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Journal articles on the topic 'Cancer – Genetic aspects'

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Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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1

Hold, Georgina L., and M. Emad El-Omar. "Genetic aspects of inflammation and cancer." Biochemical Journal 410, no. 2 (February 12, 2008): 225–35. http://dx.doi.org/10.1042/bj20071341.

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Chronic inflammation is involved in the pathogenesis of most common cancers. The aetiology of the inflammation is varied and includes microbial, chemical and physical agents. The chronically inflamed milieu is awash with pro-inflammatory cytokines and is characterized by the activation of signalling pathways that cross-talk between inflammation and carcinogenesis. Many of the factors involved in chronic inflammation play a dual role in the process, promoting neoplastic progression but also facilitating cancer prevention. A comprehensive understanding of the molecular and cellular inflammatory mechanisms involved is vital for developing preventive and therapeutic strategies against cancer. The purpose of the present review is to evaluate the mechanistic pathways that underlie chronic inflammation and cancer with particular emphasis on the role of host genetic factors that increase the risk of carcinogenesis.

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2

Hudler, Petra. "Genetic Aspects of Gastric Cancer Instability." Scientific World Journal 2012 (2012): 1–10. http://dx.doi.org/10.1100/2012/761909.

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Unravelling the molecular mechanisms underlying gastric carcinogenesis is one of the major challenges in cancer genomics. Gastric cancer is a very complex and heterogeneous disease, and although much has been learned about the different genetic changes that eventually lead to its development, the detailed mechanisms still remain unclear. Malignant transformation of gastric cells is the consequence of a multistep process involving different genetic and epigenetic changes in numerous genes in combination with host genetic background and environmental factors. The majority of gastric adenocarcinomas are characterized by genetic instability, either microsatellite instability (MSI) or chromosomal instability (CIN). It is believed that chromosome destabilizations occur early in tumour progression. This paper summarizes the most common genetic alterations leading to instability in sporadic gastric cancers and its consequences.

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3

Olsson, R. "Hepatitis and Cancer: Genetic Aspects." Scandinavian Journal of Gastroenterology 31, sup220 (January 1996): 115–20. http://dx.doi.org/10.3109/00365529609094761.

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4

R., Bohiltea. "Genetic aspects of endometrial cancer." Gineco.eu 12, no. 1 (March 20, 2016): 29–32. http://dx.doi.org/10.18643/gieu.2016.29.

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5

Karlan, Beth Y., and Deborah Krakow. "Genetic aspects of ovarian cancer." Current Opinion in Obstetrics and Gynecology 6, no. 1 (February 1994): 105. http://dx.doi.org/10.1097/00001703-199402000-00017.

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6

Steel, M., A. Thompson, and J. Clayton. "Genetic aspects of breast cancer." British Medical Bulletin 47, no. 2 (1991): 504–18. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072488.

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7

Latil, Alain, and R. Lidereau. "Genetic aspects of prostate cancer." Virchows Archiv 432, no. 5 (May 19, 1998): 389–406. http://dx.doi.org/10.1007/s004280050183.

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8

Hecht, Jonathan L., and George L. Mutter. "Molecular and Pathologic Aspects of Endometrial Carcinogenesis." Journal of Clinical Oncology 24, no. 29 (October 10, 2006): 4783–91. http://dx.doi.org/10.1200/jco.2006.06.7173.

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Endometrial cancer is the most common gynecological malignancy, with 41,000 new cases projected in the United States for 2006. Two different clinicopathologic subtypes are recognized: the estrogen-related (type I, endometrioid) and the non–estrogen-related types (type II, nonendometrioid such as papillary serous and clear cell). The morphologic differences in these cancers are mirrored in their molecular genetic profile with type I showing defects in DNA-mismatch repair and mutations in PTEN, K-ras, and beta-catenin, and type II showing aneuploidy and p53 mutations. This article reviews the genetic aspects of endometrial carcinogenesis and progression. We will define the precursor lesion of type I endometrioid cancer and the role of genetics and estrogen in its progression.

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9

Hill, R. P. "Genetic aspects of metastasis." Current Opinion in ONCOLOGY 2, no. 1 (February 1990): 157–62. http://dx.doi.org/10.1097/00001622-199002000-00026.

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10

Krasteva, M., Sv Angelova, and Zl Gospodinova. "Molecular-Genetic Aspects of Breast Cancer." Acta Medica Bulgarica 41, no. 2 (December 1, 2014): 67–79. http://dx.doi.org/10.1515/amb-2014-0024.

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Summary Breast cancer is the most frequent malignancy among women. Advances in breast cancer knowledge have deciphered the involvement of a number of tumor suppressor genes and proto-oncogenes in disease pathogenesis. These genes are part of the complex biochemical pathways, which enable cell cycle control and maintenance of genome integrity. Their function may be disrupted as a result of alterations in gene sequence or misregulation of gene expression including alterations in DNA methylation pattern. The present review summarizes the main findings on major breast cancer related genes BRCA1/2, p53, ATM, CHEK2, HER2, PIK3CA and their tumorigenic inactivation/activation. The potential clinical importance of these genes with respect to patients’ prognosis and therapy are also discussed. The possible implication of other putative breast cancer related genes is also outlined. The first elaborate data on the genetic and epigenetic status of the above mentioned genes concerning Bulgarian patients with the sporadic form of the disease are presented. The studies indicate for a characteristic mutational spectrum in some of the genes for the Bulgarian patients and specific correlation between the status of different genes and clinicopathological characteristics.

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11

Morrison, Patrick J., and A. Brew Atkinson. "Genetic Aspects of Familial Thyroid Cancer." Oncologist 14, no. 6 (May 22, 2009): 571–77. http://dx.doi.org/10.1634/theoncologist.2009-0046.

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12

Berghe, H. Van Den. "Some Genetic Aspects of Breast Cancer." Acta Clinica Belgica 48, sup15 (January 1993): 17–18. http://dx.doi.org/10.1080/17843286.1993.11718347.

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13

Lichtenstein, Anatoly V. "Cancer: evolutionary, genetic and epigenetic aspects." Clinical Epigenetics 1, no. 3-4 (September 14, 2010): 85–100. http://dx.doi.org/10.1007/s13148-010-0010-6.

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14

Toren, A., G. Rechavi, and B. Ramot. "Pediatric Cancer: Environmental and Genetic Aspects." Pediatric Hematology and Oncology 13, no. 4 (January 1996): 319–31. http://dx.doi.org/10.3109/08880019609030838.

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15

Croyle, Robert T., Jennifer S. Achilles, and Caryn Lerman. "Psychologic aspects of cancer genetic testing." Cancer 80, S3 (August 1, 1997): 569–75. http://dx.doi.org/10.1002/(sici)1097-0142(19970801)80:3+<569::aid-cncr6>3.0.co;2-4.

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16

Omelchuk, E. P., D. S. Kutilin, S. N. Dimitriadi, M. A. Gusarev, and N. N. Timoshkina. "Molecular genetic aspects of prostate cancer radioresistance." Bulletin of Siberian Medicine 20, no. 3 (October 22, 2021): 182–92. http://dx.doi.org/10.20538/1682-0363-2021-3-182-192.

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Radioresistance of prostate cancer is a complex therapeutic problem. Biochemical recurrence after radiation therapy occurs in 22–69% of patients with prostate cancer. Nearly half of these patients progress to a clinical relapse within 15 years, and a third progress to castration-resistant prostate cancer. This review analyzes literature data on radioresistance mechanisms in prostate cancer cells. We searched for literature published in eLibrary, PubMed, and Scopus databases by key words: prostate cancer, radioresistance, markers. In total, 568 foreign and 178 national articles published between 1975 and 2020 were found. Of these publications, 77 articles were selected (published in 2001–2020), which reveal the molecular basis of tumor radioresistance.Modern understanding of the origin of radioresistant cancer cells focuses on processes leading to enhanced DNA repair, activation of anti-apoptotic signaling pathways, and a decrease in the level of endogenous and exogenous reactive oxygen species. The state of a tumor microenvironment, autophagy, and epithelial-mesenchymal transition also play an important role in radioresistance. Currently, the mechanisms of resistance to radiation therapy are explained by the existence of tumor stem cells, which provide genetic heterogeneity and activation of carcinogenesis signaling pathways. The tumor can also be protected from radiation by a hypoxic microenvironment. Since cancer stem cells can acquire plasticity in response to radiation therapy, search for markers of radioresistance for screening and identification of radioresistant prostate cancer is relevant.

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17

Biedler, June L. "Genetic aspects of multidrug resistance." Cancer 70, S4 (September 15, 1992): 1799–809. http://dx.doi.org/10.1002/1097-0142(19920915)70:4+<1799::aid-cncr2820701623>3.0.co;2-b.

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18

ROM, WILLIAM N, JOHN G HAY, THEODORE C LEE, YIXING JIANG, and KAM-MENG TCHOU-WONG. "Molecular and Genetic Aspects of Lung Cancer." American Journal of Respiratory and Critical Care Medicine 161, no. 4 (April 2000): 1355–67. http://dx.doi.org/10.1164/ajrccm.161.4.9908012.

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19

Pöschl, Gudrun, Felix Stickel, Xiang D. Wang, and Helmut K. Seitz. "Alcohol and cancer: genetic and nutritional aspects." Proceedings of the Nutrition Society 63, no. 1 (February 2004): 65–71. http://dx.doi.org/10.1079/pns2003323.

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Chronic alcohol consumption is a major risk factor for cancer of upper aero-digestive tract (oro-pharynx, hypopharynx, larynx and oesophagus), the liver, the colo-rectum and the breast. Evidence has accumulated that acetaldehyde is predominantly responsible for alcohol-associated carcinogenesis. Acetaldehyde is carcinogenic and mutagenic, binds to DNA and protein, destroys the folate molecule and results in secondary cellular hyper-regeneration. Acetaldehyde is produced by mucosal and cellular alcohol dehydrogenase, cytochrome P450 2E1 and through bacterial oxidation. Its generation and/or its metabolism is modulated as a result of polymorphisms or mutations of the genes responsible for these enzymes. Acetaldehyde can also be produced by oral bacteria. Smoking, which changes the oral bacterial flora, also increases salivary acetaldehyde. Cigarette smoke and some alcoholic beverages, such as Calvados, contain acetaldehyde. In addition, chronic alcohol consumption induces cytochrome P450 2E1 enxyme activity in mucosal cells, resulting in an increased generation of reactive oxygen species and in an increased activation of various dietary and environmental carcinogens. Deficiencies of riboflavin, Zn, folate and possibly retinoic acid may further enhance alcohol-associated carcinogenesis. Finally, methyl deficiency as a result of multiple alcohol-induced changes leads to DNA hypomethylation. A depletion of lipotropes, including methionine, choline, betaine and S-adenosylmethionine, as well as folate, results in the hypomethylation of oncogenes and may lead to DNA strand breaks, all of which are associated with increased carcinogenesis.

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20

Al Zeyadi, Mohammad Mohawsh. "Molecular and Genetic Aspects of Lung Cancer." Biotechnology & Biotechnological Equipment 27, no. 5 (January 2013): 4051–60. http://dx.doi.org/10.5504/bbeq.2013.0062.

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21

Kim, Wun-Jae, and Changyi Quan. "Genetic and epigenetic aspects of bladder cancer." Journal of Cellular Biochemistry 95, no. 1 (2005): 24–33. http://dx.doi.org/10.1002/jcb.20412.

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22

Meloni-Ehrig, Aurelia M. "Renal cancer: Cytogenetic and molecular genetic aspects." American Journal of Medical Genetics 115, no. 3 (October 24, 2002): 164–72. http://dx.doi.org/10.1002/ajmg.10697.

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23

Shaposhnikov, A. V., O. I. Kit, E. M. Nepomnyaschaya, and E. A. Yurieva. "Hepatocellular cancer. Current aspects of carcinogenesis." CLINICAL AND EXPERIMENTAL MORPHOLOGY 11, no. 4 (2022): 5–15. http://dx.doi.org/10.31088/cem2022.11.4.5-15.

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The modern concept of general carcinogenesis is built on the basic knowledge of exogenous and endogenous factors. They change the body–organ–cell homeostatic and tissue basis and lead to genetic and molecular alterations followed by uncontrolled abnormal cell growth. We studied hepatocellular carcinoma (HCC) as an example of malignant neoplasm carcinogenesis. The article presents some major molecular and genetic alterations resulting in HCC as well as their association with immune microenvironment that mostly determines the onset and further tumor development. These are morphological, molecular, and genetic factors on which the HCC classification we propose is based. It involves 2 tumor classes (proliferating and nonproliferating) and will enable for determining the upcoming prospects for diagnosis of and treatment for this condition. Keywords: exogenous and endogenous risk factors, molecular and genetic and structural liver alterations, classification of hepatocellular carcinoma

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24

Palomo, Laura, Pamela Acha, and Francesc Solé. "Genetic Aspects of Myelodysplastic/Myeloproliferative Neoplasms." Cancers 13, no. 9 (April 27, 2021): 2120. http://dx.doi.org/10.3390/cancers13092120.

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Myelodysplastic/myeloproliferative neoplasms (MDS/MPN) are myeloid neoplasms characterized by the presentation of overlapping features from both myelodysplastic syndromes and myeloproliferative neoplasms. Although the classification of MDS/MPN relies largely on clinical features and peripheral blood and bone marrow morphology, studies have demonstrated that a large proportion of patients (~90%) with this disease harbor somatic mutations in a group of genes that are common across myeloid neoplasms. These mutations play a role in the clinical heterogeneity of these diseases and their clinical evolution. Nevertheless, none of them is specific to MDS/MPN and current diagnostic criteria do not include molecular data. Even when such alterations can be helpful for differential diagnosis, they should not be used alone as proof of neoplasia because some of these mutations may also occur in healthy older people. Here, we intend to review the main genetic findings across all MDS/MPN overlap syndromes and discuss their relevance in the management of the patients.

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25

Sjödahl, R., and P. O. Nyström. "Genetic Aspects of Colorectal Cancer: the Surgeon's View." Scandinavian Journal of Gastroenterology 31, sup220 (January 1996): 132–36. http://dx.doi.org/10.3109/00365529609094765.

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26

Sobolev, V. V., Z. A. Nevozinskaya, A. G. Soboleva, and I. M. Korsunskaya. "Cancer of the vulva: genetic aspects of pathogenesis." Gynecology 20, no. 4 (2018): 9–11. http://dx.doi.org/10.26442/2079-5696-2018-20-4-9-11.

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27

Sobolev, V. V., Z. A. Nevozinskaya, A. G. Soboleva, and I. M. Korsunskaya. "Cancer of the vulva: genetic aspects of pathogenesis." Gynecology 20, no. 4 (August 15, 2018): 9–11. http://dx.doi.org/10.26442/2079-5696_2018.4.9-11.

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The review is devoted to genetic research in cancer of the vulva. In genetic changes, the mutation irreversibly changes the nucleotide sequence of DNA, or the number of copies of chromosomes changes per cell. In epigenetics, the nucleotide sequence remains unchanged, but gene activity is regulated by methylation of DNA or modification of histones. Most of the studies analyzed are devoted to the study of mutations in the TP53 gene. Many studies indicate that somatic mutations are more common in HPV-negative than in HPV-positive patients. Epigenetic studies in the main devoted to hypermethylation. The gene CDKN2A is most often studied in epigenetic terms. For most of the studied genes, hypermethylation occurs more often in squamous cell carcinoma of the vulva than in the precursors.

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Martianov, Aleksandr S., Ekaterina Sh Kuligina, Alexandr A. Romanko, and Evgeny N. Imyanitov. "Molecular genetic testing in colon cancer: clinical aspects." Almanac of Clinical Medicine 50, no. 1 (April 28, 2022): 1–12. http://dx.doi.org/10.18786/2072-0505-2022-50-002.

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Molecular genetic diagnostics is an essential element to plan for management of colorectal cancer (CRC) patients. The choice of systemic treatment for CRC is impossible without molecular testing of the tumor. For instance, the assessment of the KRAS and NRAS genes is mandatory for consideration of anti-EGFR agents. Tumors with BRAF V600E mutation are characterized by aggressive behavior, the necessity of intensive cytostatic regimens, as well as by sensitivity to combination therapy with BRAF and EGFR inhibitors. Inactivation of the DNA mismatch repair, the MUTYH gene or DNA polymerase epsilon (POLE) leads to an excessive tumor mutational burden; these CRC types are highly immunogenic and therefore respond to immune checkpoint inhibitors. Some colorectal carcinomas are characterized by overexpression of the HER2 oncogene, which make them sensitive to corresponding target therapies. There are CRCs with clinical signs of hereditary predisposition, which require germline genetic testing. Nowadays the molecular diagnosis of CRC is being seriously modified due to worldwide implementation of the next-generation sequencing (NGS) and hypersensitive variants of polymerase chain reaction, for example, droplet digital polymerase chain reaction (ddPCR). Non-invasive liquid biopsy is an example of another highly useful innovation that has growing importance for CRC screening, control of surgical intervention efficacy and monitoring of the disease course.

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29

Offit, Kenneth, and Peter Thom. "Ethical and Legal Aspects of Cancer Genetic Testing." Seminars in Oncology 34, no. 5 (October 2007): 435–43. http://dx.doi.org/10.1053/j.seminoncol.2007.07.007.

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30

Ramakrishnaiah, Ravikumar, Bangalore H. Durgesh, Santhosh Basavarajappa, Abdulaziz A. Al Kheraif, and Darshan Devang Divakar. "Genetic, molecular and microbiological aspects of oral cancer." Reviews in Medical Microbiology 26, no. 4 (November 2015): 134–37. http://dx.doi.org/10.1097/mrm.0000000000000051.

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31

Ursu, Radu, Radu Alexandru Truica, Alexandra Cojocaru, Diana Prepelita, Lucian Pop, Viorica Radoi, Nicolae Bacalbasa, and Irina Balescu. "Genetic factors involved in ovarian cancer." Romanian Medical Journal 69, S3 (June 20, 2022): 13–14. http://dx.doi.org/10.37897/rmj.2022.s3.3.

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Ovarian cancer is the most frequent type of gynecologic malignancy and is currently on the fifth place among different cancers worldwide. According to the estimations, ovarian cancer accounts for 1.3% of all new cancer cases. Ovarian cancer is considered a heterogeneous class of malignancies with a poor prognosis due to late diagnose and low treatment response. There are few types of ovarian cancer: epithelial ovarian cancer, germline cell ovarian cancer and stromal cell ovarian cancer. Epithelial ovarian cancers represent more than 90% of ovarian malignancies, and comprise high-grade serous carcinoma (HGSOC), low-grade serous carcinoma (LGSOC), endometrioid carcinoma, mucinous carcinoma, and clear cell carcinoma. Of these, HGSOC is the most frequent histological subtype. The diagnosis of most of OC cases, at an advanced disease stage is one of the reasons for high fatality rate and carries poor prognosis with current therapies. Several aspects can increase the risk of developing ovarian cancer, including genetic factors, such as age, postmenopausal hormonal therapy use, infertility and nulliparity. Among the genetic factors, most commonly we encounter BRCA1 and BRCA2, at approximately 17% of patients. Also these mutation rise the risk for another cancers like breast cancer, pancreatic cancer, prostatic cancer and melanoma. BRCA1 and 2 are genes involved in DNA repair and maintenance. Other genes that have a similar function are RAD511C, RAD51D, BRIP1, PALB2, CHEK2, MRE11A, RAD50, ATM and TP53.

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32

Borreani, Claudia, and Laura Gangeri. "Genetic Counselling: Communication and Psychosocial Aspects." Tumori Journal 82, no. 2 (March 1996): 147–50. http://dx.doi.org/10.1177/030089169608200209.

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The results of genetic research have a remarkable role in medicine progress. At the same time the issues of prevention, individual attitudes and behaviour have acquired more importance, not only in relation to the illness but also regarding one's health. For these reasons is important to consider this field of study and intervention as an area to face, not only from the medical point of view but also from ethical and psychological ones. If we agree on the importance of a global approach to this problem, psychosocial support, which is often considered a parallel intervention, becomes a component of genetic counselling: the focal point of the intervention becomes the person, and not only the problem. The literature of the last years is rich of studies that have deepened these themes. Some studies have been analysed and reported but it is not easy to individualise a common patrimony of knowledge. Some aspects as information, communication, risk perception and psychological consequences are presented and discussed in this paper.

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33

Janeczko-Czarnecka, Małgorzata, Ryszard Ślęzak, Wojciech Pietras, and Katarzyna Kilis Pstrusinska. "Wilms tumor (nephroblastoma) – clinical and genetic aspects." Nowotwory. Journal of Oncology 72, no. 4 (August 22, 2022): 259–64. http://dx.doi.org/10.5603/njo.2022.0040.

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34

Scott, Rodney J., and Hansjakob Müller. "Familial and genetic aspects of colorectal carcinogenesis." European Journal of Cancer 29, no. 15 (January 1993): 2163–67. http://dx.doi.org/10.1016/0959-8049(93)90056-l.

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35

Amorim, Gelbert Luiz Chamon do Carmo, Denny Fabricio Magalhães Veloso, José Carlos Vieira, and Paulo Roberto Alves. "Molecular aspects of bladder cancer." Einstein (São Paulo) 9, no. 1 (March 2011): 95–99. http://dx.doi.org/10.1590/s1679-45082011rb1593.

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ABSTRACT One of the most important objectives of genetic markers of cancer will be the possible identification of individuals at greatest risk in order to allow better management and prognosis. Many urological tumors were associated to various types of gene alterations with a great number of genes involved in the process, hindering gene therapy. This treatment uses specific techniques and one or several genes are manipulated in the laboratory in order to induce molecular alterations that may block the oncogenic process. The article addresses these issues emphasizing the importance of the new molecular biology techniques.

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36

Miller, Mike. "Colorectal Cancer: Tackling the Genetic Aspects of the Disease." JNCI: Journal of the National Cancer Institute 90, no. 14 (July 15, 1998): 1034–35. http://dx.doi.org/10.1093/jnci/90.14.1034.

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37

Lyubchenko, L. N., M. G. Filippova, O. A. Anurova, P. B. Nazliev, and I. S. Stilidi. "HEREDITARY DIFFUSE GASTRIC CANCER: GENETIC ASPECTS AND PROPHYLACTIC TOTAL GASTRECTOMY." Siberian journal of oncology 17, no. 4 (September 4, 2018): 48–52. http://dx.doi.org/10.21294/1814-4861-2018-17-4-48-52.

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For patients with an identified germline E-cadherin-1 (CDH1) mutation, prophylactic gastrectomy is the treatment of choice to eliminate the high risk of developing diffuse gastric cancer. The case report describes a rare case of hereditary diffuse gastric cancer (HDGC) associated with CDH1 gene mutation, which is reported in the Russian population for the first time. In 2013, a 28-year- old woman was referred to Clinical Oncogenetics Laboratory with a family history of gastric cancer. Molecular genetic analysis revealed CDH1 gene mutation. The lifetime risk of cancer in mutation positive members is more than 80. Histological examination of gastric biopsy specimens obtained during endoscopy revealed isolated signet ring cells in the lamina propria. Spleenpreserving D2-lymphodissection and total gastrectomy with Roux-en-Y reconstruction with a jejunal reservoir formation were performed at the Abdominal Oncology Surgery Department.

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Singh, Juhi, Puneet Kumar, Khushi Verma, Satyender Kumar Tiwary, Gopeshwar Narayan, and V. K. Dixit. "Molecular genetic changes in gastric carcinoma." International Journal of Molecular & Immuno Oncology 6 (January 8, 2021): 30–46. http://dx.doi.org/10.25259/ijmio_8_2020.

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Gastric cancer remains highly prevalent and accounts for a notable proportion of global cancer mortality and this is associated with poor survival rates. Understanding the molecular genetic changes of gastric carcinoma may offer an insight into its pathogenesis helps in identifying new biomarkers, aid prognostication, and novel treatment targets. Over a past few decades, advances in technology and high throughput analysis have improved understanding of the molecular genetic aspects of gastric cancer. In this article, hierarchy of the changes at genetic and molecular level including several aspects which are heterogenous and represents a wide spectrum such as tumor suppressor genes, oncogenes, cellcycle regulators, apoptosis, cell-adhesion molecules, loss of heterozygosity, microsatellite instability, and epigenetic changes. The classification of gastric carcinoma at molecular and genetic level as well as hereditary gastric carcinoma is elaborated. The molecular genetic aspects regarding pathogenesis, changes and aberrations of all genes and pathways which are involved in gastric cancer are addressed in this review.

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39

Li, Shuai, Tuong L. Nguyen, Tu Nguyen-Dumont, James G. Dowty, Gillian S. Dite, Zhoufeng Ye, Ho N. Trinh, et al. "Genetic Aspects of Mammographic Density Measures Associated with Breast Cancer Risk." Cancers 14, no. 11 (June 2, 2022): 2767. http://dx.doi.org/10.3390/cancers14112767.

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Cumulus, Altocumulus, and Cirrocumulus are measures of mammographic density defined at increasing pixel brightness thresholds, which, when converted to mammogram risk scores (MRSs), predict breast cancer risk. Twin and family studies suggest substantial variance in the MRSs could be explained by genetic factors. For 2559 women aged 30 to 80 years (mean 54 years), we measured the MRSs from digitized film mammograms and estimated the associations of the MRSs with a 313-SNP breast cancer polygenic risk score (PRS) and 202 individual SNPs associated with breast cancer risk. The PRS was weakly positively correlated (correlation coefficients ranged 0.05–0.08; all p < 0.04) with all the MRSs except the Cumulus-white MRS based on the “white but not bright area” (correlation coefficient = 0.04; p = 0.06). After adjusting for its association with the Altocumulus MRS, the PRS was not associated with the Cumulus MRS. There were MRS associations (Bonferroni-adjusted p < 0.04) with one SNP in the ATXN1 gene and nominally with some ESR1 SNPs. Less than 1% of the variance of the MRSs is explained by the genetic markers currently known to be associated with breast cancer risk. Discovering the genetic determinants of the bright, not white, regions of the mammogram could reveal substantial new genetic causes of breast cancer.

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40

Rumjanzeva, U., P. Rumjanzev, and A. Ilyin. "Clinical and Genetic Aspects of Sporadic Non-Medullar Thyroid Cancer." Clinical and experimental thyroidology 2, no. 1 (March 15, 2006): 16. http://dx.doi.org/10.14341/ket20062116-20.

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41

Durnev, A. D., and A. K. Zhanataev. "Relevant Aspects of Drug Genetic Toxicology." Bulletin of the Scientific Centre for Expert Evaluation of Medicinal Products 12, no. 1 (January 31, 2022): 90–109. http://dx.doi.org/10.30895/1991-2919-2022-12-1-90-109.

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Genotoxic lesions are not only a cause of genetic pathologies and cancer, but also the most common and significant factor of the etiopathology of cardiovascular and neurodegenerative disorders, reproductive losses, infertility, and aging. This requires careful monitoring of the use of potential genotoxicants including medicinal products (MPs), which are a group of compounds intentionally and routinely used by humans. Genotoxicity assesment is highly essential in preclinical drug safety studies. The aim of the study was to analyse the current situation and reveal possible ways of addressing methodological and regulatory issues in genotoxicology to enable proper conduction of drug safety preclinical studies. The article summarises basic concepts of the modern genetic toxicology development and highlights the history of research aimed at identifying mutagenic, clastogenic, and aneugenic effects. The authors analyse regulatory aspects of genotoxicological studies of MPs and consider issues of improving the strategy for genotoxicity testing. The paper gives information about the genotoxicity tests approved for MPs, recommendations for interchangeability of tests in relation to particular study characteristics. The authors carried out a comparative analysis of the tests’ pros and cons with an emphasis that the study of each MP is a separate scientific task. They discuss interpretation of results and prediction of MP carcinogenic potential in genotoxicological studies. Recommendations are given for the optimisation of the MP genotoxicity assessment strategy, considering its partial integration into general toxicity studies. The article stresses the urgent need to develop registration methods for genotoxic events in germ cells, assesses the prospects of new tests, and reviews new trends in drug genotoxicology fundamental research.

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Maher, ER, and JRW Yates. "Familial renal cell carcinoma: clinical and molecular genetic aspects." British Journal of Cancer 63, no. 2 (February 1991): 176–79. http://dx.doi.org/10.1038/bjc.1991.43.

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Toruner, Murat, Martin E. Fernandez-Zapico, and Christopher L. Pin. "New Aspects of the Epigenetics of Pancreatic Carcinogenesis." Epigenomes 4, no. 3 (August 31, 2020): 18. http://dx.doi.org/10.3390/epigenomes4030018.

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Pancreatic cancer remains among the deadliest forms of cancer with a 5 year survival rate less than 10%. With increasing numbers being observed, there is an urgent need to elucidate the pathogenesis of pancreatic cancer. While both contribute to disease progression, neither genetic nor environmental factors completely explain susceptibility or pathogenesis. Defining the links between genetic and environmental events represents an opportunity to understand the pathogenesis of pancreatic cancer. Epigenetics, the study of mitotically heritable changes in genome function without a change in nucleotide sequence, is an emerging field of research in pancreatic cancer. The main epigenetic mechanisms include DNA methylation, histone modifications and RNA interference, all of which are altered by changes to the environment. Epigenetic mechanisms are being investigated to clarify the underlying pathogenesis of pancreatic cancer including an increasing number of studies examining the role as possible diagnostic and prognostic biomarkers. These mechanisms also provide targets for promising new therapeutic approaches for this devastating malignancy.

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Bigner, S. H. "Morphologic and molecular genetic aspects of oligodendroglial neoplasms." Neuro-Oncology 1, no. 1 (January 1, 1999): 52–60. http://dx.doi.org/10.1215/15228517-1-1-52.

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Bigner, Sandra H., B. K. Ahmed Rasheed, Rodney Wiltshire, and Roger E. McLendon. "Morphologic and molecular genetic aspects of oligodendroglial neoplasms." Neuro-Oncology 1, no. 1 (January 1, 1999): 52–60. http://dx.doi.org/10.1093/neuonc/1.1.52.

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Surbone, Antonella. "The ethical challenge of genetic testing for breast cancer." Medicina e Morale 48, no. 3 (June 30, 1999): 469–84. http://dx.doi.org/10.4081/mem.1999.799.

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The scientific importance of our recently acquired ability to test for heredity predisposition to breast and ovarian cancers is paralleled only by its social and ethical relevance. Dilemmas are common in all genetic testing, but they assume particular nuances in the setting of breast cancer. Due to its devastating nature and to its increasing incidence, breast cancer is a central issue in women’s health. Breast cancer patients and women in general are often deeply involved in understanding the disease process and the treatment options, as they are in discussing the psychological, social and moral ramifications. This paper is a reflection upon some qualitative aspects of the debate that surrounds genetic testing for breast and ovarian cancer, as they have emerged in my encounters with breast cancer patients prior to their decision to consider genetic testing. The five recurrent themes identified in those conversations may or may not be representative of other practice situations, but they illustrate some fundamental philosophical, ethical and moral questions which exist at the core of our human essence and of our moral agency, and which point to the unavoidable intertwinement of medicine, culture, normativity and philosophy, vis-à-vis the many questions raised by genetics. The Author has intentionally refrained from questionnaires, which could betray the complexity of our thinking process, and from the vignettes, as they could betray confidentiality. The paper concludes that the correct answers to the dilemmas posed by genetic testing for breast cancer predisposition can only arise from a blend of medical, social and philosophical analysis.

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You, Y. Nancy, Lucas D. Lee, Benjamin W. Deschner, and David Shibata. "Colorectal Cancer in the Adolescent and Young Adult Population." JCO Oncology Practice 16, no. 1 (January 2020): 19–27. http://dx.doi.org/10.1200/jop.19.00153.

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Colorectal cancer in the young adult population is of increasing incidence and concern. Genetic predisposition and heritable syndromes contribute to this trend, but perhaps more concerning is the majority of new diagnoses that involve no traceable genetic risk factors. Prevention and early recognition, with a high suspicion in the symptomatic young adult, are critical in attenuating recent trends. Clinical management requires coordinated multidisciplinary care from diagnosis to surveillance in order to ensure appropriate management. This review provides a summary of key aspects related to colorectal cancer in adolescents and young adults, including epidemiology, biology, genetics, clinical management, and prevention.

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Giusti, Francesca, Alberto Falchetti, Francesco Franceschelli, Francesca Marini, Annalisa Tanini, and Maria Luisa Brandi. "Thyroid Cancer: Current Molecular Perspectives." Journal of Oncology 2010 (2010): 1–17. http://dx.doi.org/10.1155/2010/351679.

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The thyroid cancer is a rare oncological entity, representing no more than 1% of all human malignant neoplasms. Recently, it has been demonstrated a sharp increase in incidence of differentiated thyroid carcinoma, equally occurring in both sexes. So far, multiple genetic alterations have been identified in differentiated thyroid carcinoma, leading to investigate the clinical utility of genetic studies. In particular, molecular genetic approaches searching for gene mutations in the material collected by fine needle ago-biopsy may have a particular utility in small nodules and in those specimens with an indeterminate cytology. The expansion of knowledge about genetic mutations occurring in different thyroid tumors has characterized recent years, allowing the identification of a correlation between specific mutations and phenotypic characteristics of thyroid cancers, essential for their prognosis. This review will briefly report on the histological features and the new entity represented by thyroid microcarcinoma and will focus on both environmental and genetic aspects associated with the occurrence of thyroid cancer.

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McGee, Rose B., and Kim E. Nichols. "Introduction to cancer genetic susceptibility syndromes." Hematology 2016, no. 1 (December 2, 2016): 293–301. http://dx.doi.org/10.1182/asheducation-2016.1.293.

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AbstractThe last 30 years have witnessed tremendous advances in our understanding of the cancer genetic susceptibility syndromes, including those that predispose to hematopoietic malignancies. The identification and characterization of families affected by these syndromes is enhancing our knowledge of the oncologic and nononcologic manifestations associated with predisposing germ line mutations and providing insights into the underlying disease mechanisms. Here, we provide an overview of the cancer genetic susceptibility syndromes, focusing on aspects relevant to the evaluation of patients with leukemia and lymphoma. Guidance is provided to facilitate recognition of these syndromes by hematologists/oncologists, including descriptions of the family history features, tumor genotype, and physical or developmental findings that should raise concern for an underlying cancer genetic syndrome. The clinical implications and management challenges associated with cancer susceptibility syndromes are also discussed.

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GOELEN, G., A. RIGO, B. NEYNS, W. BETZ, and J. DE GRÈVE. "Ethical Aspects of Genetic Counseling in Familial Breast and Ovarian Cancer." Annals of the New York Academy of Sciences 833, no. 1 Cancer (December 1997): 170–72. http://dx.doi.org/10.1111/j.1749-6632.1997.tb48604.x.

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