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Mini Review - (2023) Volume 11, Issue 4

Renal Cell Cancer

Lockwood Jonathan*
1International Epidemiology Institute, USA
*Correspondence: Lockwood Jonathan, International Epidemiology Institute, USA, Email:

Received: 01-Jul-2023, Manuscript No. ipacr-23-13721; Editor assigned: 03-Jul-2023, Pre QC No. P-13721; Reviewed: 17-Jul-2023, QC No. Q-13721; Revised: 22-Jul-2023, Manuscript No. R-13721; Published: 28-Jul-2023


Malignant (cancer) cells are located in the lining of kidney tubules, which are incredibly tiny tubes. This condition is known as renal cell cancer, kidney cancer, or renal cell adenocarcinoma. On either side of the spine, above the waist, are two kidneys, one on each side. Blood is filtered and cleaned by tiny kidney tubules. Urine is created by removing waste. One lengthy tube called a ureter connects each kidney to the bladder, where the urine is excreted. Up until the urethra allows it to exit the body, the bladder stores the pee


Malignant cancer; Renal cell cancer; Kidney tubules


One of the three prevalent tumours of the urinary system, kidney cancer is believed to impact more than 400 000 individuals a year, with 40% of these patients dying from the disease. The clear cell renal cell carcinoma (ccRCC) is the type of cell that occurs most frequently in clinical settings. Even with this well-known disease kind, practitioners could have difficulty in selecting an appropriate course of action because they are only given the patient's clinical data and do not know their precise prognosis. In order to support clinical practise, efforts have also been undertaken to build a reliable prognostic model. Self-renewal and differentiation potentials, which are specialised cell capabilities of stem cells, are referred to as stemness. Intriguingly, it has been shown that cancer cells increasingly acquire stem cell-like characteristics as they advance, aiding in their expansion and metastasis. A new parameter deserving of note was created as a result of machine learning algorithm-assisted analyses of this dedifferentiated oncogenic state. This parameter is known as stemness indices, and it has been demonstrated that it can both identify the phenotype of cancer cells and correlate with the prognostics of various cancer types [1-5].

Renal cell carcinoma (RCC), which includes a variety of cancers, is the most prevalent pathological subtype of kidney cancer. 11 histologic forms of RCC, including clear cell, chromophobe, oncocytoma, and papillary of two kinds, were recognised by the World Health Organisation (WHO) in 2004. The most prevalent and dangerous form of RCC is clear cell renal cell carcinoma (ccRCC). Furthermore, a third of patients with ccRCC who have locally progressed or distant spread are classified as late-stage tumour patients, which has a very bad prognosis. Additionally, conventional therapies are ineffective since individuals with ccRCC are not responsive to both chemotherapy and radiotherapy, while immunotherapy, such as immune checkpoint inhibitors (ICIs), which target CTLA-4, PD-1/PD-L1, has been shown to be extremely effective. Genomic instability (GI), which arises from mutations in DNA repair genes and consequently encourages tumour development and metastasis as well as resistance to various treatments, is a notable hallmark of cancer. Evidence is mounting that links genetic instability to the clinical outcomes of individuals with different malignancies.

Non-coding RNAs (ncRNAs), sometimes known as RNA transcripts without the ability to code for proteins, including long non-coding RNAs (lncRNAs). The ncRNAs are classified as long ncRNAs (lncRNAs) if the cut-off value of the length is greater than 200 nucleotides; otherwise, they are found to be tiny ncRNAs. New research suggests that ncRNAs are essential for DNA repair and genomic integrity, which is vital for tumour cell survival and carcinogenesis prevention. According to Mathias et al., NORAD, a highly conserved lncRNA that is a crucial component of the topoisomerase complex NARC, is crucial for preserving genomic integrity. Additionally, NORAD is raised as a result of DNA damage, which causes chromosomal instability. By knocking off the lncRNA GUARDIN, which is closely associated to the p53 response, tumour development is inhibited and the cytotoxicity brought on by extra stress is increased. GUARDIN is crucial for preserving genomic integrity and may aid in the creation of tailored therapies. Despite the foregoing discoveries, the clinical importance and prognostic usefulness of lncRNAs associated to genomic instability remain unknown.

Around 2% of malignancies in the globe are renal cell cancers. North America and northern Europe have seen an increase in its prevalence, while other parts of the world have not. The greatest rates are now observed among black people in the United States, where the pace of rise has been roughly 3% every year. The 5-year relative survival rate increased from 30% to 40% in the 1960s to between 50% and 60% in the 1990s, indicating that survival has improved. Numerous epidemiologic research, in particular case-control studies, have looked for etiological hints. The development of renal cell carcinoma is a direct result of cigarette smoking. Obesity or having a high relative body weight has been cited in nearly every study as another important factor, particularly for women. Although the cause is uncertain, high blood pressure or its treatments may potentially be involved. It has been suggested that some occupational exposures, such as asbestos, coke oven emissions, petrol and solvents, increase the risk of certain diseases; however there is no solid evidence to support this claim or that of any other occupational hazard. One of the few consistently observed dietary findings is the inverse relationship between risk and intake of fruits and vegetables, which has been shown in a number of studies. It is doubtful that there is a connection between renal cell carcinoma and coffee, alcohol, or any other beverage. A considerable fraction of cases include genetic predisposition, perhaps through a variety of pathways. Future etiologic research should concentrate on the ways in which obesity raises risk, the impact of high blood pressure and its treatments, and the causes of the startlingly quick rise in incidence among Americans of African descent.

Although sporadic, 2% to 4% of RCCs are familial in origin. Hereditary papillary renal cancer (HPRCC), hereditary leiomyomatosis RCC, Birt-Hogg-Dube (BHD) syndrome, chromosome 3 translocation, and tuberous sclerosis (TCS1, TCS2) are among the genetic disorders linked to RCC. A dominantly inherited multisystemic condition called VHL syndrome causes tumours in a number of different organs, including the kidneys (sometimes multiple, bilateral tumours), pancreas, adrenal glands, epididymis, eyes, spine, and cerebellum. Renal cell carcinoma is the most prevalent cause of mortality and the cumulative chance of developing it by the age of 60 is greater than 70%. The VHL tumorsuppressor gene, which is located on chromosome 3p, is implicated in both spontaneous and hereditary RCC and is inactivated by a number of processes, including mutation and silencing by DNA methylation. Only the conventional (clear cell) cancer is caused by this gene. At least 50% of sporadic clear cells RCC are caused by somatic mutations in the VHL gene, while another 10% to 20% are caused by gene methylation. Increased production of angiogenetic factors such vascular endothelial growth factor is correlated with loss of VHL gene function. In vascularized tumours like RCC, overexpression of endothelial growth factor may favour development and progression. Through hypoxia-inducible factor (HIF), the VHL tumour suppressor protein (pVHL) also plays a significant part in the mammalian oxygen-sensing system. HIF causes the production of a number of genes that are involved in the control of angiogenesis, cell growth, or cell survival when pVHL is absent [6-10].


New sensitive imaging methods may have unintentionally discovered slow-growing, non-lethal tumours, increasing the likelihood of localised disease progression and contributing to the rising prevalence of RCC in most populations. However, the rising prevalence encompasses both smaller local tumours and more advanced tumours, which explains why certain nations still have high death rates. The recent levelling of RCC mortality in the United States and many European nations is probably due to the rising prevalence of early RCC diagnosis in many nations. Nevertheless, across all phases, about 50% of patients pass away within 5 years of their diagnosis. In high-risk nations, obesity and cigarette smoking may be responsible for 40% of all incidental cases. In addition to obesity, increased rates of hypertension might possibly be a factor. The risk of RCC may also be impacted by a number of additional lifestyle and occupational variables. According to a World Cancer Research Fund and American Institute for Cancer Research expert panel, there are a number of leads about dietary components, but no relationship has been regarded as causative. The disparity between populations may also be influenced by genetic differences. Better treatment options are required, as well as ongoing study into the aetiology of RCC. The ongoing investigation of environmental issues should consider RCC while looking for preventive measures.


  1. Weber KL, Randall RL, Grossman S, et al. Management of lower-extremity bone metastasis. J Bone Joint Surg Am. 2006; 88(4): 11-19.
  2. Indexed at, Google Scholar, Crossref

  3. Ruggieri P, Mavrogenis AF, Casadei R, et al. Protocol of surgical treatment of long bone pathological fractures. Injury. 2010; 41(6): 1161-1167.
  4. Indexed at, Google Scholar, Crossref

  5. Harrington KD, Sim F, Enis J, et al. Methylmethacrylate as an adjunct in internal fixation of pathological fractures. Experience with three hundred and seventy-five cases. J Bone Joint Surgery. 1976; 58(9): 1047-1055.
  6. Indexed at, Google Scholar

  7. Kumar S, Kashyap P. Antiproliferative activity and nitric oxide production of amrthanolic extract of Fraxicus micrantha on michigan cancer foundation-7 mammalian breast cancinoma cell line. J Intercult Ethnopharmacol. 2015; 4(8): 109-113.
  8. Indexed at, Google Scholar, Crossref

  9. Coleman RE, Lipton A, Roodman GD, et al. Metastasis and bone loss: advancing treatment and prevention. Cancer Treat Rev. 2010; 36(9): 615-620.
  10. Indexed at, Google Scholar, Crossref

  11. Adler RA, Gill RS. Clinical utility of denosumab for treatment of bone loss in men and women. Clin Interv Aging. 2011; 6(6): 119-124.
  12. Indexed at, Google Scholar, Crossref

  13. Kachnic LA, Pugh SL, Tai P, et al. RTOG 0518: Randomized Phase III Trial to Evaluate Zoledronic Acid for Prevention of Osteoporosis and Associated Fractures in Prostate Cancer Patients. Prostate Cancer Prostatic Dis. 2013; 16(2): 1-10.
  14. Indexed at, Google Scholar, Crossref

  15. Oboma YI, Susan BE, Elesha SO, et al. Breast cancer biomarkers at Niger delta University hospital: Comparisons with national and International trends and clinical significance. J Patphy. 2017; 903(7): 1-6.
  16. Indexed at, Google Scholar, Crossref

  17. Ruggieri P, Mavrogenis AF, Casadei R, et al. Protocol of surgical treatment of long bone pathological fractures. Injury. 2010; 41(6): 1161-1167.
  18. Indexed at, Google Scholar, Crossref

  19. Selvaggi G, Scagliotti GV. Management of bone metastases in cancer: a review. Critical reviews in oncol hematol. 2005; 56(8): 365-378.
  20. Indexed at, Google Scholar, Crossref