Relevant bibliographies by topics / Molecular subclassification

Academic literature on the topic 'Molecular subclassification'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Molecular subclassification"

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Tsukasaki, Kunihiro, Olivier Hermine, Ali Bazarbachi, Lee Ratner, Juan Carlos Ramos, William Harrington, Deirdre O’Mahony, et al. "Definition, Prognostic Factors, Treatment, and Response Criteria of Adult T-Cell Leukemia-Lymphoma: A Proposal From an International Consensus Meeting." Journal of Clinical Oncology 27, no. 3 (January 20, 2009): 453–59. http://dx.doi.org/10.1200/jco.2008.18.2428.

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Adult T-cell leukemia-lymphoma (ATL) is a distinct peripheral T-lymphocytic malignancy associated with a retrovirus designated human T-cell lymphotropic virus type I (HTLV-1). The diversity in clinical features and prognosis of patients with this disease has led to its subclassification into the following four categories: acute, lymphoma, chronic, and smoldering types. The chronic and smoldering subtypes are considered indolent and are usually managed with watchful waiting until disease progression, analogous to the management of some patients with chronic lymphoid leukemia (CLL) or other indolent histology lymphomas. Patients with aggressive ATL generally have a poor prognosis because of multidrug resistance of malignant cells, a large tumor burden with multiorgan failure, hypercalcemia, and/or frequent infectious complications as a result of a profound T-cell immunodeficiency. Under the sponsorship of the 13th International Conference on Human Retrovirology: HTLV, a group of ATL researchers joined to form a consensus statement based on established data to define prognostic factors, clinical subclassifications, and treatment strategies. A set of response criteria specific for ATL reflecting a combination of those for lymphoma and CLL was proposed. Clinical subclassification is useful but is limited because of the diverse prognosis among each subtype. Molecular abnormalities within the host genome, such as tumor suppressor genes, may account for these diversities. A treatment strategy based on the clinical subclassification and prognostic factors is suggested, including watchful waiting approach, chemotherapy, antiviral therapy, allogeneic hematopoietic stem-cell transplantation (alloHSCT), and targeted therapies.
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Köbel, Martin, and Eun Young Kang. "The Evolution of Ovarian Carcinoma Subclassification." Cancers 14, no. 2 (January 14, 2022): 416. http://dx.doi.org/10.3390/cancers14020416.

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The phenotypically informed histotype classification remains the mainstay of ovarian carcinoma subclassification. Histotypes of ovarian epithelial neoplasms have evolved with each edition of the WHO Classification of Female Genital Tumours. The current fifth edition (2020) lists five principal histotypes: high-grade serous carcinoma (HGSC), low-grade serous carcinoma (LGSC), mucinous carcinoma (MC), endometrioid carcinoma (EC) and clear cell carcinoma (CCC). Since histotypes arise from different cells of origin, cell lineage-specific diagnostic immunohistochemical markers and histotype-specific oncogenic alterations can confirm the morphological diagnosis. A four-marker immunohistochemical panel (WT1/p53/napsin A/PR) can distinguish the five principal histotypes with high accuracy, and additional immunohistochemical markers can be used depending on the diagnostic considerations. Histotypes are further stratified into molecular subtypes and assessed with predictive biomarker tests. HGSCs have recently been subclassified based on mechanisms of chromosomal instability, mRNA expression profiles or individual candidate biomarkers. ECs are composed of the same molecular subtypes (POLE-mutated/mismatch repair-deficient/no specific molecular profile/p53-abnormal) with the same prognostic stratification as their endometrial counterparts. Although methylation analyses and gene expression and sequencing showed at least two clusters, the molecular subtypes of CCCs remain largely elusive to date. Mutational and immunohistochemical data on LGSC have suggested five molecular subtypes with prognostic differences. While our understanding of the molecular composition of ovarian carcinomas has significantly advanced and continues to evolve, the need for treatment options suitable for these alterations is becoming more obvious. Further preclinical studies using histotype-defined and molecular subtype-characterized model systems are needed to expand the therapeutic spectrum for women diagnosed with ovarian carcinomas.
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Effendi, Kathryn, Wit Thun Kwa, Akihisa Ueno, and Michiie Sakamoto. "The role of molecular pathology in the precision diagnosis and subclassification of hepatocellular carcinoma." Universa Medicina 41, no. 2 (June 13, 2022): 194–206. http://dx.doi.org/10.18051/univmed.2022.v41.194-206.

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Hepatocellular carcinoma (HCC) remains a leading cause of cancer death worldwide despite recent advances in surveillance and therapeutic management. The outcomes for HCC patients remain poor, often as a result of late diagnosis or lack of effective treatments. Early detection and precise diagnosis are evidently crucial in improving the prognosis of HCC. However, HCC is a highly heterogeneous cancer with various clinical backgrounds and altered molecular pathways; these factors make its precise diagnosis more difficult. Approximately 25% of HCCs harbor actionable mutations, which are yet to be translated into clinical practice. In the era of precision medicine, molecular or genomic information are indispensable for HCC diagnosis and prognosis. Exploring genomic alterations has become a requirement for identifying the molecular subtypes of HCC. Recent studies have introduced molecular markers to help identify early HCC and to clarify its multistep process of carcinogenesis. The subclassification of tumors into proliferation class and nonproliferation class HCCs gives pointers to the HCC phenotype and facilitates the selection of appropriate treatments. In this review, we broadly summarize some of the latest insights into HCC subclassification from the perspective of molecular pathology. Immunohistochemistry-based subclassification allows improved characterization of HCC in daily clinical practice. Moreover, analysis of the immune microenvironment, intra-tumoral morphological heterogeneity, and imaging features gives additional information regarding the classification of HCC. Combinations of these approaches are expected to inform and advance the precision diagnosis and management of HCC.
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Hytiroglou, Prodromos, Paulette Bioulac-Sage, Neil D. Theise, and Christine Sempoux. "Etiology, Pathogenesis, Diagnosis, and Practical Implications of Hepatocellular Neoplasms." Cancers 14, no. 15 (July 28, 2022): 3670. http://dx.doi.org/10.3390/cancers14153670.

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Hepatocellular carcinoma (HCC), a major global contributor of cancer death, usually arises in a background of chronic liver disease, as a result of molecular changes that deregulate important signal transduction pathways. Recent studies have shown that certain molecular changes of hepatocarcinogenesis are associated with clinicopathologic features and prognosis, suggesting that subclassification of HCC is practically useful. On the other hand, subclassification of hepatocellular adenomas (HCAs), a heterogenous group of neoplasms, has been well established on the basis of genotype–phenotype correlations. Histologic examination, aided by immunohistochemistry, is the gold standard for the diagnosis and subclassification of HCA and HCC, while clinicopathologic correlation is essential for best patient management. Advances in clinico-radio-pathologic correlation have introduced a new approach for the diagnostic assessment of lesions arising in advanced chronic liver disease by imaging (LI-RADS). The rapid expansion of knowledge concerning the molecular pathogenesis of HCC is now starting to produce new therapeutic approaches through precision oncology. This review summarizes the etiology and pathogenesis of HCA and HCC, provides practical information for their histologic diagnosis (including an algorithmic approach), and addresses a variety of frequently asked questions regarding the diagnosis and practical implications of these neoplasms.
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Akhtar, Mohammed, Issam A. Al-Bozom, Mohamed Ben Gashir, and Noheir M. Taha. "Intrinsic Molecular Subclassification of Urothelial Carcinoma of the Bladder." Advances In Anatomic Pathology 26, no. 4 (July 2019): 251–56. http://dx.doi.org/10.1097/pap.0000000000000235.

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Li, Dong, Shuho Semba, Ming Wu, and Hiroshi Yokozaki. "Molecular pathological subclassification of mucinous adenocarcinoma of the colorectum." Pathology International 55, no. 12 (December 2005): 766–74. http://dx.doi.org/10.1111/j.1440-1827.2005.01903.x.

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Tsuiimoto, Gozoh. "α1-adrenoceptor (α1AR) subclassification by pharmacology and molecular cloning." Japanese Journal of Pharmacology 67 (1995): 15. http://dx.doi.org/10.1016/s0021-5198(19)46039-3.

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Thompson, Emily F., Lynn Hoang, Anne Kathrin Höhn, Andrea Palicelli, Karen L. Talia, Nairi Tchrakian, Janine Senz, et al. "Molecular subclassification of vulvar squamous cell carcinoma: reproducibility and prognostic significance of a novel surgical technique." International Journal of Gynecologic Cancer 32, no. 8 (June 28, 2022): 977–85. http://dx.doi.org/10.1136/ijgc-2021-003251.

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ObjectivesVulvar squamous cell carcinoma is subclassified into three prognostically relevant groups: (i) human papillomavirus (HPV) associated, (ii) HPV independent p53 abnormal (mutant pattern), and (iii) HPV independent p53 wild type. Immunohistochemistry for p16 and p53 serve as surrogates for HPV viral integration and TP53 mutational status. We assessed the reproducibility of the subclassification based on p16 and p53 immunohistochemistry and evaluated the prognostic significance of vulvar squamous cell carcinoma molecular subgroups in a patient cohort treated by vulvar field resection surgery.MethodsIn this retrospective cohort study, 68 cases treated by vulvar field resection were identified from the Leipzig School of Radical Pelvic Surgery. Immunohistochemistry for p16 and p53 was performed at three different institutions and evaluated independently by seven pathologists and two trainees. Tumors were classified into one of four groups: HPV associated, HPV independent p53 wild type, HPV independent p53 abnormal, and indeterminate. Selected cases were further interrogated by (HPV RNA in situ hybridization, TP53 sequencing).ResultsFinal subclassification yielded 22 (32.4%) HPV associated, 41 (60.3%) HPV independent p53 abnormal, and 5 (7.3%) HPV independent p53 wild type tumors. Interobserver agreement (overall Fleiss’ kappa statistic) for the four category classification was 0.74. No statistically significant differences in clinical outcomes between HPV associated and HPV independent vulvar squamous cell carcinoma were observed.ConclusionInterobserver reproducibility of vulvar squamous cell carcinoma subclassification based on p16 and p53 immunohistochemistry may support routine use in clinical practice. Vulvar field resection surgery showed no significant difference in clinical outcomes when stratified based on HPV status.
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Liau, Jau-Yu, Jia-Huei Tsai, Ray-Hwang Yuan, Chih-Ning Chang, Hsin-Jung Lee, and Yung-Ming Jeng. "Morphological subclassification of intrahepatic cholangiocarcinoma: etiological, clinicopathological, and molecular features." Modern Pathology 27, no. 8 (January 10, 2014): 1163–73. http://dx.doi.org/10.1038/modpathol.2013.241.

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Nagasaka, Toru, Masaharu Gunji, Noboru Hosokai, Kumiko Hayashi, Hiroshi Ikeda, Masafumi Ito, and Suguru Inao. "FISH 1p/19q deletion/imbalance for molecular subclassification of glioblastoma." Brain Tumor Pathology 24, no. 1 (May 25, 2007): 1–5. http://dx.doi.org/10.1007/s10014-006-0209-6.

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Dissertations / Theses on the topic "Molecular subclassification"

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Schwalbe, Edward Carl. "Molecular subclassification of medulloblastoma and its utility for disease prognostication." Thesis, University of Newcastle upon Tyne, 2012. http://hdl.handle.net/10443/1388.

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Medulloblastoma is the most common malignant brain tumour of childhood. Transcriptomic classification of the disease has indicated the existence of discrete molecular subgroups of medulloblastoma, although the precise number, nature and clinical significance of these subgroups remains unclear. Two groups, characterised by activation of the WNT and SHH signalling pathways, are common to all published studies. An assay for the rapid diagnosis of medulloblastoma subgroups was therefore designed, using transcriptomic gene signatures of pathway activation for the WNT and SHH signalling pathways. The successful validation of these gene signatures in vitro and in silico enabled a meta-analysis of 173 new and published cases to be performed, which defined the molecular and clinico-pathological correlates of the disease subgroups more precisely. WNT subgroup cases were associated with CTNNB1 mutation, chromosome 6 loss and classic histology and were diagnosed > 5 years of age. SHH cases predominated in infants and showed an age-dependent relationship to desmoplastic / nodular histology. WNT / SHH independent tumours showed all histologies, peaked at 3 to 6 years and were associated with chromosome 17p loss. A novel DNA methylation array-based approach was next applied to disease subclassification. Using consensus clustering, based on non-negative matrix factorisation, four methylomic subgroups were identified in a training cohort (n = 100), which were robustly validated in a test cohort (n = 130). The subgroups were characterised by significant relationships to specific clinico-pathological and molecular markers. Two subgroups were characterised by activation of the WNT and SHH signalling pathways and showed equivalent clinico-pathological and molecular characteristics to the previously defined transcriptomic subgroups. For the WNT / SHH independent subgroups, group I was associated with a loss of chromosome 17p, whereas group II was enriched for large cell / anaplastic (LCA) histology. The WNT subgroup was associated with a favourable prognosis, while no survival differences were apparent between the remaining subgroups (SHH, group I, group II). Specific methylation biomarkers were identified for the discrimination of all subgroups. Assays of DNA methylation status were robust in derivatives of FFPE tissues, enabling testing in routinely-collected clinical material. Finally, the prognostic potential of methylomic biomarkers was investigated in a large clinical trials-based cohort (n = 191), with particular focus on the non-WNT subgroups (n = 163), where subgroup membership was not prognostic. Using the Cox Boost algorithm, which adds high dimensional data to mandatory clinical covariates to form cross-validated prognostic Cox survival models, the methylation status of MXI1 and IL8 were each identified as independent prognostic markers. These were incorporated into a novel risk stratification scheme, based on the cumulative assessment of disease risk using clinical (metastatic disease; poor prognosis), pathological (LCA pathology, poor prognosis) and methylomic variables (WNT subgroup, favourable prognosis; MXI1 and IL8 status). Importantly, this scheme assigns 46% of cases to a low risk group of patients (>90% survival) who could potentially be treated less intensively, with the aim of reducing therapy-associated late effects. This model out-performed the current clinical and other state-of-the-art medulloblastoma risk classification schemes. These data provide clear precedent for the utility of DNA methylation biomarkers for disease subclassification and prognostication in medulloblastoma, and their clinical application in diagnostic tumour biopsies.
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Books on the topic "Molecular subclassification"

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Weller, Michael, Michael Brada, Tai-Tong Wong, and Michael A. Vogelbaum. Astrocytic tumours: diffuse astrocytoma, anaplastic astrocytoma, glioblastoma, and gliomatosis cerebri. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0003.

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Astrocytic gliomas are primary brain tumours thought to originate from neural stem or progenitor cells. They are assigned grades II, III, or IV by the World Health Organization according to degree of malignancy as defined by histology. The following molecular markers are increasingly used for diagnostic subclassification or clinical decision-making: 1p/19q co-deletion status, O6-methylguanine-DNA methyltransferase (MGMT) promoter methylation status, and isocitrate dehydrogenase 1 and 2 mutation status. Extent of resection is a favourable prognostic factor, but surgery is never curative. Radiotherapy prolongs progression-free survival across all astrocytic glioma entities. Alkylating agent chemotherapy is an active treatment in particular for patients with MGMT promoter-methylated tumours. Anti-angiogenic therapies have failed to improve survival, and the current focus of major clinical trials is on novel targeted agents or on immunotherapy.
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Book chapters on the topic "Molecular subclassification"

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Wickenhauser, Claudia, Daniel Bethmann, Zipei Feng, Shawn M. Jensen, Carmen Ballesteros-Merino, Chiara Massa, Andre Steven, et al. "Multispectral Fluorescence Imaging Allows for Distinctive Topographic Assessment and Subclassification of Tumor-Infiltrating and Surrounding Immune Cells." In Methods in Molecular Biology, 13–31. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8979-9_2.

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Athauda, Avani, and Ian Chau. "Advances in Molecular Subclassification of Colorectal Cancer." In Advances in the Molecular Understanding of Colorectal Cancer. IntechOpen, 2019. http://dx.doi.org/10.5772/intechopen.80679.

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Conference papers on the topic "Molecular subclassification"

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Thompson, EF, L. Hoang, AK Höhn, A. Palicelli, KL Talia, N. Tchrakian, J. Senz, et al. "231 Molecular subclassification of vulvar squamous cell carcinoma: prognostic significance and reproducibility." In ESGO 2021 Congress. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/ijgc-2021-esgo.616.

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Bramsen, Jesper B., Mads H. Rasmussen, Halit Ongen, Søren Vang, Philippe Lamy, Manel B. Esteller, Emmanouil T. Dermitzakis, Torben F. Orntoft, and Claus L. Andersen. "Abstract 2630: Integration of tumor microenvironment and molecular subclassification of colorectal cancer identifies patient subsets with poor prognosis." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2630.

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Ferreira, Nancy, Darley Ferreira, and Thais Ferreira. "GENETIC EVALUATION OF MICROCALCIFICATIONS AS A PROGNOSTIC FACTOR." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2101.

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Introduction: Breast cancer is the most recurring type of cancer among women, with reduced mortality at an initial stage of lesion. From a radiological perspective, perceived microcalcifications may be associated with histological findings such as proliferative injuries with or without atypical features and ductal carcinoma in situ. Currently, percutaneous and vacuum biopsies allow for the correlation between anatomoradiological and identification of previous lesions and those that offer the risk of cancer. No biomarker has been established to predict the risk of cancer in women diagnosed with benign mammary disease. Doing so could strengthen the possibility of stratifying the individual risk of benign injuries for cancer. The platelet-derived growth factor receptor A (PDGFRA) plays its part in tumor oncogenesis, angiogenesis, and metastasis, and its activation is found in some kinds of cancer. In contrast, DNA methylation standards are initial changes to the development of cancer and may be helpful in its early identification, being regulated by a family of enzymes called DNMTs (DNA methyltransferase). Methods: The aim of this study was to evaluate the profile of BI-RADS® 4 and 5 mammary microcalcification women carriers and determine the level of the gene expression of possible molecular markers in 37 patients with mammary microcalcification (paraffin blocks) and 26 patients with breast cancer (fresh in RNA later tissue) cared for at the Hospital Barão de Lucena’s Mastology Ambulatory. Anatomoradiological aspects along with clinical findings have been evaluated , and percentage rates have been calculated. The PDGFRA and DNMTs (DMNT3a) gene expressions have been established using quantitative polymerase chain reaction (qPCR), with the use of β-actin as reference gene. Discussion: In the patients with mammary microcalcification, the average age was 55.9; predominantly whiteskinned subjects (p<0.014). Most of them were mothers (p<0.001), and the average menarche age was 13. The subgroups that presented greater significance were patients classified BI-RADS® in category IV (67.6%) and histological findings of nonproliferative lesion (p<0.001). Lesions of the ductal carcinoma in situ type (100%) presented positive estrogen and progesterone receptors, and 94.6% have undergone sectorectomy surgery by prior needling (p<0.001). The most damaged breast was the left one (62.2%), and the most affected quadrant was the top lateral one (59.5%) (p<0.001). There was no family history in 83.8% of the cases. In the tested microcalcification samples, it was not possible to observe the expression of PDGFRA. Nevertheless, 15 out of 37 patients with microcalcification showed an increase in the gene expression of DMNT3a, most of them greater than Luminal and triple-negative cancer types. Conclusion: The data presented here highlight the improvement on the description of BI-RADS® 4 subclassification in order to better conduct the clinical decision and also demonstrated the potential of DNMTs evaluation in microcalcification samples as a strategy to access the understanding about the role of these molecules in the breast cancer development.
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