samples, with an average of 74 donors and 1010 samples collected per month. The predominant diagnosis is breast carcinoma, with 933 donors, followed by colorectal carcinoma (383 donors), prostate carcinoma (221 donors), bladder carcinoma (81 donors), exocrine pancreatic carcinoma (15 donors) and metachronous colorectal cancer metastases to liver (14 donors). Forty percent of the total sample count originates from macroscopically healthy cancer-neighboring tissue, while contribution from tumors is 12%, which adds to the uniqueness of our collection for cancer predisposition studies. Moreover, we developed two program packages, enabling registration of patients, clinical data and samples at the participating hospitals as well as the central system of sample/data management at coordinating center. The approach used by us may serve as a model for dispersed biobanking from multiple satellite hospitals. Our biobanking resource ought to stimulate research into genetic mechanisms underlying the development of common cancers. It will allow all available "-omics" approaches on DNA-, RNA-, protein- and tissue levels to be applied. The collected samples can be made available to other research groups.

cancer biology↗