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12. Rigid tumours contain soft cancer cells

Author

Fuhs, Thomas, Wetzel, Franziska, Fritsch, Anatol W., Li, Xinzhi, Stange, Roland, Pawlizak, Steve, Kießling, Tobias R., Morawetz, Erik, Grosser, Steffen, Sauer, Frank, Lippoldt, Jürgen, Renner, Frederic, Friebe, Sabrina, Zink, Mareike, Bendrat, Klaus, Braun, Jürgen, Oktay, Maja H., Condeelis, John, Briest, Susanne, Wolf, Benjamin, Horn, Lars-Christian, Höckel, Michael, Aktas, Bahriye, Marchetti, M. Cristina, Manning, M. Lisa, Niendorf, Axel, Bi, Dapeng, and Käs, Josef A.

Published
2022
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22. MSI testing: What’s new? What should be considered?

Author

Rüschoff, Josef, Baretton, Gustavo, Bläker, Hendrik, Dietmaier, Wolfgang, Dietel, Manfred, Hartmann, Arndt, Horn, Lars-Christian, Jöhrens, Korinna, Kirchner, Thomas, Knüchel, Ruth, Mayr, Doris, Merkelbach-Bruse, Sabine, Schildhaus, Hans-Ulrich, Schirmacher, Peter, Tiemann, Markus, Tiemann, Katharina, Weichert, Wilko, and Büttner, Reinhard

Published
2021
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23. MSI-Testung: Was ist neu? Was ist zu beachten?

Author

Rüschoff, Josef, Baretton, Gustavo, Bläker, Hendrik, Dietmaier, Wolfgang, Dietel, Manfred, Hartmann, Arndt, Horn, Lars-Christian, Jöhrens, Korinna, Kirchner, Thomas, Knüchel, Ruth, Mayr, Doris, Merkelbach-Bruse, Sabine, Schildhaus, Hans-Ulrich, Schirmacher, Peter, Tiemann, Markus, Tiemann, Katharina, Weichert, Wilko, and Büttner, Reinhard

Published
2021
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24. Molecular Subtypes of Vulvar Squamous Cell Carcinoma: The Significance of HPV-Independent/p53 Wild Type.

Author

Horn, Lars-Christian, Brambs, Christine E., Gilks, Blake, Hoang, Lien, Singh, Naveena, Hiller, Grit Gesine Ruth, Hering, Kathrin, McAlpine, Jessica N., Jamieson, Amy, Alfaraidi, Mona, Aktas, Bahriye, Dornhöfer, Nadja, and Höhn, Anne Kathrin

Subjects
*SQUAMOUS cell carcinoma, *COMPUTER-assisted molecular modeling, *VULVAR tumors, *PAPILLOMAVIRUSES, *IMMUNOHISTOCHEMISTRY, *GENE expression profiling, *ONCOGENES, *GENETIC mutation, *MOLECULAR biology, *STAINS & staining (Microscopy)
Abstract

Simple Summary: The distinct histopathogenetic pathways of vulvar squamous cell neoplasia have led to a shift from a morphology-based to an etiology/molecular-based histopathologic classification, adopted in the most recent WHO Classification of Female Genital Tumours. There are two main categories: HPV-associated (HPVa) and HPV-independent (HPVi) vulvar squamous neoplasia. Most HPVi VSCCs have an underlying TP53 mutation, but attention has recently focused on the uncommon third molecular subtype: TP53 wild-type HPVi VSCC. We review this shift to the etiology/molecular-based classification of VSCC, emphasizing the diagnostic and treatment implications of this change and highlighting the third molecular subtype. Vulvar carcinoma is a rare disease, meeting the criteria for a "rare cancer", but its incidence is increasing, especially in women <60 years of age. Squamous cell carcinoma (VSCC) accounts for the overwhelming majority of vulvar carcinomas and is the focus of this review. As with many cancers, the increased understanding of molecular events during tumorigenesis has led to the emergence of the molecular subclassification of VSCC, which is subclassified into tumors that arise secondary to high-risk human papillomavirus infection (HPV-associated, or HPVa) and those that arise independently of HPV (HPVi), most commonly in the setting of a chronic inflammatory condition of the vulvar skin. This latter group of HPVi VSCC arises in most cases secondary to mutations in TP53, but recently, attention has focused on the uncommon TP53 wild-type HPVi VSCC. These three molecular subtypes of VSCC (HPVa, HPVi p53 abnormal, and HPVi p53 wild type), as well as their precursor lesions, cannot be diagnosed based on a routine histopathological examination or immunostaining for p53 and p16 as surrogate markers for TP53 mutation and high-risk HPV infection, respectively, are required. The molecular subtyping of VSCC shows high reproducibility and provides important prognostic information. HPVa VSCC has the most favorable prognosis, while HPVi VSCC with TP53 mutations (p53abn) has the worst prognosis, and HPVi VSCC with wild-type TP53 (p53wt) has an intermediate prognosis. In this review, we discuss the evidence supporting this molecular subclassification and its implications for the diagnosis and treatment of VSCC and its precursors. [ABSTRACT FROM AUTHOR]

Published
2024
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25. Changes in the tumour microenvironment mark the transition from serous borderline tumour to low‐grade serous carcinoma.

Author

Vallejos, Rodrigo, Zhantuyakova, Almira, Negri, Gian Luca, Martin, Spencer D, Spencer, Sandra E, Thornton, Shelby, Leung, Samuel, Lynch, Branden, Qin, Yimei, Chow, Christine, Liang, Brooke, Zdravko, Sabrina, Douglas, J Maxwell, Milne, Katy, Mateyko, Bridget, Nelson, Brad H, Howitt, Brooke E, Kommoss, Felix KF, Horn, Lars‐Christian, and Hoang, Lien

Subjects
REGULATORY T cells, OVARIAN tumors, TUMOR microenvironment, BIOMARKERS, T cells
Abstract

Low‐grade serous ovarian carcinoma (LGSC) is a rare and lethal subtype of ovarian cancer. LGSC is pathologically, biologically, and clinically distinct from the more common high‐grade serous ovarian carcinoma (HGSC). LGSC arises from serous borderline ovarian tumours (SBTs). The mechanism of transformation for SBTs to LGSC remains poorly understood. To better understand the biology of LGSC, we performed whole proteome profiling of formalin‐fixed, paraffin‐embedded tissue blocks of LGSC (n = 11), HGSC (n = 19), and SBTs (n = 26). We identified that the whole proteome is able to distinguish between histotypes of the ovarian epithelial tumours. Proteins associated with the tumour microenvironment were differentially expressed between LGSC and SBTs. Fibroblast activation protein (FAP), a protein expressed in cancer‐associated fibroblasts, is the most differentially abundant protein in LGSC compared with SBT. Multiplex immunohistochemistry (IHC) for immune markers (CD20, CD79a, CD3, CD8, and CD68) was performed to determine the presence of B cells, T cells, and macrophages. The LGSC FAP+ stroma was associated with greater abundance of Tregs and M2 macrophages, features not present in SBTs. Our proteomics cohort reveals that there are changes in the tumour microenvironment in LGSC compared with its putative precursor lesion, SBT. These changes suggest that the tumour microenvironment provides a supportive environment for LGSC tumourigenesis and progression. Thus, targeting the tumour microenvironment of LGSC may be a viable therapeutic strategy. © 2024 The Pathological Society of Great Britain and Ireland. [ABSTRACT FROM AUTHOR]

Published
2024
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26. Different contractility modes control cell escape from multicellular spheroids and tumor explants

Author

Blauth, Eliane, primary, Grosser, Steffen, additional, Sauer, Frank, additional, Merkel, Mario, additional, Kubitschke, Hans, additional, Warmt, Enrico, additional, Morawetz, Erik W., additional, Friedrich, Philip, additional, Wolf, Benjamin, additional, Briest, Susanne, additional, Hiller, Grit Gesine Ruth, additional, Horn, Lars-Christian, additional, Aktas, Bahriye, additional, and Käs, Josef A., additional

Published
2024
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37. Invasives Karzinom der Vagina

Author

Ackermann, Sven, Dannecker, Christian, Horn, Lars-Christian, Alt-Radtke, Celine, Schnürch, Hans-Georg, Hantschmann, Peer, Weikel, Wolfgang, Wölber, Linn, Marnitz-Schulze, Simone, Barinoff, Jana, Mehlhorn, Grit, Günthert, Andreas, Mallmann, Peter, Schnürch, Hans-Georg, editor, Hampl, Monika, editor, and Wölber, Linn, editor

Published
2018
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38. Vaginale intraepitheliale Neoplasie (VaIN)

Author

Ackermann, Sven, Dannecker, Christian, Horn, Lars-Christian, Schnürch, Hans-Georg, Hantschmann, Peer, Denecke, Agnieszka, Petry, Karl Ulrich, Mehlhorn, Grit, Schnürch, Hans-Georg, editor, Hampl, Monika, editor, and Wölber, Linn, editor

Published
2018
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