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Journal articles on the topic 'Cancer pathogenesis'

Author: Grafiati

Published: 10 January 2023

Last updated: 28 January 2023

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1

Montironi, Rodolfo, and Per-Uno Malmström. "Bladder cancer: pathogenesis." Scandinavian Journal of Urology and Nephrology 42, sup218 (January 2008): 93–94. http://dx.doi.org/10.1080/03008880802291899.

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2

Berger, Hilmar, Miguel S. Marques, Rike Zietlow, Thomas F. Meyer, Jose C. Machado, and Ceu Figueiredo. "Gastric cancer pathogenesis." Helicobacter 21 (August 16, 2016): 34–38. http://dx.doi.org/10.1111/hel.12338.

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3

Bukhtoyarov, Oleg V., and Denis M. Samarin. "Pathogenesis of Cancer: Cancer Reparative Trap." Journal of Cancer Therapy 06, no. 05 (2015): 399–412. http://dx.doi.org/10.4236/jct.2015.65043.

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4

Franco, Omar E., Aubie K. Shaw, Douglas W. Strand, and Simon W. Hayward. "Cancer associated fibroblasts in cancer pathogenesis." Seminars in Cell & Developmental Biology 21, no. 1 (February 2010): 33–39. http://dx.doi.org/10.1016/j.semcdb.2009.10.010.

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5

Szabó, Diána, Adrienn Zsippai, Melinda Bendes, Zsófia Tömböl, Péter M. Szabó, Károly Rácz, and Péter Igaz. "Pathogenesis of adrenocortical cancer." Orvosi Hetilap 151, no. 29 (July 1, 2010): 1163–70. http://dx.doi.org/10.1556/oh.2010.28931.

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A mellékvesekéreg-carcinoma ritka, rossz prognózisú daganat. Döntően sporadikus előfordulású, de ismertek nagyon ritka öröklődő formái is, amelyek a patogenezis megértésében nagy segítséget nyújtanak. A mellékvesekéreg-daganatokra hajlamosító öröklődő szindrómák közé tartozik a Li–Fraumeni-szindróma, a Beckwith–Wiedemann-szindróma, a familiáris adenomatosus polyposis, illetve a döntően benignus daganatokkal társuló multiplex endokrin neoplasia 1-es típusa (MEN1), Carney-komplex és McCune–Albright-szindróma. A mellékvesekéreg-daganatok patogenezisében szereplő főbb mechanizmusok közé tartozik az inzulinszerű növekedési faktor-2 fokozott expressziója, a Wnt/β-katenin és a cAMP-proteinkináz-A jelátviteli utak aktivációja, valamint a p53 és MEN1 gének mutációi. A mellékvesekéreg-carcinoma kezelésében a gyógyszeres lehetőségek meglehetősen korlátozottak. Az utóbbi évek molekuláris-bioinformatikai kutatásai számos eddig ismeretlen patogenetikai út szerepét vetették fel, amelyek új gyógyszeres támadáspontok lehetőségét is jelenthetik. E tanulmányban a szerzők az öröklődő daganatszindrómák patogenezisét, a sporadikus daganatokban észlelt eltéréseket és a legújabb molekuláris-bioinformatikai eredményeket ismertetik.

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6

Yoon, Cheol-Yong, and Seok-Soo Byun. "Pathogenesis of Prostate Cancer." Journal of the Korean Medical Association 53, no. 2 (2010): 98. http://dx.doi.org/10.5124/jkma.2010.53.2.98.

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7

N, Gupta, Mujapara AK, Boraste A, Khairnar Y, Vamsi KK, Jhadav A, Gupta M, et al. "Toxicogenomics and cancer pathogenesis." International Journal of Genetics 1, no. 2 (December 30, 2009): 47–60. http://dx.doi.org/10.9735/0975-2862.1.2.47-60.

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8

Miller, York E. "Pathogenesis of Lung Cancer." American Journal of Respiratory Cell and Molecular Biology 33, no. 3 (September 2005): 216–23. http://dx.doi.org/10.1165/rcmb.2005-0158oe.

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9

Arnold, C. N., and H. E. Blum. "Colorectal cancer: molecular pathogenesis." DMW - Deutsche Medizinische Wochenschrift 130, no. 14 (April 2005): 880–82. http://dx.doi.org/10.1055/s-2005-865102.

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10

Ponz de Leon, M., and A. Percesepe. "Pathogenesis of colorectal cancer." Digestive and Liver Disease 32, no. 9 (December 2000): 807–21. http://dx.doi.org/10.1016/s1590-8658(00)80361-8.

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11

Berger, Nathan A. "Obesity and cancer pathogenesis." Annals of the New York Academy of Sciences 1311, no. 1 (April 2014): 57–76. http://dx.doi.org/10.1111/nyas.12416.

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12

Laviano, Alessandro, and Filippo Rossi-Fanelli. "Pathogenesis of cancer anorexia." Nutrition 19, no. 1 (January 2003): 67–68. http://dx.doi.org/10.1016/s0899-9007(02)00941-3.

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13

Jass, Jeremy R. "Pathogenesis of colorectal cancer." Surgical Clinics of North America 82, no. 5 (October 2002): 891–904. http://dx.doi.org/10.1016/s0039-6109(02)00047-6.

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14

Milsom, Jeffrey W. "Pathogenesis of Colorectal Cancer." Surgical Clinics of North America 73, no. 1 (February 1993): 1–11. http://dx.doi.org/10.1016/s0039-6109(16)45925-6.

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15

Figueiredo, Ceu, Susana Costa, Andreas Karameris, and Jose Carlos Machado. "Pathogenesis of Gastric Cancer." Helicobacter 20 (September 2015): 30–35. http://dx.doi.org/10.1111/hel.12254.

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16

Murtaugh, L. Charles. "Pathogenesis of Pancreatic Cancer." Toxicologic Pathology 42, no. 1 (October 31, 2013): 217–28. http://dx.doi.org/10.1177/0192623313508250.

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17

Bertherat, Jérôme, and Xavier Bertagna. "Pathogenesis of adrenocortical cancer." Best Practice & Research Clinical Endocrinology & Metabolism 23, no. 2 (April 2009): 261–71. http://dx.doi.org/10.1016/j.beem.2008.10.006.

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18

Khalyfa, Ahamed A., Shil Punatar, Rida Aslam, and Alex Yarbrough. "Exploring the Inflammatory Pathogenesis of Colorectal Cancer." Diseases 9, no. 4 (October 30, 2021): 79. http://dx.doi.org/10.3390/diseases9040079.

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Colorectal cancer is one of the most commonly diagnosed cancers worldwide. Traditionally, mechanisms of colorectal cancer formation have focused on genetic alterations including chromosomal damage and microsatellite instability. In recent years, there has been a growing body of evidence supporting the role of inflammation in colorectal cancer formation. Multiple cytokines, immune cells such T cells and macrophages, and other immune mediators have been identified in pathways leading to the initiation, growth, and metastasis of colorectal cancer. Outside the previously explored mechanisms and pathways leading to colorectal cancer, initiatives have been shifted to further study the role of inflammation in pathogenesis. Inflammatory pathways have also been linked to some traditional risk factors of colorectal cancer such as obesity, smoking and diabetes, as well as more novel associations such as the gut microbiome, the gut mycobiome and exosomes. In this review, we will explore the roles of obesity and diet, smoking, diabetes, the microbiome, the mycobiome and exosomes in colorectal cancer, with a specific focus on the underlying inflammatory and metabolic pathways involved. We will also investigate how the study of colon cancer from an inflammatory background not only creates a more holistic and inclusive understanding of this disease, but also creates unique opportunities for prevention, early diagnosis and therapy.

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19

Byrne, Frances L., Amy R. Martin, Melidya Kosasih, Beth T. Caruana, and Rhonda Farrell. "The Role of Hyperglycemia in Endometrial Cancer Pathogenesis." Cancers 12, no. 5 (May 8, 2020): 1191. http://dx.doi.org/10.3390/cancers12051191.

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Endometrial cancer is one of the most common cancers in women worldwide and its incidence is increasing. Epidemiological evidence shows a strong association between endometrial cancer and obesity, and multiple mechanisms linking obesity and cancer progression have been described. However, it remains unclear which factors are the main drivers of endometrial cancer development. Hyperglycemia and type 2 diabetes mellitus are common co-morbidities of obesity, and there is evidence that hyperglycemia is a risk factor for endometrial cancer independent of obesity. This review aims to explore the association between hyperglycemia and endometrial cancer, and discuss the evidence supporting a role for increased glucose metabolism in endometrial cancer and how this phenotype may contribute to endometrial cancer growth and progression. Finally, the potential role of blood glucose lowering strategies, including drugs and bariatric surgery, for the treatment of this malignancy will be discussed.

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20

Pratap, Pushpendra D., Syed Tasleem Raza, Ghazala Zaidi, Shipra Kunwar, Ale Eba, and Muneshwar Rajput. "IMPACT OF OXIDATIVE STRESS IN THE PATHOGENESIS OF CERVICAL CANCER: THERAPEUTIC APPROCHES." Era's Journal of Medical Research 9, no. 2 (December 2022): 249–55. http://dx.doi.org/10.24041/ejmr2022.39.

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Cervical cancer (CC) is acknowledged as the most ubiquitous carcinoma among females along with the utmost prevalence in developing nations. The major cause of CC is HPV exposure, especially HPV16 and 18. Inflammation is linked to the carcinogenesis of CC in addition to HPV infection. Although the precise cause of CC is yet unknown, using oral contraceptives, being immunosuppressed, and smoking may enhance the risk of the disease. Oxidative stress (OS), in addition to HPV, is linked to cervical cancer. Across several clinical and preclinical research, the dysfunctional redox system and the impact of oxidative stress throughout the aetiology of CC have been examined. Redox homeostasis must therefore be maintained, which calls for both enzymatic and nonenzymatic redox regulators. In this study, we explored the therapeutic strategies used to preserve redox balance, lower cervical cancer mortality, and illustrate the contribution of oxidative stress in the aetiology of the disease.

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21

Dranoff, Glenn. "Cytokines in cancer pathogenesis and cancer therapy." Nature Reviews Cancer 4, no. 1 (January 2004): 11–22. http://dx.doi.org/10.1038/nrc1252.

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22

Mahamane Salissou, Maibouge Tanko, Daud Gharib Zainab, Susan L.Mutambu, Mahaman Yacoubou Abdoul Razak, Fadzai Mukora Mutseyekwa, and Sungano Mharakurwa. "Involvement of Rab25 Biomarker in Pathogenesis of Ovarian Cancer." Asian Journal of Medicine and Biomedicine 5, no. 2 (October 29, 2021): 36–41. http://dx.doi.org/10.37231/ajmb.2021.5.2.431.

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Ovarian tumor is the third leading common gynecologic tumor and the common leading cause of death in gynecological cancers to the entire global and studies suggested that Rab25 is insinuated in the pathological process of ovarian cancer. Despite the availability of biomarkers for ovarian cancer detection, there are no specific markers that enable the early detection of ovarian cancers which open an avenue to Rab25 to be review. A number of genes and proteins have been reported to be involved in the pathogenesis of ovarian cancers. Of them, Ras-related protein 25 (Rab25) is suggested to be linked to increased risk of ovarian cancer development. Rab25, an intracellular transport protein, belongs to the Rab small GTPase family and regulates various aspects of internalized membrane protein recycling and trafficking occurring inside the cells to the cell membrane. It is known to be involved in cell proliferation, and prevents apoptosis and invasion in ovarian cancer. Rab25 is highly found in epithelial cells and the expression of Rab25 proteins has been implicated to be ubiquitous. Upregulation of Rab25 has also been strongly shown to intensify the cancer cell proliferation and to prevent apoptosis in vitro and in vivo .Here in we will review the past and current studies implicating Rab 25 as potential biomarker in ovarian cancer in addition to pathogenesis

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23

Knowles, Margaret A. "FGFR3 – a Central Player in Bladder Cancer Pathogenesis?" Bladder Cancer 6, no. 4 (December 14, 2020): 403–23. http://dx.doi.org/10.3233/blc-200373.

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The identification of mutations in FGFR3 in bladder tumors in 1999 led to major interest in this receptor and during the subsequent 20 years much has been learnt about the mutational profiles found in bladder cancer, the phenotypes associated with these and the potential of this mutated protein as a target for therapy. Based on mutational and expression data, it is estimated that >80% of non-muscle-invasive bladder cancers (NMIBC) and ∼40% of muscle-invasive bladder cancers (MIBC) have upregulated FGFR3 signalling, and these frequencies are likely to be even higher if alternative splicing of the receptor, expression of ligands and changes in regulatory mechanisms are taken into account. Major efforts by the pharmaceutical industry have led to development of a range of agents targeting FGFR3 and other FGF receptors. Several of these have entered clinical trials, and some have presented very encouraging early results in advanced bladder cancer. Recent reviews have summarised the drugs and related clinical trials in this area. This review will summarise what is known about the effects of FGFR3 and its mutant forms in normal urothelium and bladder tumors, will suggest when and how this protein contributes to urothelial cancer pathogenesis and will highlight areas that may benefit from further study.

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24

Bardhan, Kankana, and Kebin Liu. "Epigenetics and Colorectal Cancer Pathogenesis." Cancers 5, no. 4 (June 5, 2013): 676–713. http://dx.doi.org/10.3390/cancers5020676.

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25

Ibeanu, Okechukwu A. "Molecular pathogenesis of cervical cancer." Cancer Biology & Therapy 11, no. 3 (February 2011): 295–306. http://dx.doi.org/10.4161/cbt.11.3.14686.

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26

Yamaoka, Yoshio, and David Y. Graham. "Helicobacter pylorivirulence and cancer pathogenesis." Future Oncology 10, no. 8 (June 2014): 1487–500. http://dx.doi.org/10.2217/fon.14.29.

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27

Mackman, Nigel. "Pathogenesis of cancer-associated thrombosis." HemaSphere 2 (June 2018): 34–36. http://dx.doi.org/10.1097/hs9.0000000000000073.

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28

Park, Won Sang. "Molecular Pathogenesis of Gastric Cancer." Journal of the Korean Medical Association 53, no. 4 (2010): 270. http://dx.doi.org/10.5124/jkma.2010.53.4.270.

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29

Bluming, Avrum Z. "Progesterone and breast cancer pathogenesis." Journal of Molecular Endocrinology 66, no. 1 (January 2021): C1—C2. http://dx.doi.org/10.1530/jme-20-0262.

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30

Abdulkareem, ImranHaruna. "Aetio-pathogenesis of breast cancer." Nigerian Medical Journal 54, no. 6 (2013): 371. http://dx.doi.org/10.4103/0300-1652.126284.

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31

Král, Jan, Jana Slyšková, Pavel Vodička, and Julius Špičák. "Molecular Pathogenesis of Colorectal Cancer." Klinicka onkologie 29, no. 6 (December 15, 2016): 419–27. http://dx.doi.org/10.14735/amko2016419.

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32

Fong, Kwun M., Yoshitaka Sekido, and John D. Minna. "Molecular pathogenesis of lung cancer." Journal of Thoracic and Cardiovascular Surgery 118, no. 6 (December 1999): 1136–52. http://dx.doi.org/10.1016/s0022-5223(99)70121-2.

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33

Segev, Dorry L., Christopher Umbricht, and Martha A. Zeiger. "Molecular pathogenesis of thyroid cancer." Surgical Oncology 12, no. 2 (August 2003): 69–90. http://dx.doi.org/10.1016/s0960-7404(03)00037-9.

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34

Hilgers, Werner, Christophe Rosty, and StephanA Hahn. "Molecular pathogenesis of pancreatic cancer." Hematology/Oncology Clinics of North America 16, no. 1 (February 2002): 17–35. http://dx.doi.org/10.1016/s0889-8588(01)00005-3.

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35

Hoops, Timothy C., and Peter G. Traber. "MOLECULAR PATHOGENESIS OF COLORECTAL CANCER." Hematology/Oncology Clinics of North America 11, no. 4 (August 1997): 609–33. http://dx.doi.org/10.1016/s0889-8588(05)70453-6.

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36

Ozturk, Mehmet, Tugce Batur, Umut Ekin, Aybike Erdogan, Evin İscan, Umur Keles, Ozden Oz, and Cigdem Ozen. "Molecular Pathogenesis of Liver Cancer." Journal of Gastrointestinal Cancer 48, no. 3 (July 17, 2017): 222–24. http://dx.doi.org/10.1007/s12029-017-9957-2.

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37

Knowles, Margaret A. "Molecular pathogenesis of bladder cancer." International Journal of Clinical Oncology 13, no. 4 (August 2008): 287–97. http://dx.doi.org/10.1007/s10147-008-0812-0.

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38

De Paoli, Paolo, and Antonino Carbone. "Pathogenesis of HIV-Associated Cancer." Journal of Clinical Oncology 32, no. 27 (September 20, 2014): 3078–79. http://dx.doi.org/10.1200/jco.2014.56.0680.

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39

Zöchbauer-Müller, Sabine, Adi F. Gazdar, and John D. Minna. "Molecular Pathogenesis of Lung Cancer." Annual Review of Physiology 64, no. 1 (March 2002): 681–708. http://dx.doi.org/10.1146/annurev.physiol.64.081501.155828.

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40

Goral, Vedat. "Pancreatic Cancer: Pathogenesis and Diagnosis." Asian Pacific Journal of Cancer Prevention 16, no. 14 (September 2, 2015): 5619–24. http://dx.doi.org/10.7314/apjcp.2015.16.14.5619.

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41

Figueiredo, Ceu, Maria A. Garcia-Gonzalez, and Jose C. Machado. "Molecular Pathogenesis of Gastric Cancer." Helicobacter 18 (September 2013): 28–33. http://dx.doi.org/10.1111/hel.12083.

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42

Arnold, Christian N., Ajay Goel, Hubert E. Blum, and C. Richard Boland. "Molecular pathogenesis of colorectal cancer." Cancer 104, no. 10 (November 15, 2005): 2035–47. http://dx.doi.org/10.1002/cncr.21462.

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43

Sirnes, Solveig, Guro E. Lind, Jarle Bruun, Tone A. Fykerud, Marc Mesnil, Ragnhild A. Lothe, Edgar Rivedal, Matthias Kolberg, and Edward Leithe. "Connexins in colorectal cancer pathogenesis." International Journal of Cancer 137, no. 1 (May 5, 2014): 1–11. http://dx.doi.org/10.1002/ijc.28911.

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44

Francavilla, Antonio, and David H. Van Thiel. "Hepatic cancer pathogenesis and detection." Digestive Diseases and Sciences 36, no. 7 (July 1991): 961. http://dx.doi.org/10.1007/bf01297148.

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45

Maitra, Anirban, Scott E. Kern, and Ralph H. Hruban. "Molecular pathogenesis of pancreatic cancer." Best Practice & Research Clinical Gastroenterology 20, no. 2 (April 2006): 211–26. http://dx.doi.org/10.1016/j.bpg.2005.10.002.

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46

Lee, Yool. "Roles of circadian clocks in cancer pathogenesis and treatment." Experimental & Molecular Medicine 53, no. 10 (October 2021): 1529–38. http://dx.doi.org/10.1038/s12276-021-00681-0.

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AbstractCircadian clocks are ubiquitous timing mechanisms that generate approximately 24-h rhythms in cellular and bodily functions across nearly all living species. These internal clock systems enable living organisms to anticipate and respond to daily changes in their environment in a timely manner, optimizing temporal physiology and behaviors. Dysregulation of circadian rhythms by genetic and environmental risk factors increases susceptibility to multiple diseases, particularly cancers. A growing number of studies have revealed dynamic crosstalk between circadian clocks and cancer pathways, providing mechanistic insights into the therapeutic utility of circadian rhythms in cancer treatment. This review will discuss the roles of circadian rhythms in cancer pathogenesis, highlighting the recent advances in chronotherapeutic approaches for improved cancer treatment.

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47

Moses, Michael A., Andrea L. George, Nozomi Sakakibara, Kanwal Mahmood, Roshini M. Ponnamperuma, Kathryn E. King, and Wendy C. Weinberg. "Molecular Mechanisms of p63-Mediated Squamous Cancer Pathogenesis." International Journal of Molecular Sciences 20, no. 14 (July 23, 2019): 3590. http://dx.doi.org/10.3390/ijms20143590.

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The p63 gene is a member of the p53/p63/p73 family of transcription factors and plays a critical role in development and homeostasis of squamous epithelium. p63 is transcribed as multiple isoforms; ΔNp63α, the predominant p63 isoform in stratified squamous epithelium, is localized to the basal cells and is overexpressed in squamous cell cancers of multiple organ sites, including skin, head and neck, and lung. Further, p63 is considered a stem cell marker, and within the epidermis, ΔNp63α directs lineage commitment. ΔNp63α has been implicated in numerous processes of skin biology that impact normal epidermal homeostasis and can contribute to squamous cancer pathogenesis by supporting proliferation and survival with roles in blocking terminal differentiation, apoptosis, and senescence, and influencing adhesion and migration. ΔNp63α overexpression may also influence the tissue microenvironment through remodeling of the extracellular matrix and vasculature, as well as by enhancing cytokine and chemokine secretion to recruit pro-inflammatory infiltrate. This review focuses on the role of ΔNp63α in normal epidermal biology and how dysregulation can contribute to cutaneous squamous cancer development, drawing from knowledge also gained by squamous cancers from other organ sites that share p63 overexpression as a defining feature.

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48

Turpin, Brian K., Whitney M. Miller, Eric S. Mullins, Jay L. Degen, Matthew J. Flick, Brett P. Monia, Robert MacLeod, Alexey S. Revenko, and Joseph S. Palumbo. "Thrombin Supports Colitis and Colitis-Associated Cancer Pathogenesis." Blood 118, no. 21 (November 18, 2011): 2237. http://dx.doi.org/10.1182/blood.v118.21.2237.2237.

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Abstract Abstract 2237 Chronic inflammation has been recognized as a major factor in the development and progression of multiple cancers. A prime example of this is the strong association between colitis and colon cancer. However, the specific factors that regulate disadvantageous immune processes in the context of inflammation-associated cancers remain poorly defined. Growing evidence suggests that hemostatic system components, traditionally associated with the maintenance of vascular integrity and prevention of blood loss, also directly regulate inflammatory processes. Furthermore, thrombin and several thrombin targets (e.g., PARs, fibrinogen, factor XIII) have been shown to regulate tumor cell proliferation and apoptosis, support metastasis, and protect tumor cells from innate immune surveillance mechanisms in other experimental contexts. A logical extension of these findings is the hypothesis that thrombin, as a master regulator of both inflammatory processes and tumor cell biology, is a major determinant of the progression of inflammation-driven cancers such as colitis-associated colon cancer (CAC). To test this hypothesis, we induced CAC in mice carrying prothrombin levels 50% of normal (fII+/−) and WT mice in parallel using an established two step protocol consisting of azoxymethane (AOM) and dextran sodium sulfate (DSS) exposure. The modest diminution in prothrombin levels imposed by the fII+/− genotype resulted in a dramatic diminution in the number of colonic adenomas formed after AOM/DSS challenge relative to WT mice. In order to determine if the diminution in adenoma formation observed in fII+/− mice was coupled to thrombin function, wildtype mice challenged with AOM/DSS were treated with daily i.p. injections of hirudin, a direct thrombin inhibitor, or saline carrier. Similar to the finding in mice with a genetically-imposed diminution in circulating prothrombin, hirudin treatment significantly blunted adenoma formation. To determine if reduction of thrombin generation improved the inflammation preceding the development of colonic adenomas, we used a novel, highly-specific factor XI antisense oligonucleotide “gapmer” (ISIS Pharmaceuticals) to inhibit hepatic factor XI synthesis prior to DSS challenge. Gapmer-mediated diminution of fXI levels to ∼15% of normal resulted in a dramatic improvement in colitis related symptoms. Gapmer-treated mice had less intestinal bleeding and weight loss associated with DSS challenge relative to mice treated with a control oligonucleotide. Consistent with these gross observations, microscopic analyses of colonic tissue showed that fXI gapmer treatment significantly limited mucosal ulceration. Factor XI gapmer treatment also significantly diminished local levels of several inflammatory cytokines known to play a role in colon cancer progression (i.e., IL-6, IL-1β, IL-12). These results demonstrate that thrombin is a crucial driver of the pathogenesis of colitis-associated colon cancer and suggest that therapies directed at thrombin or thrombin generation could treat or prevent inflammation-driven colon cancer. As pathological inflammation has been estimated to account for as many as 1 in 5 cancer-related deaths, thrombin-directed therapies could have broad applicability to multiple malignancies. Disclosures: Mullins: Baxter: Consultancy. Monia:Isis Pharmaceuticals: Employment. MacLeod:Isis Pharmaceuticals: Employment. Revenko:Isis Pharmaceuticals: Employment. Palumbo:Novo Nordisk: Research Funding.

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49

Smallridge, Robert C., Laura A. Marlow, and John A. Copland. "Anaplastic thyroid cancer: molecular pathogenesis and emerging therapies." Endocrine-Related Cancer 16, no. 1 (March 2009): 17–44. http://dx.doi.org/10.1677/erc-08-0154.

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Anaplastic thyroid cancer (ATC) is a rare malignancy. While external beam radiation therapy has improved locoregional control, the median survival of ∼ 4 months has not changed in more than half a century due to uncontrolled systemic metastases. The objective of this study was to review the literature in order to identify potential new strategies for treating this highly lethal cancer. PubMed searches were the principal source of articles reviewed. The molecular pathogenesis of ATC includes mutations in BRAF, RAS, catenin (cadherin-associated protein), beta 1, PIK3CA, TP53, AXIN1, PTEN, and APC genes, and chromosomal abnormalities are common. Several microarray studies have identified genes and pathways preferentially affected, and dysregulated microRNA profiles differ from differentiated thyroid cancers. Numerous proteins involving transcription factors, signaling pathways, mitosis, proliferation, cell cycle, apoptosis, adhesion, migration, epigenetics, and protein degradation are affected. A variety of agents have been successful in controlling ATC cell growth both in vitro and in nude mice xenografts. While many of these new compounds are in cancer clinical trials, there are few studies being conducted in ATC. With the recent increased knowledge of the many critical genes and proteins affected in ATC, and the extensive array of targeted therapies being developed for cancer patients, there are new opportunities to design clinical trials based upon tumor molecular profiling and preclinical studies of potentially synergistic combinatorial novel therapies.

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50

Djuraev, Mirdjalol Dehkanovich, Nodir Maxammatkulovich Rahimov, Mavluda Nigmatovna Karimova, and Shakhnoza Shavkatovna Shakhanova. "Current Views On The Pathogenesis Of The Parietal-Visceral Pathway Of Gastric Cancer Metastasis." American Journal of Medical Sciences and Pharmaceutical Research 03, no. 03 (March 31, 2021): 94–103. http://dx.doi.org/10.37547/tajmspr/volume03issue03-14.

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Abstract:

Metastases to the peritoneum occur in 55-60% of patients with gastric cancer and are associated with a 5-year overall survival of 2%. Treatment options for these patients are limited, and targeted therapy or immunotherapy is not available. Rational therapeutic targets have yet to be found.In this review, we present the published literature and our own recent experience in molecular biology to identify important molecules and signalling pathways as well as cellular immunity involved in GC peritoneal metastases.

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