Bibliografias temáticas / Genetic of cancer

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Literatura científica selecionada sobre o tema "Genetic of cancer"

Autor: Grafiati
Publicado: 21 de dezembro de 2024

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Artigos de revistas sobre o assunto "Genetic of cancer"

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Niendorf, Kristin Baker. "Genetic Library: Cancer Genetics". Journal of Genetic Counseling 11, n.º 5 (outubro de 2002): 429–34. http://dx.doi.org/10.1023/a:1016854001384.

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Gleich, Lyon L., e Frank N. Salamone. "Molecular Genetics of Head and Neck Cancer". Cancer Control 9, n.º 5 (setembro de 2002): 369–78. http://dx.doi.org/10.1177/107327480200900502.

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Background Head and neck cancers have multiple genetic abnormalities that influence tumor behavior and may be useful in developing new treatments. Methods Genetic alterations implicated in head and neck cancer oncogenesis and behavior are reviewed, and molecular techniques for detection and treatment are evaluated. Results The large number of genetic changes present in head and neck cancer cells precludes meaningful use of simple molecular tests and treatments. Detection of abnormalities in multiple genes provides better prognostic information than the detection and assessment of single mutations. Screening tests that rely on amplification of genetic material present in bodily fluids are hindered by the genomic complexity of head and neck cancer. Introduction of genetic material into head and neck cancer cells for gene therapy has shown some efficacy. Conclusions Head and neck cancers comprise a complex genetic disease. Although much has been learned about the molecular genetics of head and neck cancers, continued study of multiple genes is critical for further progress. Gene therapy, although promising, must also overcome this complexity.
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Stankov, Karmen, e Giovanni Romeo. "Cloning of the genes for non-medullary thyroid cancer: Methods and advances". Archive of Oncology 14, n.º 1-2 (2006): 30–34. http://dx.doi.org/10.2298/aoo0602030s.

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In last ten years, significant advances have occurred in thyroid endocrinology, as a consequence of the generalized use of molecular biology techniques. New genes involved in the development of thyroid cancer have been identified, which had a great impact on our understanding of thyroid cancer predisposition. All cancers are genetic in origin because they arise from mutations in a single somatic cell, but the genetic changes in sporadic cancers are confined to a particular tissue. In inherited cancers, a predisposing mutation is present in all somatic cells and in the germ line, which enables the transmission of risk to the next generation. Cancer genetics offers a model of how information on the genetics of inherited cancers could affect identification of individuals at increased genetic risk.
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Hamby, Lori, e Constance A. Griffin. "Genetic Library Video Reviews: Cancer Genetics". Journal of Genetic Counseling 12, n.º 2 (abril de 2003): 185–92. http://dx.doi.org/10.1023/a:1022615408076.

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Benninger, Michael S., Daniel Vandyke, Carol Bradford e Thomas Carey. "Genetics of Head and Neck Cancer (Introduction)". Otolaryngology–Head and Neck Surgery 112, n.º 5 (maio de 1995): P90. http://dx.doi.org/10.1016/s0194-5998(05)80212-8.

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Educational objectives: To review basic genetics and cytogenetics as they relate to human cancers and head and neck cancer and to become familiar with the basis of genetics of human cancer and successes in molecular and genetic research of squamous cell cancer.
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Woodman-Ross, Jacynda, Sierra O. Green, Jessica Corredor, Elissa Dodd-Eaton, Nathaniel Hernandez, Susan K. Peterson, Wenyi Wang e Banu K. Arun. "Abstract OT2-13-01: Willingness to Participate in a Trial Comparing Standard Genetic Counseling versus Genetic Counseling with Personalized Cancer Risks Estimates in Patients with Li-Fraumeni Syndrome". Cancer Research 83, n.º 5_Supplement (1 de março de 2023): OT2–13–01—OT2–13–01. http://dx.doi.org/10.1158/1538-7445.sabcs22-ot2-13-01.

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Abstract Background: Individuals with Li-Fraumeni Syndrome (LFS) have increased risk of developing breast cancer, sarcomas, brain tumors, leukemia, and other cancers throughout their lifetime. LFS is primarily caused by autosomal dominant germline mutations in the TP53 tumor suppressor gene. Due to the large number of cancers caused by LFS, and their variable age of presentation, each LFS family often presents very differently. Currently, standard genetic counseling for patients with LFS often involves general lifetime risk predictions for developing several primary cancers. At present, there are no standard tools available to help genetics providers obtain a personalized risk assessment for a patient with LFS based on their unique personal and family history data. To address this, the LFSPRO risk model was developed to estimate the likelihood of a proband having LFS, to provide cancer-specific risks of a first primary cancer, and to estimate risk of time to second primary cancer diagnosis by utilizing detailed personal and family history information. Specific Aims: This study aims to understand patients’ willingness to participate in a randomized trial comparing standard genetic counseling practice to personalized genetic counseling via LFSPRO risk estimates. Trial Design: Eligible patients or parents/guardians are invited via email to complete a survey assessing interest in a hypothetical clinical trial scenario where patients are randomized to receive one of two types of post-disclosure genetic counseling approaches: standard genetic counseling for TP53 results, involving generic risk predictions for developing cancers, or personalized risk information provided from LFSPRO. Following the hypothetical scenario, participants are asked about their perceived benefits and barriers to this research scenario and interest in receiving personalized risk results. Demographic information is also collected. Eligibility Criteria: Individuals who receive genetic counseling through MD Anderson Cancer Center genetics clinics specifically for TP53 genetic testing and who consent to undergo TP53 genetic testing or individuals who genetic testing already indicates a TP53 germline mutation are offered this survey. Patients must be 13 years or older to complete the survey, otherwise a parent/guardian may complete the survey on their behalf. Patients must have English fluency. Statistical methods: Descriptive statistics will be used to analyze the data and summarize the opinion of the participants. Accrual: Enrollment is set to open in July 2022. Currently, 157 patients have been identified to be invited to participate in the study. Funding: This research is supported by the Cancer Research and Prevention Institute of Texas. Contact: Jacynda Woodman-Ross, MS, CGC, The University of Texas MD Anderson Cancer Center, jawoodman@mdanderson.org Citation Format: Jacynda Woodman-Ross, Sierra O. Green, Jessica Corredor, Elissa Dodd-Eaton, Nathaniel Hernandez, Susan K. Peterson, Wenyi Wang, Banu K. Arun. Willingness to Participate in a Trial Comparing Standard Genetic Counseling versus Genetic Counseling with Personalized Cancer Risks Estimates in Patients with Li-Fraumeni Syndrome [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr OT2-13-01.
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Abdukhakimov, Abdulla Nusratillayevich, e Muqaddas Tukhtabievna Tukhtaboeva. "Molecular Genetic Factors Of Breast Cancer Development (Review)". American Journal of Medical Sciences and Pharmaceutical Research 02, n.º 07 (31 de julho de 2020): 112–16. http://dx.doi.org/10.37547/tajmspr/volume02issue07-14.

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Lee, John, Arushi Tripathy, Tannaz Guivatchian, Erika Koeppe, Elena Stoffel e Wajd Al-Holou. "EPCO-21. IDENTIFYING FACTORS THAT PREDICT GENETIC PREDISPOSITION TO BRAIN TUMOR FORMATION". Neuro-Oncology 25, Supplement_5 (1 de novembro de 2023): v128. http://dx.doi.org/10.1093/neuonc/noad179.0484.

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Abstract INTRODUCTION Increasing evidence suggests that glioma formation may have a greater hereditary component than initially thought. Identification of individuals with a genetic predisposition is critical for appropriate monitoring and treatment. OBJECTIVE To analyze the personal and family histories of patients with intrinsic brain tumors seen in a cancer genetics clinic to inform referral practices. METHODS A prospective database of cancer genetics data from a large multidisciplinary cancer genetics clinic was queried for brain tumors from 2007-2023. Genetic test results, age of brain cancer diagnosis, number/types of distinct cancers, oncologic family history, and personal and family history of cancer syndromes were recorded. Fisher’s exact tests and ANOVA were used for analysis. RESULTS Sixty-five patients with intrinsic brain tumors, which included 53 high and low grade gliomas, were identified. There were 33 males; the mean age of diagnosis was 34.6±23.4. Fifty-three (81.5%) had genetic testing performed. Of these, 19 (35.8%) were found to have germline pathogenic variants (PV), 10 (18.9%) had variants of unknown significance (VUS), and 24 (45.3%) were found to have no mutations. Patients with PVs were younger than patients with normal genetic screening (28.1 vs 41.5 years, p= 0.06), and patients with either PV or VUS were significantly younger (p= 0.04) than patients with normal screening. Regarding personal cancer history, patients with and without PVs had a similar history of personal cancers (p= 0.20). Regarding family history, only 1 patient with PV had a family history of brain cancer compared to 15 in patients with negative testing (5.3% vs 44.1%, p= 0.004). CONCLUSIONS Only younger age at presentation was identified as a predictor of a PV or VUS. A lack of personal/family history of cancer does not preclude a genetic predisposition to cancer. We recommend that younger patients with intrinsic brain tumors should be referred for genetic testing.
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Lahiri, Sayoni, Sara Pirzadeh-Miller, Kelsey Moriarty e Nisa Kubiliun. "Implementation of a Population-Based Cancer Family History Screening Program for Lynch Syndrome". Cancer Control 30 (abril de 2023): 107327482311750. http://dx.doi.org/10.1177/10732748231175011.

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Objectives Lynch syndrome increases risks for colorectal and other cancers. Though published Lynch syndrome cancer risk-management guidelines are effective for risk-reduction, the condition remains under-recognized. The Cancer Genetics Program at an academic medical center implemented a population-based cancer family history screening program, Detecting Unaffected Individuals with Lynch syndrome, to aid in identification of individuals with Lynch syndrome. Methods In this retrospective cohort study, simple cancer family history screening questionnaires were used to identify those at risk for Lynch syndrome. Program navigators triaged and educated those who screened positive about hereditary cancer, and genetic counseling and testing services, offering genetic counseling if eligible. Genetic counseling was provided primarily via telephone. Genetic counselors performed hereditary cancer risk assessment and offered genetic testing via hereditary cancer panels to those eligible. Remote service delivery models via telephone genetic counseling and at-home saliva testing were used to increase access to medical genetics services. Results This program screened 212,827 individuals, over half of whom were considered underserved, and identified 133 clinically actionable genetic variants associated with hereditary cancer. Of these, 47 (35%) were associated with Lynch syndrome while notably, 70 (53%) were not associated with hereditary colorectal cancer. Of 3,344 patients offered genetic counseling after initial triage, 2,441 (73%) elected to schedule the appointment and 1,775 individuals (73%) completed genetic counseling. Among underserved patients, telephone genetic counseling completion rates were significantly higher than in-person appointment completion rates ( P < .05). While remote service delivery improved appointment completion rates, challenges with genetic test completion using at-home saliva sample collection kits were observed, with 242 of 1592 individuals (15%) not completing testing. Conclusion Population-based cancer family history screening and navigation can help identify individuals with hereditary cancer syndromes across diverse patient populations, but logistics of certain downstream service delivery models can impact outcomes.
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Luo, Jian-Hua, e Yan Ping Yu. "Genetic factors underlying prostate cancer". Expert Reviews in Molecular Medicine 5, n.º 12 (15 de abril de 2003): 1–26. http://dx.doi.org/10.1017/s1462399403006057.

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Prostate cancer is one of the leading causes of cancer-related death in the USA. In the past decade, tremendous progress has been made in the identification and understanding of the genetic factors related to prostate cancer development. Unlike many other types of cancers, only a small fraction of prostate cancer cases are aggressive and life-threatening. The factors related to prostate cancer development and progression appear complex and diverse. This review summarises some of the important findings in the areas of genome and gene expression abnormalities in prostate cancer, and aims to provide a comprehensive view of new developments in these areas.
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Teses / dissertações sobre o assunto "Genetic of cancer"

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Michael, Agnieszka. "Genetic immunotherapy for cancer". Thesis, St George's, University of London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.437318.

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Singh, Rashmi. "Genetic predisposition to prostate cancer". Thesis, Institute of Cancer Research (University Of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416575.

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Skoglund, Johanna. "Genetic studies of colorectal cancer /". Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-098-5/.

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Wiklund, Fredrik. "Genetic epidemiology of prostate cancer". Doctoral thesis, Umeå : Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-281.

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Lutke, Holzik Martijn Frederik. "Genetic predisposition to testicular cancer". [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2007. http://irs.ub.rug.nl/ppn/304254797.

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González-Zuloeta, Ladd Angela Maria. "Genetic determinants of breast cancer". [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2007. http://hdl.handle.net/1765/10525.

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黎子韻 e Tsz-wan Kristi Lai. "Genetic polymorphisms in ovarian cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31970618.

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Cheung, Chin-ling, e 張展寧. "Genetic analysis of nasopharyngeal cancer". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44659866.

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Cheng, Timothy. "Genetic susceptibility to endometrial cancer". Thesis, University of Oxford, 2015. http://ora.ox.ac.uk/objects/uuid:3a559ae0-156f-48a2-a64e-b03a13c562df.

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Endometrial cancer (EC) is the fourth most common cancer affecting women in the UK. Those with a family history of EC have an increased risk compared with the general population. Highly penetrant germline mutations in mismatch repair (MMR) genes and DNA polymerases account for only a small proportion of the familial aggregation. The aim of this thesis is to investigate the genetic susceptibility to EC in the general population using cases and controls of European ancestry. A GWAS meta-analysis totalling 7,737 EC cases and 37,144 controls yielded five novel EC risk loci of genome-wide significance (P < 5x10−8). In decreasing order of significance, these were at chromosomes 13q22.1 (rs11841589, near KLF5), 6q22.31 (rs13328298, in LOC643623 and near HEY2 and NCOA7), 8q24.21 (rs4733613, telomeric to MYC), 15q15.1 (rs937213, in EIF2AK4, near BMF) and 14q32.33 (rs2498796, in AKT1, near SIVA1). A second independent EC signal was found in the 8q24 locus. The association found in a previous EC GWAS at HNF1B on chromosome 17 was replicated at a higher significance, with the most significant SNP being rs11263763. CYP19A1 SNPs have previously been associated with EC and higher circulating levels of oestrogen from candidate studies, but I confirmed this locus to be genome-wide significant for the first time. Functional annotation and in vitro studies for the EC risk loci at the intergenic region of chromosome 13q22 suggested that the functional SNP sits within a transcriptional repressor for KLF5, with the higher-risk allele reducing repressor activity. The propensity for germline MMR and DNA polymerase muations to cause both EC and colorectal cancer (CRC) prompted me to search for common variants associated with both cancer phenotypes. An EC CRC GWAS meta-analysis showed little evidence of shared susceptibility loci. However, this meta-analysis revealed a novel genome-wide significant risk locus: rs3184504, a missense SH2B3 SNP that has not previously been associated with either EC or CRC. This thesis has enhanced the understanding of genetic susceptibility to sporadic EC and increased the number of genome-wide EC-associated variants to seven.
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Lai, Tsz-wan Kristi. "Genetic polymorphisms in ovarian cancer". Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25176493.

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Livros sobre o assunto "Genetic of cancer"

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1959-, Eeles Rosalind A., ed. Genetic predisposition to cancer. 2a ed. London: Arnold, 2004.

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1959-, Eeles Rosalind A., ed. Genetic predisposition to cancer. London: Chapman & Hall Medical, 1996.

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Côté, Gilbert B. Cancer cytogenetics lookup. Ontario, Canada: Canell, 1999.

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Hoda, Anton-Guirgis, e Lynch Henry T, eds. Biomarkers, genetics, and cancer. New York: Van Nostrand Reinhold, 1985.

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Garte, Seymour. Genetic Susceptibility to Cancer. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4989-5.

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Eeles, Rosalind A., Bruce A. J. Ponder, Douglas F. Easton e Alan Horwich, eds. Genetic Predisposition to Cancer. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-4501-3.

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T, Lynch Henry, e Hirayama Takeshi 1923-, eds. Genetic epidemiology of cancer. Boca Raton, Fla: CRC Press, 1989.

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1959-, Eeles Rosalind A., ed. Genetic predisposition to cancer. London: Chapman & Hall Medical, 1996.

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1938-, Lindahl T., e Imperial Cancer Research Fund (Great Britain)., eds. Genetic instability in cancer. Plainview, NY: Cold Spring Harbor Laboratory Press, 1996.

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W, Weber, Mulvihill John J. 1943- e Narod Steven A, eds. Familial cancer management. Boca Raton: CRC Press, 1996.

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Capítulos de livros sobre o assunto "Genetic of cancer"

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Sakr, Rita A., e Hassan Ghazal. "Genetic Testing for Cancer Risk in the UAE". In Cancer Care in the United Arab Emirates, 235–43. Singapore: Springer Nature Singapore, 2024. http://dx.doi.org/10.1007/978-981-99-6794-0_15.

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AbstractHereditary cancers are estimated to account for 10% of all cancers. Clinical genetics initially provided genetic testing to cancer patients and/or those with a strong family history of cancer. Hereditary cancer gene testing became more widely available as a result of research into inherited genes and the revolutionary development of genetic testing technologies. As a result, testing has been expanded to include medical specialties other than clinical genetics. The increased testing rate resulted in the identification of more patients with pathogenic mutations, but it also resulted in a very high detection rate of variants of uncertain significance, which can cause further confusion among families and distress in patients. Therefore, a crucial suggestion would be that multigene testing should be considered only after proper evaluation for clinical suspicion of hereditary cancer susceptibility, which would be best offered by clinical genetics and/or doctors trained in oncogenetics.
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Robinson, Murray O. "Telomerase and Cancer". In Genetic Engineering, 209–22. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4199-8_12.

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Landolph, Joseph R. "Genetic Toxicology". In Encyclopedia of Cancer, 1–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_2385-3.

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Landolph, Joseph R. "Genetic Toxicology". In Encyclopedia of Cancer, 1877–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_2385.

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Landolph, Joseph R. "Genetic Toxicology". In Encyclopedia of Cancer, 1528–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2385.

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Schneider, Katherine, Kristen Shannon, Anu Chittenden, Elaine Hiller e Stephanie Kieffer. "Cancer Genetic Counseling". In The Molecular Basis of Human Cancer, 477–95. Totowa, NJ: Humana Press, 2002. http://dx.doi.org/10.1007/978-1-59259-125-1_21.

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Elieff, Michelle P., Antonio Lopez-Beltran, Rodolfo Montironi e Liang Cheng. "Familial Cancer Syndromes". In Molecular Genetic Pathology, 449–66. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-405-6_18.

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Harrison, Beth T., Rodolfo Montironi, Antonio Lopez-Beltran, Michelle P. Elieff e Liang Cheng. "Familial Cancer Syndrome". In Molecular Genetic Pathology, 607–43. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4800-6_23.

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Zirn, Birgit, e Karl Mehnert. "F Cancer". In Guide for Genetic Consultation, 107–27. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-04345-2_6.

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Berk, Terri. "Genetic Counseling Overview". In Hereditary Colorectal Cancer, 425–29. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-6603-2_24.

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Trabalhos de conferências sobre o assunto "Genetic of cancer"

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Rodrigues, Milena de Freitas, Ariane Silva da Rocha, David Siqueira Gonçalves, Maria Paula Curado e Maria Nirvana da Cruz Formiga. "Hereditary cancer syndromes in patients with second primary breast cancer". In Brazilian Breast Cancer Symposium 2023. Mastology, 2023. http://dx.doi.org/10.29289/259453942023v33s1067.

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Objective: The objective of this study was to evaluate the presence of hereditary cancer syndromes (HCS) in patients with a diagnosis of two primary breast carcinomas and analyze the frequency of pathogenic variants in high- and moderatepenetrance genes. Methodology: This is a retrospective unicentric cohort study on patients with a diagnosis of two primary breast cancers, diagnosed between January 2000 to December 2020, at A.C. Camargo Cancer Center, Brazil. The association between categorical variables was analyzed by the chi-square test or Fisher’s exact test. For survival curves, the Kaplan-Meier method and log-rank test were used to describe the survival curve differences. Results: Medical records of breast cancer patients were reviewed from 2000 to 2020, and a frequency of 600 patients with two primary breast tumors (metachronous or synchronous) was observed. In total, 190 (31.7%) patients performed genetic testing and 35 (5.8%) patients presented a pathogenic or likely-pathogenic germline variant in cancer predisposing genes. Conclusion: Our results revealed a low rate of genetic testing among patients with two primary breast cancers in a cancer center and a frequency of carrier patients lower than expected.
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Rotaru, Ludmila, e Tudor Rotaru. "Ovarian cancer – genetic aspects". In XIth International Congress of Geneticists and Breeders from the Republic of Moldova. Scientific Association of Geneticists and Breeders of the Republic of Moldova, Institute of Genetics, Physiology and Plant Protection, Moldova State University, 2021. http://dx.doi.org/10.53040/cga11.2021.041.

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Reis, Gabriel Baêta Branquinho, Hugo Francisco da Fonseca Neto, Alice Jardim Zaccariotti, Daniel Bispo de Sousa, Silvaleide Ataides Assunção, Thiago Martins de Abreu, Fernando Santos de Azevedo e Lanúscia Morais de Santana. "INVASIVE DUCTAL CARCINOMA IN A PATIENT WITH LI-FRAUMENI SYNDROME: A CASE REPORT". In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2105.

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Introduction/Objectives: Breast cancer is one of the most common malignancies among women, with 10% resulting from genetic predisposition. Li-Fraumeni syndrome is an autosomal dominant disease that predisposes to multiple primary tumors and is responsible for less than 0.1% of breast cancers, being considered in early-onset tumors. The aim of this report was to describe a fast evolution of three primary tumors in a young patient with Li-Fraumeni syndrome, including ductal breast carcinoma. Case Report: In 2017, a 27-year-old female patient was diagnosed with malignant cancer of the right breast, Luminal HER KI67 70%, clinical stage IV (liver and lung), underwent first-line cancer treatment, maintaining endocrinotherapy and Double Block, with a positive genetic panel test for TP53 mutation, inferring SLF. In 2018, screening colonoscopy showed colon adenocarcinoma, pT53pN1, treated with total colectomy with ileal pouch, followed by suspension of endocrinotherapy and maintenance of Double Block and adjuvant FOLFOX. At the end of chemotherapy, endocrinotherapy was adopted again. Reassessment tests showed partial response in the liver, but the primary nodules were unchanged. Biopsy after thoracoscopy described lung adenocarcinoma, pT3pN2, submitted to adjuvant with Gemzar and Navelbine, followed by Double Block and interruption of endocrinotherapy. It evolved with the appearance of nodules in the right breast, suggestive of progression of breast disease, under treatment with Xeloda, Herceptin, and Perjeta, showing good clinical response. Discussion: Breast cancer in young people increases the possibility of heredity, thus raising the need for investigations of genetic syndromes. Although rare, the identification of FHL brings an important implication for the genetic counseling. Early diagnosis is the best form of management, enabling the preventive screening and intervention of multiple malignancies. Conclusion: Cases of breast cancer in young women should raise a suspected diagnosis of Li-Fraumeni syndrome, which can change the therapeutic and investigation of other cancers at an early stage.
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Sudakov, A. I., E. P. Kulikov, S. A. Mertsalov, A. A. Nikiforov e V. A. Grigorenko. "GENETIC POLYMORPHISM AND COLORECTAL CANCER". In NOVEL TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2022. http://dx.doi.org/10.47501/978-5-6044060-2-1.105-109.

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The article analyzes the relationship of polymorphism of a number of genes with some features of colorectal cancer, such as the aggressiveness of its course and development of the disease, the effectiveness of preoperative chemoradiotherapy. The data obtained can be used to deter-mine individual tactics for treating patients.
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Monteagudo, Ángel, e José Santos. "Evolutionary Optimization of Cancer Treatments in a Cancer Stem Cell Context". In GECCO '15: Genetic and Evolutionary Computation Conference. New York, NY, USA: ACM, 2015. http://dx.doi.org/10.1145/2739480.2754640.

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Kim, Min Kyu, Soo Youn Bae e Jee Yeon Lee. "Abstract 1303: Genetic cancer incidence". In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1303.

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Mansour, Nashat, Rouba Zantout e Mirvat El-Sibai. "Mining breast cancer genetic data". In 2013 9th International Conference on Natural Computation (ICNC). IEEE, 2013. http://dx.doi.org/10.1109/icnc.2013.6818131.

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Abujamous, Lama, Abdelghani Tbakhi, Mohammed Odeh, Osama Alsmadi, Faten F. Kharbat e Hikmat Abdel-Razeq. "Towards Digital Cancer Genetic Counseling". In 2018 1st International Conference on Cancer Care Informatics (CCI). IEEE, 2018. http://dx.doi.org/10.1109/cancercare.2018.8618229.

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Looi, LM. "The Genetic Basis of Cancer". In 2nd International University of Malaya Research Imaging Symposium (UMRIS) 2005: Fundamentals of Molecular Imaging. Kuala Lumpur, Malaysia: Department of Biomedical Imaging, University of Malaya, 2005. http://dx.doi.org/10.2349/biij.1.1.e7-40.

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Saleem, Jabar, e Amna Arsahd. "Detection of Genetic Colon Cancer". In 2021 International Conference on Innovative Computing (ICIC). IEEE, 2021. http://dx.doi.org/10.1109/icic53490.2021.9692971.

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Relatórios de organizações sobre o assunto "Genetic of cancer"

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Neuhausen, Susan L. Genetic Epidemiology of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, junho de 2005. http://dx.doi.org/10.21236/ada442276.

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Neuhausen, Susan L. Genetic Epidemiology of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, março de 2006. http://dx.doi.org/10.21236/ada454886.

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Couch, Fergus J. Genetic Modifiers of Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, junho de 2012. http://dx.doi.org/10.21236/ada566979.

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Buchsbaum, Donald J. Genetic Radiotherapy of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, dezembro de 2003. http://dx.doi.org/10.21236/ada422767.

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Couch, Fergus J. Genetic Modifiers of Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, junho de 2013. http://dx.doi.org/10.21236/ada590500.

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Couch, Fergus. Genetic Modifiers of Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, junho de 2011. http://dx.doi.org/10.21236/ada549466.

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Neuhausen, Susan L. Genetic Epidemiology of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, março de 2007. http://dx.doi.org/10.21236/ada470273.

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Hait, William. Genetic Susceptibility to Cancer Chemotherapy in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, julho de 2000. http://dx.doi.org/10.21236/ada396563.

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Hait, William N. Genetic Susceptibility to Cancer Chemotherapy in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, julho de 2001. http://dx.doi.org/10.21236/ada398401.

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Halt, William N. Genetic Susceptibility to Cancer Chemotherapy in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, julho de 1999. http://dx.doi.org/10.21236/ada382957.

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