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Artículos de revistas sobre el tema "Cancer – Molecular aspects"

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Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 29 de julio de 2024

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1

Amorim, Gelbert Luiz Chamon do Carmo, Denny Fabricio Magalhães Veloso, José Carlos Vieira y Paulo Roberto Alves. "Molecular aspects of bladder cancer". Einstein (São Paulo) 9, n.º 1 (marzo de 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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2

Tong, Xiao W., Dirk G. Kieback, Rajagopal Ramesh y Scott M. Freeman. "MOLECULAR ASPECTS OF OVARIAN CANCER". Hematology/Oncology Clinics of North America 13, n.º 1 (febrero de 1999): 109–33. http://dx.doi.org/10.1016/s0889-8588(05)70156-8.

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3

Cronauer, M. V. y Z. Culig. "Molecular aspects of prostate cancer". World Journal of Urology 30, n.º 3 (7 de marzo de 2012): 277–78. http://dx.doi.org/10.1007/s00345-012-0853-x.

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4

Kausch, I. y A. Böhle. "Molecular Aspects of Bladder Cancer". European Urology 41, n.º 1 (enero de 2002): 15–29. http://dx.doi.org/10.1016/s0302-2838(01)00007-0.

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5

Wenham, Robert M., Johnathan M. Lancaster y Andrew Berchuck. "Molecular aspects of ovarian cancer". Best Practice & Research Clinical Obstetrics & Gynaecology 16, n.º 4 (agosto de 2002): 483–97. http://dx.doi.org/10.1053/beog.2002.0298.

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6

Hynes, Nancy y Robert B. Dickson. "Molecular aspects of breast cancer". Journal of Mammary Gland Biology and Neoplasia 1, n.º 2 (abril de 1996): 137–38. http://dx.doi.org/10.1007/bf02013637.

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7

Hecht, Jonathan L. y George L. Mutter. "Molecular and Pathologic Aspects of Endometrial Carcinogenesis". Journal of Clinical Oncology 24, n.º 29 (10 de octubre de 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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8

Krasteva, M., Sv Angelova y Zl Gospodinova. "Molecular-Genetic Aspects of Breast Cancer". Acta Medica Bulgarica 41, n.º 2 (1 de diciembre de 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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9

Tsikouras, Panagiotis, Sofia Bouchlariotou, Nikolaos Vrachnis, Alexandros Dafopoulos, Georgios Galazios, Roland Csorba y Georg Friedrich von Tempelhoff. "Endometrial cancer: molecular and therapeutic aspects". European Journal of Obstetrics & Gynecology and Reproductive Biology 169, n.º 1 (julio de 2013): 1–9. http://dx.doi.org/10.1016/j.ejogrb.2013.01.018.

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10

Yashina, D. P. y Z. A. Afanasyeva. "Molecular genetic aspects of adrenocortical cancer". Advances in Molecular Oncology 10, n.º 2 (10 de julio de 2023): 42–57. http://dx.doi.org/10.17650/2313-805x-2023-10-2-42-57.

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Adrenocortical cancer is a rare tumor originating from cortical adrenal cells, endowed with aggressive potential, a rapidly progressing course and an unfavorable prognosis. The complexity of early diagnosis of the disease is due to several factors: the variability of clinical manifestations associated with the initial multiregulatory influence of steroid hormones on the body’s homeostasis, the rare occurrence of the tumor and, as a result, the lack of understanding of the molecular mechanisms of its carcinogenesis.The increased interest in recent years among oncologists and endocrinologists in understanding the fundamental and clinical aspects of adrenocortical cancer and the search for potential targets for new drugs has led to a detailed study of the cellular and molecular genetic mechanisms involved in normal adrenal ontogenesis and their role in tumor transformation. This review presents the currently known molecular genetic processes and their mediating auto-, para-, endocrine factors involved in normal adrenal ontogenesis and carcinogenesis. The paper analyzes results of trials published in international and Russian journals on molecular oncology and endocrinology indexed in the PubMed, CyberLeninka, Web of Science, Science Direct and eLIBRARY databases.

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11

Osório-Costa, Felipe, Guilherme Z. Rocha, Marília M. Dias y José B. C. Carvalheira. "Epidemiological and molecular mechanisms aspects linking obesity and cancer". Arquivos Brasileiros de Endocrinologia & Metabologia 53, n.º 2 (marzo de 2009): 213–26. http://dx.doi.org/10.1590/s0004-27302009000200013.

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About 25% of cancer cases globally are due to excess weight and a sedentary lifestyle. These results are alarming, as the world knows a pandemy of obesity and, in consequence, insulin resistance. Obesity may increase risk for various cancers by several mechanisms, including increasing sex and metabolic hormones, and inflammation. Here, we present a review of epidemiological and molecular evidences linking obesity and cancer - particularly colorectal, post-menopausal breast, endometrial, pancreatic, high grade prostate, hepatocellular, gallbladder, kidney and esophageal adenocarcinoma. The expected striking increase in the incidence of cancer in the near future related to obesity turns the knowledge of this field of great impact as it is needed to the development of strategies to prevent and treat this disease.

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12

Omelchuk, E. P., D. S. Kutilin, S. N. Dimitriadi, M. A. Gusarev y N. N. Timoshkina. "Molecular genetic aspects of prostate cancer radioresistance". Bulletin of Siberian Medicine 20, n.º 3 (22 de octubre de 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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13

Ferreira, Luciana Bueno, Etel Gimba, João Vinagre, Manuel Sobrinho-Simões y Paula Soares. "Molecular Aspects of Thyroid Calcification". International Journal of Molecular Sciences 21, n.º 20 (19 de octubre de 2020): 7718. http://dx.doi.org/10.3390/ijms21207718.

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In thyroid cancer, calcification is mainly present in classical papillary thyroid carcinoma (PTC) and in medullary thyroid carcinoma (MTC), despite being described in benign lesions and in other subtypes of thyroid carcinomas. Thyroid calcifications are classified according to their diameter and location. At ultrasonography, microcalcifications appear as hyperechoic spots ≤ 1 mm in diameter and can be named as stromal calcification, bone formation, or psammoma bodies (PBs), whereas calcifications > 1 mm are macrocalcifications. The mechanism of their formation is still poorly understood. Microcalcifications are generally accepted as a reliable indicator of malignancy as they mostly represent PBs. In order to progress in terms of the understanding of the mechanisms behind calcification occurring in thyroid tumors in general, and in PTC in particular, we decided to use histopathology as the basis of the possible cellular and molecular mechanisms of calcification formation in thyroid cancer. We explored the involvement of molecules such as runt-related transcription factor-2 (Runx-2), osteonectin/secreted protein acidic and rich in cysteine (SPARC), alkaline phosphatase (ALP), bone sialoprotein (BSP), and osteopontin (OPN) in the formation of calcification. The present review offers a novel insight into the mechanisms underlying the development of calcification in thyroid cancer.

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14

Smith, Malcolm G. "Cellular and molecular aspects of gastric cancer". World Journal of Gastroenterology 12, n.º 19 (2006): 2979. http://dx.doi.org/10.3748/wjg.v12.i19.2979.

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15

ROM, WILLIAM N, JOHN G HAY, THEODORE C LEE, YIXING JIANG y KAM-MENG TCHOU-WONG. "Molecular and Genetic Aspects of Lung Cancer". American Journal of Respiratory and Critical Care Medicine 161, n.º 4 (abril de 2000): 1355–67. http://dx.doi.org/10.1164/ajrccm.161.4.9908012.

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16

Schalken, Jack A. "Molecular aspects of hormone-independent prostate cancer". BJU International 100, s2 Prostate Can (julio de 2007): 52–55. http://dx.doi.org/10.1111/j.1464-410x.2007.06956.x.

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17

SHIMOSATO, YUKIO. "Biological and molecular aspects of lung cancer". Juntendo Medical Journal 36, n.º 4 (1991): 470–77. http://dx.doi.org/10.14789/pjmj.36.470.

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18

DeMarzo, Angelo M., William G. Nelson, William B. Isaacs y Jonathan I. Epstein. "Pathological and molecular aspects of prostate cancer". Lancet 361, n.º 9361 (marzo de 2003): 955–64. http://dx.doi.org/10.1016/s0140-6736(03)12779-1.

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19

Trent, Ron J. A. "Molecular aspects of cancer and its therapy". Pathology 31, n.º 3 (1999): 301. http://dx.doi.org/10.1016/s0031-3025(16)34800-0.

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20

PANANI, A. y C. ROUSSOS. "Cytogenetic and molecular aspects of lung cancer". Cancer Letters 239, n.º 1 (28 de julio de 2006): 1–9. http://dx.doi.org/10.1016/j.canlet.2005.06.030.

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21

Gharibi, A., Y. Adamian y J. A. Kelber. "Cellular and molecular aspects of pancreatic cancer". Acta Histochemica 118, n.º 3 (abril de 2016): 305–16. http://dx.doi.org/10.1016/j.acthis.2016.01.009.

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22

Katenkamp, D. "Molecular Aspects of Cancer and its Therapy". Experimental and Toxicologic Pathology 52, n.º 5 (octubre de 2000): 454. http://dx.doi.org/10.1016/s0940-2993(00)80081-0.

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23

Al Zeyadi, Mohammad Mohawsh. "Molecular and Genetic Aspects of Lung Cancer". Biotechnology & Biotechnological Equipment 27, n.º 5 (enero de 2013): 4051–60. http://dx.doi.org/10.5504/bbeq.2013.0062.

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24

Vahakangas, K. "Ethical aspects of molecular epidemiology of cancer". Carcinogenesis 25, n.º 4 (24 de octubre de 2003): 465–71. http://dx.doi.org/10.1093/carcin/bgh043.

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25

Meloni-Ehrig, Aurelia M. "Renal cancer: Cytogenetic and molecular genetic aspects". American Journal of Medical Genetics 115, n.º 3 (24 de octubre de 2002): 164–72. http://dx.doi.org/10.1002/ajmg.10697.

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26

Gavrish, Yu E., A. S. Artemieva, A. A. Sidoruk, A. N. Baltrukova, E. A. Ulrikh, I. V. Berlev y A. F. Urmancheeva. "MOLECULAR SUBCLASSIFICATION OF ENDOMETRIAL CANCER: AGE ASPECTS". Профилактическая и клиническая медицина, n.º 2 (2023): 41–54. http://dx.doi.org/10.47843/2074-9120_2023_2_41.

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27

Hold, Georgina L. y M. Emad El-Omar. "Genetic aspects of inflammation and cancer". Biochemical Journal 410, n.º 2 (12 de febrero de 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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28

Miranda, M., F. Amicarelli, A. Bonfigli, A. Poma, O. Zarivi y D. Botti. "Molecular aspects of melanoma clonogenicity". Melanoma Research 3, n.º 1 (marzo de 1993): 72. http://dx.doi.org/10.1097/00008390-199303000-00263.

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29

Grande, Enrique, Juan José Díez, Carles Zafon y Jaume Capdevila. "Thyroid Cancer: Molecular Aspects and New Therapeutic Strategies". Journal of Thyroid Research 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/847108.

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Despite that thyroid cancer accounts for over 90% of tumors that arise from the endocrine system, these tumors barely represent 2% of solid tumors in adults. Many entities are grouped under the general term of thyroid cancer, and they differ in histological features as well as molecular and clinical behavior. Thus, the prognosis for patients with thyroid cancer ranges from a survival rate of >97% at 5 years, in the case of differentiated thyroid tumors sensitive to radioactive iodine, to a 4-month median survival for anaplastic tumors. The high vascularity in these tumors and the important role that oncogenic mutations may have in the RAS/RAF/MEK pathway and oncogenicity (as suggested by activating mutations and rearrangements of theRETgene) have led to the development of multitarget inhibitors in different histological subgroups of patients. The correct molecular characterization of patients with thyroid cancer is thought to be a key aspect for the future clinical management of these patients.

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30

Shaposhnikov, A. V., O. I. Kit, E. M. Nepomnyaschaya y E. A. Yurieva. "Hepatocellular cancer. Current aspects of carcinogenesis". CLINICAL AND EXPERIMENTAL MORPHOLOGY 11, n.º 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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31

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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32

Mareel, Marc y Ancy Leroy. "Clinical, Cellular, and Molecular Aspects of Cancer Invasion". Physiological Reviews 83, n.º 2 (1 de abril de 2003): 337–76. http://dx.doi.org/10.1152/physrev.00024.2002.

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Invasion causes cancer malignancy. We review recent data about cellular and molecular mechanisms of invasion, focusing on cross-talk between the invaders and the host. Cancer disturbs these cellular activities that maintain multicellular organisms, namely, growth, differentiation, apoptosis, and tissue integrity. Multiple alterations in the genome of cancer cells underlie tumor development. These genetic alterations occur in varying orders; many of them concomitantly influence invasion as well as the other cancer-related cellular activities. Examples discussed are genes encoding elements of the cadherin/catenin complex, the nonreceptor tyrosine kinase Src, the receptor tyrosine kinases c-Met and FGFR, the small GTPase Ras, and the dual phosphatase PTEN. In microorganisms, invasion genes belong to the class of virulence genes. There are numerous clinical and experimental observations showing that invasion results from the cross-talk between cancer cells and host cells, comprising myofibroblasts, endothelial cells, and leukocytes, all of which are themselves invasive. In bone metastases, host osteoclasts serve as targets for therapy. The molecular analysis of invasion-associated cellular activities, namely, homotypic and heterotypic cell-cell adhesion, cell-matrix interactions and ectopic survival, migration, and proteolysis, reveal branching signal transduction pathways with extensive networks between individual pathways. Cellular responses to invasion-stimulatory molecules such as scatter factor, chemokines, leptin, trefoil factors, and bile acids or inhibitory factors such as platelet activating factor and thrombin depend on activation of trimeric G proteins, phosphoinositide 3-kinase, and the Rac and Rho family of small GTPases. The role of proteolysis in invasion is not limited to breakdown of extracellular matrix but also causes cleavage of proinvasive fragments from cell surface glycoproteins.

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33

Machado, Gabriela Conrado, Júlia Lima De Morais, Natália Dundi Carvalho y Eriston Vieira Gomes. "A transformação maligna no câncer de esôfago: Aspectos moleculares / Malignant transformation in esophageal cancer: Molecular aspects". Brazilian Journal of Development 7, n.º 8 (31 de agosto de 2021): 86256–68. http://dx.doi.org/10.34117/bjdv7n8-704.

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34

Tappia, Paramjit S. y Bram Ramjiawan. "Biomarkers for Early Detection of Cancer: Molecular Aspects". International Journal of Molecular Sciences 24, n.º 6 (9 de marzo de 2023): 5272. http://dx.doi.org/10.3390/ijms24065272.

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35

Likhobabin, Z. V., K. E. Raish, A. A. Aripova, O. V. Bulgakova, G. S. Ainagulova y R. I. Bersimbay. "The molecular aspects of asbestos-induced carcinogenesis". BULLETIN of the L.N. Gumilyov Eurasian National University. BIOSCIENCE Series 137, n.º 4 (2021): 6–21. http://dx.doi.org/10.32523/2616-7034-2021-137-4-6-21.

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One of the key problems of modern healthcare is the prevention and personalized medicine of diseases caused by exposure to adverse environmental factors. According to the World Health Organization and the International Agency for Research on Cancer, all forms of asbestos have adverse effects on the human body and can induce various forms of cancer. It has been evidenced by the inclusion of asbestos in the first category of the list of carcinogens. Today the Republic of Kazakhstan is one of the largest asbestos-producing countries. An understanding of the key mechanisms of carcinogenesis due to inhalation of asbestos is needed to effectively diagnose asbestos-induced cancer in the early stages of development. The article reports on the most modern concepts of the genetic and molecular mechanisms of carcinogenesis mediated by the effect of chrysotile asbestos and confirms the danger of this compound to human health.

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36

Martianov, Aleksandr S., Ekaterina Sh Kuligina, Alexandr A. Romanko y Evgeny N. Imyanitov. "Molecular genetic testing in colon cancer: clinical aspects". Almanac of Clinical Medicine 50, n.º 1 (28 de abril de 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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37

Bornschein, Jan, Jochen Weigt, Michael Selgrad y Peter Malfertheiner. "Molecular aspects in the diagnosis of gastric cancer". Expert Opinion on Medical Diagnostics 3, n.º 5 (26 de junio de 2009): 585–96. http://dx.doi.org/10.1517/17530050902862175.

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38

Friess, Helmut, Jörg Kleeff, Murray Korc y Markus W. Büchler. "Molecular Aspects of Pancreatic Cancer and Future Perspectives". Digestive Surgery 16, n.º 4 (1999): 281–90. http://dx.doi.org/10.1159/000018737.

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39

Kleeff, Friess, Berberat, Martignoni, Z'graggen y Büchler. "Pancreatic Cancer - New Aspects of Molecular Biology Research". Swiss Surgery 6, n.º 5 (1 de octubre de 2000): 231–34. http://dx.doi.org/10.1024/1023-9332.6.5.231.

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Pancreatic ductal adenocarcinoma (PDAC) presently has an incidence of approximately 8 to 10 cases per 100000 citizens in European countries, and the incidence has been increasing throughout the last decades. Approximately 30000 patients die every year from PDAC in Western Europe and most of the newly diagnosed patients present with an already unresectable tumor stage. Self-sufficiency in growth signals, insensitivity to antigrowth signals, and evasion of apoptosis are hallmarks of malignant growth. In PDAC a variety of growth factors are expressed at increased levels. For example, the concomitant presence of the EGF-receptor and its ligands EGF, TGF-alpha, and/or amphiregulin is associated with enhanced tumor aggressiveness and shorter survival periods following tumor resection. In addition, PDACs often exhibit alterations in growth inhibitory pathways such as Smad4 mutations and Smad6 and Smad7 overexpression, and evade apoptosis through p53 mutations and aberrant expression of apoptosis regulating genes such as members of the Bcl family. Taken together, the abundance of growth promoting factors and the disturbance of growth inhibitory and apoptotic pathways give pancreatic cancer cells a distinct growth advantage which clinically results in rapid tumor progression and poor survival prognosis.

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40

Ceci, Francesco, Paolo Castellucci, Juliano J. Cerci y Stefano Fanti. "New aspects of molecular imaging in prostate cancer". Methods 130 (noviembre de 2017): 36–41. http://dx.doi.org/10.1016/j.ymeth.2017.07.009.

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41

Modos, O., D. Keresztes, P. Nyirády, A. Szendröi, J. Tímár, A. M. Szász, H. Reis et al. "Molecular and therapeutic aspects of advanced urachal cancer". European Urology Supplements 16, n.º 11 (noviembre de 2017): e2840. http://dx.doi.org/10.1016/s1569-9056(17)31982-6.

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42

Papadopoulos, Georgios, Dimitrios Delakas, Lydia Nakopoulou y Theodoros Kassimatis. "Statins and prostate cancer: Molecular and clinical aspects". European Journal of Cancer 47, n.º 6 (abril de 2011): 819–30. http://dx.doi.org/10.1016/j.ejca.2011.01.005.

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43

Palmirotta, Raffaele, Erica Silvestris, Stella D’Oronzo, Angela Cardascia y Franco Silvestris. "Ovarian cancer: Novel molecular aspects for clinical assessment". Critical Reviews in Oncology/Hematology 117 (septiembre de 2017): 12–29. http://dx.doi.org/10.1016/j.critrevonc.2017.06.007.

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Ramakrishnaiah, Ravikumar, Bangalore H. Durgesh, Santhosh Basavarajappa, Abdulaziz A. Al Kheraif y Darshan Devang Divakar. "Genetic, molecular and microbiological aspects of oral cancer". Reviews in Medical Microbiology 26, n.º 4 (noviembre de 2015): 134–37. http://dx.doi.org/10.1097/mrm.0000000000000051.

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Rebucci, Magali y Carine Michiels. "Molecular aspects of cancer cell resistance to chemotherapy". Biochemical Pharmacology 85, n.º 9 (mayo de 2013): 1219–26. http://dx.doi.org/10.1016/j.bcp.2013.02.017.

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Pinker, Katja, Wolfgang Bogner, Stephan Gruber, Peter Brader, Siegfried Trattnig, Georgios Karanikas y Thomas H. Helbich. "Molecular Imaging in Breast Cancer – Potential Future Aspects". Breast Care 6, n.º 2 (2011): 110–19. http://dx.doi.org/10.1159/000328275.

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Bornschein, Jan, Theodore Rokkas, Michael Selgrad y Peter Malfertheiner. "Gastric Cancer: Clinical Aspects, Epidemiology and Molecular Background". Helicobacter 16 (septiembre de 2011): 45–52. http://dx.doi.org/10.1111/j.1523-5378.2011.00880.x.

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Iovanna, Juan y José Luis Neira. "Pancreatic Cancer: Molecular, Biochemical, Chemopreventive, and Therapeutic Aspects". Scientific World JOURNAL 10 (2010): 1967–70. http://dx.doi.org/10.1100/tsw.2010.184.

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Resumen

Pancreatic cancer (PC) is the fourth leading cause of cancer death, with a median survival of 6 months and a dismal 5-year survival rate of 35%, a figure which has remained relatively unchanged over the past 25 years. PC is one of the most difficult diseases to treat due to late initial diagnosis and to resistance to the usual treatments. The presence of occult or clinical metastases at the time of diagnosis, together with the lack of effective chemotherapies, contributes to the high mortality in patients with PC. Its lethal nature stems from its propensity to disseminate rapidly to the lymphatic system and distant organs. Yet, understanding and stopping metastasis may prove to be one of the great potential strategies of treating PC. There is a dire need for the design of new and targeted therapeutic strategies that can overcome the drug resistance and improve the clinical outcome for patients diagnosed with the illness. The knowledge of the molecular aspects of PC is very important, and it is likely to be helpful in the design of newer drugs and the molecular selection of existing agents for targeted therapy. The inhibition of signal pathways can be carried out not only by small molecules, able to bind to selected regions of the target protein, but also by using large molecules as antibodies. The pathway to successful new therapies has been inhibited because of the rapidity with which agents tend to move into randomized, controlled trials without the extensive early testing necessary to optimize treatment regimens. However, lessons have been learned and our collective research effort has generated a substantial platform of knowledge from which further work will spring. The bioavailability of compounds such as antisense oligonucleotides and siRNAs in humans remains a big hurdle, which will require further improvement of gene-delivery strategies. Finally, the long-term goal of the therapy individualization for patients is possible if factors that predict treatment response, such as biological markers, could be determined accurately. These approaches are likely to comprise a mixture of targeted agents in combination with conventional chemotherapy and radiotherapy. For a clinically significant effect to be achieved, treatment strategies should either be in the form of (1) a horizontal approach, in which several oncogenic pathways (as those described in this series of reviews) are inhibited; or (2) a vertical approach, whereby multiple levels of a major pathway are targeted. Combination therapies, together with improved diagnostic tools and predictive markers, are ultimately desired in order to improve the bleak outlook for patients diagnosed with PC.

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Tomasik, Bartłomiej, Michał Bieńkowski, Zuzanna Górska, Klaudia Gutowska, Paulina Kumięga, Jacek Jassem y Renata Duchnowska. "Molecular aspects of brain metastases in breast cancer". Cancer Treatment Reviews 114 (marzo de 2023): 102521. http://dx.doi.org/10.1016/j.ctrv.2023.102521.

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Puram, Sidharth V. y James W. Rocco. "Molecular Aspects of Head and Neck Cancer Therapy". Hematology/Oncology Clinics of North America 29, n.º 6 (diciembre de 2015): 971–92. http://dx.doi.org/10.1016/j.hoc.2015.07.003.

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