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Cell Jan 2000
Review
Topics: Animals; Apoptosis; Cell Transformation, Neoplastic; Gene Expression Regulation, Neoplastic; Humans; Neoplasms; Neoplasms, Experimental; Neovascularization, Pathologic
PubMed: 10647931
DOI: 10.1016/s0092-8674(00)81683-9 -
Indian Journal of Cancer 2016Cancer is one of the most dreaded diseases of the 20th century and spreading further with continuance and increasing incidence in the 21st century. The situation is so... (Review)
Review
Cancer is one of the most dreaded diseases of the 20th century and spreading further with continuance and increasing incidence in the 21st century. The situation is so alarming that every fourth person is having a lifetime risk of cancer. India registers more than 11 lakh new cases of cancer every year, whereas, this figure is above 14 million worldwide. Is cancer curable? The short answer to this question is "Yes." In fact, all cancers are curable if they are caught early enough. Cancer cells continue to grow unless one of four things occur: (1) The cancerous mass is removed surgically; (2) using chemotherapy or another type of cancer-specific medication, such as hormonal therapy; (3) using radiation therapy; or (4) the cancer cells shrink and disappear on their own.
Topics: Humans; Neoplasms; Survival Rate
PubMed: 28244479
DOI: 10.4103/0019-509X.200658 -
Signal Transduction and Targeted Therapy Jun 2020Ferroptosis is a new form of programmed cell death characterized by the accumulation of iron-dependent lethal lipid peroxides. Recent discoveries have focused on... (Review)
Review
Ferroptosis is a new form of programmed cell death characterized by the accumulation of iron-dependent lethal lipid peroxides. Recent discoveries have focused on alterations that occur in lipid metabolism during ferroptosis and have provided intriguing insights into the interplay between ferroptosis and lipid metabolism in cancer. Their interaction regulates the initiation, development, metastasis, therapy resistance of cancer, as well as the tumor immunity, which offers several potential strategies for cancer treatment. This review is a brief overview of the features characterizing the interaction between ferroptosis and lipid metabolism, and highlights the significance of this interaction in cancer.
Topics: Animals; Ferroptosis; Humans; Lipid Metabolism; Neoplasm Metastasis; Neoplasms
PubMed: 32606298
DOI: 10.1038/s41392-020-00216-5 -
Developmental Cell May 2021Tumors undergo metabolic transformations to sustain uncontrolled proliferation, avoid cell death, and seed in secondary organs. An increased focus on cancer lipid... (Review)
Review
Tumors undergo metabolic transformations to sustain uncontrolled proliferation, avoid cell death, and seed in secondary organs. An increased focus on cancer lipid metabolism has unveiled a number of mechanisms that promote tumor growth and survival, many of which are independent of classical cellular bioenergetics. These mechanisms include modulation of ferroptotic-mediated cell death, support during tumor metastasis, and interactions with the cells of the tumor microenvironment. As such, targeting lipid metabolism for anti-cancer therapies is attractive, with recent work on small-molecule inhibitors identifying compounds to target lipid metabolism. Here, we discuss these topics and identify open questions.
Topics: Animals; Diet; Ferroptosis; Humans; Lipid Metabolism; Neoplasms; Signal Transduction; Tumor Microenvironment
PubMed: 33945792
DOI: 10.1016/j.devcel.2021.04.013 -
Clinical Cancer Research : An Official... May 2018Pathogenic germline variants cause a hereditary cancer predisposition syndrome with a variety of manifestations. In addition to conferring increased cancer risks for... (Review)
Review
Pathogenic germline variants cause a hereditary cancer predisposition syndrome with a variety of manifestations. In addition to conferring increased cancer risks for pleuropulmonary blastoma (PPB) and ovarian sex cord-stromal tumors, particularly Sertoli-Leydig cell tumor, individuals with pathogenic germline variants may also develop lung cysts, cystic nephroma, renal sarcoma and Wilms tumor, nodular hyperplasia of the thyroid, nasal chondromesenchymal hamartoma, ciliary body medulloepithelioma, genitourinary embryonal rhabdomyosarcoma, and brain tumors including pineoblastoma and pituitary blastoma. In May 2016, the International PPB Registry convened the inaugural International Symposium to develop consensus testing and surveillance and treatment recommendations. Attendees from North America, Europe, and Russia provided expert representation from the disciplines of pediatric oncology, endocrinology, genetics, genetic counseling, radiology, pediatric surgery, pathology, and clinical research. Recommendations are provided for genetic testing; prenatal management; and surveillance for -associated pulmonary, renal, gynecologic, thyroid, ophthalmologic, otolaryngologic, and central nervous system tumors and gastrointestinal polyps. Risk for most -associated neoplasms is highest in early childhood and decreases in adulthood. Individual and caregiver education and judicious imaging-based surveillance are the primary recommended approaches. These testing and surveillance recommendations reflect a consensus of expert opinion and current literature. As research expands, guidelines for screening and treatment will continue to be updated. .
Topics: Algorithms; DEAD-box RNA Helicases; Disease Management; Female; Genetic Association Studies; Genetic Predisposition to Disease; Genetic Testing; Genotype; Global Health; Humans; Inheritance Patterns; Mass Screening; Mutation; Neoplastic Syndromes, Hereditary; Penetrance; Prenatal Diagnosis; Prevalence; Public Health Surveillance; Ribonuclease III; Risk Assessment
PubMed: 29343557
DOI: 10.1158/1078-0432.CCR-17-3089 -
Cell Metabolism Jan 2018The benefits of exercise training for cancer patients are becoming increasingly evident. Physical exercise has been shown to reduce cancer incidence and inhibit tumor... (Review)
Review
The benefits of exercise training for cancer patients are becoming increasingly evident. Physical exercise has been shown to reduce cancer incidence and inhibit tumor growth. Here we provide the status of the current molecular understanding of the effect of exercise on cancer. We propose that exercise has a role in controlling cancer progression through a direct effect on tumor-intrinsic factors, interplay with whole-body exercise effects, alleviation of cancer-related adverse events, and improvement of anti-cancer treatment efficacy. These findings have wide-ranging societal implications, as this understanding may lead to changes in cancer treatment strategies.
Topics: Carcinogenesis; Exercise; Humans; Immunity; Models, Biological; Neoplasms
PubMed: 29056514
DOI: 10.1016/j.cmet.2017.09.015 -
Cancer Discovery Feb 2022Pediatric tumors are uncommon, yet are the leading cause of cancer-related death in childhood. Tumor types, molecular characteristics, and pathogenesis are unique, often... (Review)
Review
Pediatric tumors are uncommon, yet are the leading cause of cancer-related death in childhood. Tumor types, molecular characteristics, and pathogenesis are unique, often originating from a single genetic driver event. The specific diagnostic challenges of childhood tumors led to the development of the first World Health Organization (WHO) Classification of Pediatric Tumors. The classification is rooted in a multilayered approach, incorporating morphology, IHC, and molecular characteristics. The volume is organized according to organ sites and provides a single, state-of-the-art compendium of pediatric tumor types. A special emphasis was placed on "blastomas," which variably recapitulate the morphologic maturation of organs from which they originate. SIGNIFICANCE: In this review, we briefly summarize the main features and updates of each chapter of the inaugural WHO Classification of Pediatric Tumors, including its rapid transition from a mostly microscopic into a molecularly driven classification systematically taking recent discoveries in pediatric tumor genomics into account.
Topics: Brain Neoplasms; Child; Genomics; Humans; World Health Organization
PubMed: 34921008
DOI: 10.1158/2159-8290.CD-21-1094 -
DICER1 tumor predisposition syndrome: an evolving story initiated with the pleuropulmonary blastoma.Modern Pathology : An Official Journal... Jan 2022DICER1 syndrome (OMIM 606241, 601200) is a rare autosomal dominant familial tumor predisposition disorder with a heterozygous DICER1 germline mutation. The most common... (Review)
Review
DICER1 syndrome (OMIM 606241, 601200) is a rare autosomal dominant familial tumor predisposition disorder with a heterozygous DICER1 germline mutation. The most common tumor seen clinically is the pleuropulmonary blastoma (PPB), a lung neoplasm of early childhood which is classified on its morphologic features into four types (IR, I, II and III) with tumor progression over time within the first 4-5 years of life from the prognostically favorable cystic type I to the unfavorable solid type III. Following the initial report of PPB, its association with other cystic neoplasms was demonstrated in family studies. The detection of the germline mutation in DICER1 provided the opportunity to identify and continue to recognize a number seemingly unrelated extrapulmonary neoplasms: Sertoli-Leydig cell tumor, gynandroblastoma, embryonal rhabdomyosarcomas of the cervix and other sites, multinodular goiter, differentiated and poorly differentiated thyroid carcinoma, cervical-thyroid teratoma, cystic nephroma-anaplastic sarcoma of kidney, nasal chondromesenchymal hamartoma, intestinal juvenile-like hamartomatous polyp, ciliary body medulloepithelioma, pituitary blastoma, pineoblastoma, primary central nervous system sarcoma, embryonal tumor with multilayered rosettes-like cerebellar tumor, PPB-like peritoneal sarcoma, DICER1-associated presacral malignant teratoid neoplasm and other non-neoplastic associations. Each of these neoplasms is characterized by a second somatic mutation in DICER1. In this review, we have summarized the salient clinicopathologic aspects of these tumors whose histopathologic features have several overlapping morphologic attributes particularly the primitive mesenchyme often with rhabdomyoblastic and chondroid differentiation and an uncommitted spindle cell pattern. Several of these tumors have an initial cystic stage from which there is progression to a high grade, complex patterned neoplasm. These pathologic findings in the appropriate clinical setting should serve to alert the pathologist to the possibility of a DICER1-associated neoplasm and initiate appropriate testing on the neoplasm and to alert the clinician about the concern for a DICER1 mutation.
Topics: Causality; Germ-Line Mutation; Humans; Lung Neoplasms; Pleural Neoplasms; Pulmonary Blastoma; Ribonuclease III; Syndrome
PubMed: 34599283
DOI: 10.1038/s41379-021-00905-8 -
Pathologica Jun 2023Among non-small cell lung cancers (NSCLCs), sarcomatoid carcinomas account for 3%. They are rare tumours with a poor prognosis, classified into three subgroups, namely...
Among non-small cell lung cancers (NSCLCs), sarcomatoid carcinomas account for 3%. They are rare tumours with a poor prognosis, classified into three subgroups, namely pleomorphic carcinoma, pulmonary blastoma and carcinosarcoma. In the 5th edition of WHO Classification of Thoracic Tumours more space is given to SMARC4-deficient lung cancers. Although studies on SMARCA4-deficient lung tumours are limited, a small percentage of SMARCA4 loss is present within NSCLCs. This finding is clinically relevant, as the loss of the SMARCA4 gene is associated with a worse prognosis. In our study, we analysed the presence of the main catalytic subunit of the SMARCA4 gene, the BRG1 protein, in 60 sarcomatoid lung tumours. The results of our study show that 5.3% of sarcomatoid carcinomas have BRG1-loss in tumour cells, proving that a non-negligible amount of lung sarcomatoid carcinomas are SMARCA4-deficient. These data open the debate on the necessity of including the detection of SMARCA4 within a standardised immunohistochemical panel.
Topics: Humans; Diagnosis, Differential; Neoplasms, Glandular and Epithelial; Carcinoma, Non-Small-Cell Lung; Lung Neoplasms; Carcinoma; Lung; DNA Helicases; Nuclear Proteins; Transcription Factors
PubMed: 37387441
DOI: 10.32074/1591-951X-847