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Journal articles on the topic 'Kidney Cancer'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 March 2025

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1

Franjic, Sinisa. "A Few Words about Kidney Cancer." Clinical Case Reports and Trails 1, no. 1 (December 15, 2022): 01–03. http://dx.doi.org/10.58489/2836-2217/001.

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Kidney cancer is a malignant disease that affects a large number of adults around the world. The kidneys are paired organs, extremely important for the normal functioning of the body. Each person has two kidneys, left and right, located along the spine and below the ribs. The kidneys are the main filters in the human body and perform multiple functions. They are responsible for fluid control, excretion of toxins, mineral salts, production of the hormone erythropoietin which stimulates the production of red blood cells. Each kidney works independently and a person can live with one kidney. When the kidneys are severely damaged, this leads to the need for dialysis. Kidney tumor refers to abnormal tissue growth within the kidney, and can be benign or malignant. This disease affects men more often than women aged 55 to 75 years. The disease develops within one or both kidneys, while in an advanced stage it spreads to the lymph nodes and bloodstream. It is important to know that early diagnosis and effective methods can help treat this type of cancer.

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2

Nasir, Muhammad Umar, Muhammad Zubair, Taher M. Ghazal, Muhammad Farhan Khan, Munir Ahmad, Atta-ur Rahman, Hussam Al Hamadi, Muhammad Adnan Khan, and Wathiq Mansoor. "Kidney Cancer Prediction Empowered with Blockchain Security Using Transfer Learning." Sensors 22, no. 19 (October 2, 2022): 7483. http://dx.doi.org/10.3390/s22197483.

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Kidney cancer is a very dangerous and lethal cancerous disease caused by kidney tumors or by genetic renal disease, and very few patients survive because there is no method for early prediction of kidney cancer. Early prediction of kidney cancer helps doctors start proper therapy and treatment for the patients, preventing kidney tumors and renal transplantation. With the adaptation of artificial intelligence, automated tools empowered with different deep learning and machine learning algorithms can predict cancers. In this study, the proposed model used the Internet of Medical Things (IoMT)-based transfer learning technique with different deep learning algorithms to predict kidney cancer in its early stages, and for the patient’s data security, the proposed model incorporates blockchain technology-based private clouds and transfer-learning trained models. To predict kidney cancer, the proposed model used biopsies of cancerous kidneys consisting of three classes. The proposed model achieved the highest training accuracy and prediction accuracy of 99.8% and 99.20%, respectively, empowered with data augmentation and without augmentation, and the proposed model achieved 93.75% prediction accuracy during validation. Transfer learning provides a promising framework with the combination of IoMT technologies and blockchain technology layers to enhance the diagnosing capabilities of kidney cancer.

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3

Rambe, Tri Putra Rahmad Ramadani, and M. Hidayat Surya Atmaja. "Kidney cancer with complications in Dr. Soetomo Regional Public Hospital, Surabaya, Indonesia." International journal of health sciences 6, S1 (March 22, 2022): 1832–41. http://dx.doi.org/10.53730/ijhs.v6ns1.4944.

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Kidney cancer is a disease in which kidney cells become malignant and grow uncontrollably, forming a mass or tumor. Before discussing further kidney cancer, it is important to briefly know the kidneys. The kidneys are two bean-shaped organs located in the lower abdomen on the left and right of the spine. The primary function of the kidneys is to excrete and excrete water, salt, and other unnecessary substances and turn them into urine. The urine collects in the renal pelvis (the funnel-shaped part of each kidney), then travels to the ureters (the tube between the kidneys and bladder), and finally to the bladder, where it is stored before urination. Another function of the kidneys is to help control blood pressure by making the renin hormone and forming red blood cells by forming the hormone erythropoietin. In the United States, an estimated 76,080 adults were diagnosed with kidney cancer, and 13,780 of them died from the disease in 2021. Meanwhile, a total of 2,394 new cases of kidney cancer were found in Indonesia with 1,358 total deaths in 2020. More than half of patients with kidney cancer are diagnosed at an advanced stage.

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4

Graham, Jeffrey. "ASCO GU22 – Kidney Cancer Highlights." Kidney Cancer Journal 20, no. 1 (March 16, 2022): 32–33. http://dx.doi.org/10.52733/kcj20n1-gu2.

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The 2022 ASCO Genitourinary Cancers Symposium took place in San Francisco between February 17-19th. As always, the scientific program contained several exciting abstracts with a focus on prostate cancer, bladder cancer, and kidney cancer. Here we will highlight key abstracts related to kidney cancer/renal cell carcinoma presented at this year’s symposium.

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5

Dean, Erin. "Kidney cancer." Cancer Nursing Practice 16, no. 8 (October 10, 2017): 11. http://dx.doi.org/10.7748/cnp.16.8.11.s12.

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6

_, _. "Kidney Cancer." Journal of the National Comprehensive Cancer Network 4, no. 10 (November 2006): 1072. http://dx.doi.org/10.6004/jnccn.2006.0089.

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An estimated 38,890 Americans will be diagnosed with kidney cancer and 12,840 will die of this disease in the United States in 2006. Renal cell carcinoma (RCC) constitutes approximately 2% of all malignancies, with a median age at diagnosis of 65 years. Smoking and obesity are among the risk factors for RCC development, and tumor grade, local extent of the tumor, presence of regional nodal metastases, and evidence of metastatic disease at presentation are the most important prognostic determinants of 5-year survival. These guidelines discuss evaluation, staging, treatment, and management after treatment. For the most recent version of the guidelines, please visit NCCN.org

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7

Motzer, Robert J., Neeraj Agarwal, Clair Beard, Graeme B. Bolger, Barry Boston, Michael A. Carducci, Toni K. Choueiri, et al. "Kidney Cancer." Journal of the National Comprehensive Cancer Network 7, no. 6 (June 2009): 618–30. http://dx.doi.org/10.6004/jnccn.2009.0043.

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8

Motzer, Robert J., Neeraj Agarwal, Clair Beard, Sam Bhayani, Graeme B. Bolger, Michael A. Carducci, Sam S. Chang, et al. "Kidney Cancer." Journal of the National Comprehensive Cancer Network 9, no. 9 (September 2011): 960–77. http://dx.doi.org/10.6004/jnccn.2011.0082.

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9

Owens, Brian. "Kidney cancer." Nature 537, no. 7620 (September 2016): S97. http://dx.doi.org/10.1038/537s97a.

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10

Laino, Charlene. "Kidney Cancer." Oncology Times 30, no. 8 (April 2008): 16–18. http://dx.doi.org/10.1097/01.cot.0000319616.21951.54.

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11

DiGiulio, Sarah. "Kidney Cancer." Oncology Times 34, no. 10 (May 2012): 12–14. http://dx.doi.org/10.1097/01.cot.0000415254.40472.f9.

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12

DiGiulio, Sarah. "Kidney cancer." Oncology Times UK 9, no. 6 (June 2012): 17. http://dx.doi.org/10.1097/01.otu.0000415649.34364.a9.

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13

Vogelzang, Nicholas J., and Walter M. Stadler. "Kidney cancer." Lancet 352, no. 9141 (November 1998): 1691–96. http://dx.doi.org/10.1016/s0140-6736(98)01041-1.

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14

DiGiulio, Sarah. "Kidney Cancer." Nephrology Times 5, no. 5 (May 2012): 13–14. http://dx.doi.org/10.1097/01.nep.0000415389.49208.c3.

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15

Wallen, Eric M., Raj S. Pruthi, Geoffrey F. Joyce, and Matthew Wise. "Kidney Cancer." Journal of Urology 177, no. 6 (June 2007): 2006–19. http://dx.doi.org/10.1016/j.juro.2007.01.126.

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16

Chowdhury, Nivedita, and Charles G. Drake. "Kidney Cancer." Urologic Clinics of North America 47, no. 4 (November 2020): 419–31. http://dx.doi.org/10.1016/j.ucl.2020.07.009.

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17

Linehan, W. Marston, and W. Kimryn Rathmell. "Kidney cancer." Urologic Oncology: Seminars and Original Investigations 30, no. 6 (November 2012): 948–51. http://dx.doi.org/10.1016/j.urolonc.2012.08.021.

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18

LaFollette, Sandra S. "Kidney Cancer." AORN Journal 56, no. 1 (July 1992): 31–48. http://dx.doi.org/10.1016/s0001-2092(07)66647-2.

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19

Halperin, Edward C. "Kidney cancer." Lancet 353, no. 9152 (February 1999): 594. http://dx.doi.org/10.1016/s0140-6736(05)75656-7.

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20

Johansson, Martin E., and Håkan Axelson. "Kidney cancer." Seminars in Cancer Biology 23, no. 1 (February 2013): 1–2. http://dx.doi.org/10.1016/j.semcancer.2012.05.006.

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21

Hancock, S. Brandon, and Christos S. Georgiades. "Kidney Cancer." Cancer Journal 22, no. 6 (2016): 387–92. http://dx.doi.org/10.1097/ppo.0000000000000225.

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22

Torpy, Janet M. "Kidney Cancer." JAMA 292, no. 1 (July 7, 2004): 134. http://dx.doi.org/10.1001/jama.292.1.134.

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23

Forum, Canadian Kidney Cancer. "Management of Kidney Cancer: Canadian Kidney Cancer Forum." Canadian Urological Association Journal 6, no. 1 (February 26, 2013): 16. http://dx.doi.org/10.5489/cuaj.367.

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24

Hasumi, Hisashi, Masaya Baba, Yukiko Hasumi, Martin Lang, Ying Huang, HyoungBin F. Oh, Masayuki Matsuo, et al. "Folliculin-interacting proteins Fnip1 and Fnip2 play critical roles in kidney tumor suppression in cooperation with Flcn." Proceedings of the National Academy of Sciences 112, no. 13 (March 16, 2015): E1624—E1631. http://dx.doi.org/10.1073/pnas.1419502112.

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Folliculin (FLCN)-interacting proteins 1 and 2 (FNIP1, FNIP2) are homologous binding partners of FLCN, a tumor suppressor for kidney cancer. Recent studies have revealed potential functions for Flcn in kidney; however, kidney-specific functions for Fnip1 and Fnip2 are unknown. Here we demonstrate that Fnip1 and Fnip2 play critical roles in kidney tumor suppression in cooperation with Flcn. We observed no detectable phenotype in Fnip2 knockout mice, whereas Fnip1 deficiency produced phenotypes similar to those seen in Flcn-deficient mice in multiple organs, but not in kidneys. We found that absolute Fnip2 mRNA copy number was low relative to Fnip1 in organs that showed phenotypes under Fnip1 deficiency but was comparable to Fnip1 mRNA copy number in mouse kidney. Strikingly, kidney-targeted Fnip1/Fnip2 double inactivation produced enlarged polycystic kidneys, as was previously reported in Flcn-deficient kidneys. Kidney-specific Flcn inactivation did not further augment kidney size or cystic histology of Fnip1/Fnip2 double-deficient kidneys, suggesting pathways dysregulated in Flcn-deficient kidneys and Fnip1/Fnip2 double-deficient kidneys are convergent. Heterozygous Fnip1/homozygous Fnip2 double-knockout mice developed kidney cancer at 24 mo of age, analogous to the heterozygous Flcn knockout mouse model, further supporting the concept that Fnip1 and Fnip2 are essential for the tumor-suppressive function of Flcn and that kidney tumorigenesis in human Birt–Hogg–Dubé syndrome may be triggered by loss of interactions among Flcn, Fnip1, and Fnip2. Our findings uncover important roles for Fnip1 and Fnip2 in kidney tumor suppression and may provide molecular targets for the development of novel therapeutics for kidney cancer.

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25

Burnasheva, E. V., Y. V. Shatokhin, I. V. Snezhko, and A. A. Matsuga. "KIDNEY INJURY IN CANCER THERAPY." Nephrology (Saint-Petersburg) 22, no. 5 (October 8, 2018): 17–24. http://dx.doi.org/10.24884/1561-6274-2018-22-5-17-24.

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Кidney injury is a frequent and significant complication of cancer and cancer therapy. The kidneys are susceptible to injury from malignant infiltration, damage by metabolites of malignant cells, glomerular injury, nephrotoxic drugs including chemotherapeutic agents. Also bone marrow transplantation complications, infections with immune suppression (including septicemia), tumor lysis syndrome should be taken into account. Chemotherapeutic agents are a common cause of acute kidney injury but can potentially lead to chronic kidney disease development in cancer patients. This article summarizes risk factors of acute kidney injury in cancer patients. Risk factors are divided into two groups. The systemic are decrease of total circulating blood volume, infiltration of kidney tissue by tumor cells, dysproteinemia, electrolyte disturbances. The local (renal) risk factors are microcirculation disturbances, drugs biotransformation with formation of reactive oxygen intermediates, high concentration of nephrotoxic agents in proximal tubules and its sensitivity to ischemia. Drug-related risk factors include: drugs combination with cytotoxic effect high doses long term use necessity, direct cytotoxic effect of not only chemotherapeutic agents but also its metabolites, mean solubility forming intratubular precipitates. Early diagnosis, timely prevention and treatment of these complications provide significantly improve nononcologic results of treatment.

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26

Blitzer, Grace, Susan Tsai, Mohammed Aldakkak, Robert Hellman, Douglas B. Evans, Kathleen K. Christians, Ben George, Paul S. Ritch, William Adrian Hall, and Beth Erickson. "Should functional renal scans be obtained prior to upper abdominal radiation for pancreatic cancer?" Journal of Clinical Oncology 35, no. 4_suppl (February 1, 2017): 442. http://dx.doi.org/10.1200/jco.2017.35.4_suppl.442.

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442 Background: Upper abdominal irradiation for pancreas cancer is given in close proximity to the radiation sensitive kidneys. While contemporary 3D and intensity modulated radiation therapy (IMRT) can decrease the total dose of radiation delivered to the kidneys; these plans may potentially exceed the established kidney dose constraints, especially if one kidney is providing most of the renal function. Less than 10% of the general population is estimated to have asymmetrical kidney function. Functional kidney scans using MAG3 clearance can give information about the contribution of each kidney to total renal function. We sought to determine if functional renal scans should be used to identify patients with occult renal dysfunction. Methods: Patients with resectable and borderline resectable pancreatic cancer who received abdominal irradiation therapy and had pre-radiation functional renal scans between 2009-2015 were studied. Asymmetrical kidney function was defined as a difference between the two kidneys that was ≥ 40%/60% on a functional renal scan. Serum studies (BUN, Cr, GFR) were routinely obtained pre-simulation. Restaging abdominal CT scans prior to radiation were screened for disparity in kidney size. Medical history that suggested decreased renal function was also collected. Results: Of the 205 patients examined, 24 (11.7%) had asymmetrical kidney function identified on pre-radiation functional renal scans. Of the patients with asymmetrical kidney function, 4 (2%) had a 75%/25% split or greater and 20 (9.7%) had kidney function between 60%/40% and 75%/25%. Elevated Cr or BUN, a GFR < 60, or a past medical history suggesting abnormal renal function were not significantly associated with asymmetrical kidney function. Only six (25%) of patients with asymmetrical kidney function scans had a notable difference in kidney size. Conclusions: In our series, approximately 12% of patients with pancreatic cancer have asymmetrical kidney function not identified by size, serum BUN, Cr, GFR, or a significant past medical history of renal compromise. These results provide important insight for cases when radiation plans may approach or exceed accepted dose constraints for the kidneys.

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27

Peired, Anna Julie, Elena Lazzeri, Francesco Guzzi, Hans-Joachim Anders, and Paola Romagnani. "From kidney injury to kidney cancer." Kidney International 100, no. 1 (July 2021): 55–66. http://dx.doi.org/10.1016/j.kint.2021.03.011.

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28

Yuk, Hyeong-Dong, Kyoung-Hwa Lee, Hye-Sun Lee, Seung-Hwan Jeong, Yongseok Kho, Chang-Wook Jeong, Hyeon-Hoe Kim, Ja-Hyeon Ku, and Cheol Kwak. "PDLIM2 Suppression Inhibit Proliferation and Metastasis in Kidney Cancer." Cancers 13, no. 12 (June 15, 2021): 2991. http://dx.doi.org/10.3390/cancers13122991.

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We evaluated the expression of PDLIM2 in human kidney cancer cell lines from primary or metastatic origins and found that PDLIM2 expression was highly elevated in metastatic kidney cancers. We evaluated the effect of PDLIM2 inhibition by RNA interference method. PDLIM2 knockdown showed the decreased proliferation and metastatic character in human metastatic kidney cancer cells. By repeated round of orthotopic injection of RenCa mouse kidney cancer cell line, we obtained metastatic prone mouse kidney cancer cell lines. PDLIM2 expression was highly expressed in these metastatic prone cells comparing parental cells. In addition, we evaluated the in vivo efficacy of PDLIM2 knockout on the tumor formation and metastasis of kidney cancer cells using a PDLIM2 knockout mice. The experimental metastasis model with tail vein injection and orthotopic metastasis model injected into kidney all showed reduced lung metastasis cancer formation in PDLIM2 knockout mice comparing control Balb/c mice. Overall, our findings indicate that PDLIM2 is required for cancer formation and metastasis in metastatic kidney cancer, indicating that PDLIM2 may be a new therapeutic target for metastatic kidney cancer.

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29

Wang, Yichen, Sarah Moody, Behnoush Abedi-Ardekani, Calli Latimer, Saamin Cheema, Jingwei Wang, Stephen Fitzgerald, Laura Humphreys, Paul Brennan, and Michael R. Stratton. "Abstract 1168: Mutational processes in tumour-adjacent normal kidneys across countries with varying cancer incidence rates." Cancer Research 83, no. 7_Supplement (April 4, 2023): 1168. http://dx.doi.org/10.1158/1538-7445.am2023-1168.

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Abstract In recent years, large-scale whole genome sequencing of multiple types of cancer across multiple continents has been conducted as part of the “Mutographs” Cancer Grand Challenge to uncover unknown causes of cancer through detection of signatures of mutational processes operative during cancer development. Distinct mutational signatures have recently been detected by “Mutographs” in Renal Clear Cell Carcinomas (RCC) from different parts of the world. However, whether the detected mutational signatures are present in normal tissues or are initiated after tumorigenesis remains unknown. In general, there has been a lack of knowledge of somatic mutations in normal cells primarily due to technological barriers to detection of somatic mutations in highly polyclonal normal tissues. However, a recently developed duplex sequencing technology, NanoSeq, uses copies of both strands of each DNA molecule to reduce sequencing errors to 10−9. With NanoSeq, we are able to detect somatic mutations in polyclonal tissues including the normal kidney. In this study, we used NanoSeq to sequence 288 tumor-adjacent normal kidney samples from multiple countries with varying RCC incidence. Subsequently, we conducted agnostic signature extraction using a Hierarchical Dirichlet Process to investigate whether the region specific mutational signatures found in cancers can be extracted from normal kidney tissue. The normal kidney tissues we sequenced have paired RCC whole genome sequencing data from the same individual. Therefore, the mutational profiles of normal kidney can be compared to paired cancer samples to ascertain the timing of the mutational processes causing the mutational signatures found in the cancers. We confirmed that a predominantly T>C mutational signature that is highly enriched in Japanese RCC is present in normal kidney samples. A strong transcriptional strand bias in this signature provides circumstantial evidence that it is likely to have been caused by DNA damaging agents causing bulky DNA adducts which may be of environmental origin. A subset of RCC samples from Serbia and Romania had mutational signatures caused by aristolochic acids (AA). We found different dominant AA-related signatures in tumors compared to their matched normal tissues, potentially indicating different mutagenic or repair mechanisms between normal and cancer cells. Levels of SBS40, which is of unknown cause, were elevated in normal kidneys from the Czech Republic compared to other countries, and may contribute to the high RCC incidence in this country. In summary, this study provides the first systematic investigation of somatic mutations in normal kidney, revealing different mutational processes in different geographic regions and in cancer versus normal kidneys. Citation Format: Yichen Wang, Sarah Moody, Behnoush Abedi-Ardekani, Calli Latimer, Saamin Cheema, Jingwei Wang, Stephen Fitzgerald, Laura Humphreys, Paul Brennan, Michael R. Stratton. Mutational processes in tumour-adjacent normal kidneys across countries with varying cancer incidence rates [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 1168.

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30

Goodman, Alice. "Advanced Kidney Cancer." Oncology Times 29, no. 12 (June 2007): 8. http://dx.doi.org/10.1097/01.cot.0000282580.73692.0c.

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31

Fromer, Margot J. "Metastatic Kidney Cancer." Oncology Times 27, no. 3 (February 2005): 16. http://dx.doi.org/10.1097/01.cot.0000288813.54319.2c.

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32

Dixon, Carl F. "Kidney Cancer Association." Oncology Times 24, no. 9 (September 2002): 4. http://dx.doi.org/10.1097/01.cot.0000289199.30118.78.

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33

Kelley, Celeste. "Kidney Cancer Association." Neoplasia 4, no. 5 (2002): 464. http://dx.doi.org/10.1038/sj.neo.7900261.

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34

Yuan, Yan, Guillermo Marshall, Catterina Ferreccio, Craig Steinmaus, Jane Liaw, Michael Bates, and Allan H. Smith. "Kidney Cancer Mortality." Epidemiology 21, no. 1 (January 2010): 103–8. http://dx.doi.org/10.1097/ede.0b013e3181c21e46.

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35

Libertino, John A. "Editorial: Kidney Cancer." Journal of Urology 155, no. 2 (February 1996): 466–67. http://dx.doi.org/10.1016/s0022-5347(01)66419-x.

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36

Fromer, Margot J. "Metastatic kidney cancer." Oncology Times 2, no. 4 (April 2005): 6–8. http://dx.doi.org/10.1097/01434893-200504000-00003.

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37

Hwang, Jonathan J., Edward M. Uchio, W. Marston Linehan, and McClellan M. Walther. "Hereditary kidney cancer." Urologic Clinics of North America 30, no. 4 (November 2003): 831–42. http://dx.doi.org/10.1016/s0094-0143(03)00054-5.

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38

Alekseev, B. Ya, A. S. Kalpinsky, N. V. Vorobyev, K. M. Nyushko, K. Yu Kanukoev, and A. D. Kaprin. "Bilateral kidney cancer." Onkologiya. Zhurnal imeni P.A.Gertsena 5, no. 1 (2016): 55. http://dx.doi.org/10.17116/onkolog20165155-62.

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39

Linehan, W. Marston, Peter A. Pinto, Gennady Bratslavsky, Elizabeth Pfaffenroth, Maria Merino, Cathy D. Vocke, Jorge R. Toro, et al. "Hereditary kidney cancer." Cancer 115, S10 (April 28, 2009): 2252–61. http://dx.doi.org/10.1002/cncr.24230.

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40

Rasmussen, Robert, Thomas Sanford, Anil V. Parwani, and Ivan Pedrosa. "Artificial Intelligence in Kidney Cancer." American Society of Clinical Oncology Educational Book, no. 42 (April 2022): 1–11. http://dx.doi.org/10.1200/edbk_350862.

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Artificial intelligence is rapidly expanding into nearly all facets of life, particularly within the field of medicine. The diagnosis, characterization, management, and treatment of kidney cancer is ripe with areas for improvement that may be met with the promises of artificial intelligence. Here, we explore the impact of current research work in artificial intelligence for clinicians caring for patients with renal cancer, with a focus on the perspectives of radiologists, pathologists, and urologists. Promising preliminary results indicate that artificial intelligence may assist in the diagnosis and risk stratification of newly discovered renal masses and help guide the clinical treatment of patients with kidney cancer. However, much of the work in this field is still in its early stages, limited in its broader applicability, and hampered by small datasets, the varied appearance and presentation of kidney cancers, and the intrinsic limitations of the rigidly structured tasks artificial intelligence algorithms are trained to complete. Nonetheless, the continued exploration of artificial intelligence holds promise toward improving the clinical care of patients with kidney cancer.

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41

Forum, Canadian Kidney Cancer. "Management of kidney cancer: Canadian Kidney Cancer Forum Consensus Update." Canadian Urological Association Journal 3, no. 3 (April 26, 2013): 200. http://dx.doi.org/10.5489/cuaj.1069.

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42

Jewett, Michael A. S., J. J. Knox, and C. Kollmannsberger. "Management of kidney cancer: Canadian Kidney Cancer Forum Consensus Statement." Canadian Urological Association Journal 2, no. 3 (April 2, 2013): 175. http://dx.doi.org/10.5489/cuaj.567.

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43

Duha, Diki Arma, Edward Usfie Harahap, Rachmat Budi Santoso, and Ikhlas Arief Bramono. "Kidney Cancer Profile in National Cancer Center (NCC) - Dharmais Cancer Hospital." Indonesian Journal of Cancer 16, no. 4 (December 28, 2022): 226. http://dx.doi.org/10.33371/ijoc.v16i4.904.

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Background: Kidney cancer is one of the most prevalent cancers in urology. The higher prevalence of risk factors, as well as better diagnostic modalities, has led to a reported increase worldwide. The study aims to describe the profile and management pattern of kidney cancer patients at a tertiary referral center over seven years.Methods: A descriptive study was conducted to assess the profile and management of kidney patients in the national cancer center (NCC) - Dharmais Hospital Jakarta between January 2013 and December 2020. The variables collected included age, gender, stage (AJCC staging), histopathological result, and management, using the total sampling method.Results: A total of 53 kidney cancer cases were documented in NCC - Dharmais Hospital Jakarta from 2013 to 2020. Overall, males are more prevalent than females, with a sex ratio of 2.3:1. The most frequent age group was 51–65 years. The most common histological subtype was a clear cell in the renal cell carcinoma (RCC) subtype and sarcoma in the non-RCC subtype. Noticeably, end-stage (stage IV) was found in more than half of patients (65.6%), with no patient found in stage I. Radical nephrectomy was preferable to cytoreductive nephrectomy. Conclusions: : An increasing trend of kidney cancer incidence was found between 2013 and 2020 with most patients diagnosed with stage IV.

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44

Muscella, Antonella, Leonardo Resta, Luca Giulio Cossa, and Santo Marsigliante. "Immunolocalization of the AT-1R Ang II Receptor in Human Kidney Cancer." Biomolecules 13, no. 8 (July 28, 2023): 1181. http://dx.doi.org/10.3390/biom13081181.

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This study aimed to evaluate AT1-R expression in normal and cancerous human kidneys, how these expressions are modified, and AT1-R functionality. AT-1R mRNA expression, determined by real-time PCR, was detected in all samples. AT-1R mRNA increased in well-differentiated cancer (G1, p < 0.01) and decreased 2.9-fold in undifferentiated cancer (G4, p < 0.001) compared with normal kidney tissues. Immunocytochemistry analysis showed that the AT-1R was expressed in the normal tubular epithelium. The glomerulus was also immunoreactive, and as expected, the smooth muscle cells of the vessel walls also expressed the receptor. A total of 35 out of 42 tumors were AT-1R positive, with the cell tumors showing varying numbers of immunoreactive cells, which were stained in a diffuse cytoplasmic and membranous pattern. Computer-assisted counting of the stained tumor cells showed that the number of AT-1R-positive cells increased in the well-differentiated cancers. The functionality of AT-1R was assessed in primary cultures of kidney epithelial cells obtained from three G3 kidney cancer tissues and corresponding histologically proven non-malignant tissue adjacent to the tumor. Indeed, Ang II stimulated, in a dose-dependent manner, the 24 h proliferation of normal kidney cells and cancer cells in the primary culture and phosphorylated extracellular regulated kinases 1 and 2. In conclusion, Ang II may be involved in the growth or function of neoplastic kidney tissue.

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45

SeokShin, Hong, Hyun JinJung, and Jae ShinPark. "Bladder cancer presenting as a retroperitoneal urinoma of kidney." International Journal of Medical Reviews and Case Reports 2, Reports in Surgery and Dermatolo (2018): 1. http://dx.doi.org/10.5455/ijmrcr.retroperitoneal-urinoma-kidney.

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Lee, Kyoung-Hwa, Byung-Chan Kim, Seung-Hwan Jeong, Chang Wook Jeong, Ja Hyeon Ku, Cheol Kwak, and Hyeon Hoe Kim. "Histone Demethylase LSD1 Regulates Kidney Cancer Progression by Modulating Androgen Receptor Activity." International Journal of Molecular Sciences 21, no. 17 (August 24, 2020): 6089. http://dx.doi.org/10.3390/ijms21176089.

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Kidney cancer is one of the most difficult cancers to treat by targeted and radiation therapy. Therefore, identifying key regulators in this cancer is especially important for finding new drugs. We focused on androgen receptor (AR) regulation by its epigenetic co-regulator lysine-specific histone demethylase 1 (LSD1) in kidney cancer development. LSD1 knock-down in kidney cancer cells decreased expression of AR target genes. Moreover, the binding of AR to target gene promoters was reduced and histone methylation status was changed in LSD1 knock-down kidney cancer cells. LSD1 knock-down also slowed growth and decreased the migration ability of kidney cancer cells. We found that pargyline, known as a LSD1 inhibitor, can reduce AR activity in kidney cancer cells. The treatment of kidney cancer cells with pargyline delayed growth and repressed epithelial–mesenchymal transition (EMT) markers. These effects were additively enhanced by co-treatment with the AR inhibitor enzalutamide. Down-regulation of LSD1 in renal cancer cells (RCC) attenuated in vivo tumor growth in a xenograft mouse model. These results provide evidence that LSD1 can regulate kidney cancer cell growth via epigenetic control of AR transcription factors and that LSD1 inhibitors may be good candidate drugs for treating kidney cancer.

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Buchberger, David, Paul Kreinbrink, and Jordan Kharofa. "Proton Therapy in the Treatment of Anal Cancer in Pelvic Kidney Transplant Recipients: A Case Series." International Journal of Particle Therapy 6, no. 1 (June 1, 2019): 28–34. http://dx.doi.org/10.14338/ijpt-19-00067.1.

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Abstract Purpose: The incidence of anal cancer in patients with kidney transplants has increased. The definitive treatment for anal cancer is chemotherapy and intensity-modulated radiation therapy. In kidney transplant recipients, sparing the pelvic kidney in the process of delivering radiation to the anus can be challenging. Intensity-modulated proton therapy (IMPT) has been proposed as an alternative to intensity-modulated radiation therapy for the treatment of anal cancer in this population, given its increased ability to spare organs-at-risk. Case Series: We present 4 cases of patients with transplanted pelvic kidneys who subsequently developed anal cancer and were treated with IMPT from 2017 to 2019. Conclusion: Use of IMPT appears to be an acceptable option for the treatment of anal cancer in patients with a pelvic kidney.

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Saly, Danielle L., and Mark A. Perazella. "The adverse kidney effects of cancer immunotherapies." Journal of Onco-Nephrology 2, no. 2-3 (June 2018): 56–68. http://dx.doi.org/10.1177/2399369318808806.

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Cancer therapies are a common cause of acute and chronic kidney disease, which are increasingly being seen by nephrologists in clinical practice. Conventional chemotherapeutic drugs and novel targeted agents are effective cancer therapies but their use is complicated by nephrotoxicity. Cancer immunotherapies exploit various properties of immune cells to enhance immune-mediated tumor killing. Interferon and high-dose interleukin-2 are older immunotherapies first employed clinically in the 1980s and 1990s to treat a number of different cancers. While effective, these two therapies have well-known systemic toxicities, which include acute kidney disease. The emergence of the new cancer immunotherapies over the past decade brings more effective treatment options. The immune checkpoint inhibitors and chimeric antigen receptor T cells are exciting additions to the cancer treatment armamentarium. These agents effectively treat a several and a growing list of cancers that have otherwise failed other therapies. However, as with the conventional and targeted cancer agents, drug-induced acute and chronic kidney disease is an untoward effect of this group of drugs. We will undertake a case-based review: the newer immunotherapies followed by the older therapies, interferon and interleukin-2.

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Tichanek, Filip, Asta Försti, Akseli Hemminki, Otto Hemminki, and Kari Hemminki. "Survival in Kidney and Bladder Cancers in Four Nordic Countries through a Half Century." Cancers 15, no. 10 (May 16, 2023): 2782. http://dx.doi.org/10.3390/cancers15102782.

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Kidney and bladder cancers share etiology and relatively good recent survival, but long-term studies are rare. We analyzed survival for these cancers in Denmark, Finland, Norway (NO), and Sweden (SE) over a 50-year period (1971–2020). Relative 1- and 5-year survival data were obtained from the NORDCAN database, and we additionally calculated conditional 5/1-year survival. In 2016–2020, 5-year survivals for male kidney (79.0%) and bladder (81.6%) cancers were best in SE. For female kidney cancer, NO survival reached 80.0%, and for bladder cancer, SE survival reached 76.1%. The magnitude of 5-year survival improvements during the 50-year period in kidney cancer was over 40% units; for bladder cancer, the improvement was over 20% units. Survival in bladder cancer was worse for women than for men, particularly in year 1. In both cancers, deaths in the first year were approximately as many as in the subsequent 4 years. We could document an impressive development for kidney cancer with tripled male and doubled female 5-year survival in 50 years. Additionally, for bladder cancer, a steady improvement was recorded. The current challenges are to curb early mortality and target treatment to reduce long-term mortality.

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Billia, Michele, and Carlo Terrone. "Case Presentation: Kidney Cancer in Transplanted Kidney." European Urology Focus 2, no. 2 (June 2016): 221–22. http://dx.doi.org/10.1016/j.euf.2016.01.011.

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