What Percent Of 68 Is 17 – 25 percent of 68 equals 17. It can be easily calculated by dividing 25 by 100 and multiplying the answer by 68 to get 17.
The easiest way to get this answer is to solve a simple percent math problem. You must find 25% of the 68 if they are sales or real life problems. Divide 25 by 100, multiply the answer by 68, and get 25% of 68 in seconds.
What Percent Of 68 Is 17
This article will explain the whole process of how to find any percentage value of any quantity or number in simple and easy steps.
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The percentage can be understood with a simple explanation. Take 68 and divide it into 100 equal parts. The number of 25 parts out of a total of 100 parts is called 25 percent, which is 17 in this example.
This percentage can be plotted on a pie chart for visualization. Let’s say the entire pie chart corresponds to a value of 68. Now we find 25 percent of 68, which is 17. The area occupied by the value of 17 will be 25 percent of the total value of 68. The rest of the region of the pie chart will be 75 percent of the total value of 68. 100% of 68 will cover the entire pie chart because 68 is the total value.
Any given number or amount can be expressed as a percentage to give a better understanding of the total amount. A percentage can be thought of as a quantity that divides any number into hundreds of equal parts for better representation and understanding of large numbers.
Percentage scaling or normalization is a very simple and convenient way of presenting numbers in relative sizes. Such designations are widely used in many industrial sectors where relative proportions are used.
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By Zhuo Huang 1, †, Ying Tang 2, †, Yuyan Wei 1, Jingyu Qian 1, Yifan Kang 1, Duohao Wang 1, Miao Xu 1, Ling Nie 1, Xueqin Chen 1, Ni Chen Zho 1, * and Qia, *
Received: 2023 January 31 / Revised: 2023 March 27 / Adopted: 2023 May 6 / Published 2023 May 9
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(This article is from the Special Issue Current Understanding of Heterogeneity in Prostate Cancer and Renal Cell Carcinoma)
Neuroendocrine differentiation (NED), characterized by the expression of neuroendocrine markers such as chromogranin A (CgA), is frequently observed in advanced prostate cancer (PCa), the prognostic significance of which is still controversial. Here, we specifically address the potential prognostic value of CgA expression in patients with late-stage PCa with distant metastases and its change over time from metastatic hormone-sensitive prostate cancer (mHSPC) to metastatic castration-resistant prostate cancer. (mCRPC). CgA expression was assessed immunohistochemically in mHSPC primary biopsies and mCPRC second biopsies in sixty-eight patients, and its correlation with prognosis (along with conventional clinicopathological parameters) was analyzed using the Kaplan-Meier method and risk modeling. Cox proportional. . We found that CgA expression was an independent adverse prognostic factor in both mHSPC (CgA positivity ≥ 1%, HR = 2.16, 95% CI: 1.04–4.26, p = 0.031) and mCRPC ( CgA ≥ 10%, HR = 20.19, % CI: 3.04-329.9, p = 0.008). CgA positivity generally increased from mHSPC to mCRPC and was a negative predictor. Assessment of CgA expression can help in the clinical evaluation of advanced patients with distant metastases.
Prostate cancer (PCa) is the second most common malignancy among men and the fifth leading cause of death worldwide [1]. Although the prevalence of PCa is much lower in Asia, it is also increasing rapidly in East and West Asia [2]. Most prostate cancers are adenocarcinomas, initially hormone-sensitive prostate cancers (HSPC) with expression of androgen receptor (AR) and prostate-specific antigen (PSA). Typical first-line androgen deprivation therapy (ADT) generally results in the development of castration-resistant prostate cancer (CRPC) [3]. Although potent AR pathway inhibitors (ARPIs) such as enzalutamide, abiraterone acetate, and apalutamide have therapeutic effects in CRPC, these tumors almost inevitably develop AR-independent pathways to support tumor growth after prolonged use of ARPIs [ Four. Five]. . Some CRPCs can develop into treatment-emergent neuroendocrine prostate cancer (t-NEPC), which is characterized by neuroendocrine carcinoma morphology, expression of neuroendocrine markers, loss of AR expression, and independence of AR signaling [ 6, 7]. In the latest WHO classification of prostate cancer, prostate t-NEPC was considered a single and independent type [6].
However, several prostate adenocarcinomas have also been observed to show variable expression of neuroendocrine markers (also known as neuroendocrine differentiation [NED]) and distant metastases at diagnosis. These patients are thought to have metastatic hormone-sensitive prostate cancer (mHSPC) with NED that is responsive to androgen deprivation therapy and may progress to metastatic castration-resistant prostate cancer (mCRPC). Although it is generally accepted that NED is associated with adverse outcomes [8, 9, 10], the prognosis of advanced prostate cancer in NED may differ from that in NEPC [7, 11].
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Therefore, further evaluation of the prognostic impact of NED in advanced prostate cancer, including mHSPC and mCRPC, is warranted. Among the various neuroendocrine markers used in different groups, chromogranin A (CgA) is the most specific compared to synaptophysin (Syn), CD56, and neuron-specific enolase (NSE). In this study, we specifically evaluated the prognostic value of CgA expression in initial biopsies obtained from 68 mHSPC patients at diagnosis and in second prostate biopsies obtained after these patients progressed to the mCRPC stage.
West China Hospital Cases 2009-2017. were collected and retrospectively reviewed, and sixty-eight patients were selected according to the following inclusion and exclusion criteria. Inclusion criteria required that patients (1) be diagnosed for the first time with metastatic acinic adenocarcinoma of the prostate on primary biopsy; (2) not having previously received diagnostic or therapeutic procedures for CaP; (3) received maximal androgen blockade therapy, including surgical or medical castration with ADT; (4) mCRPC was diagnosed according to the CRPC diagnostic guidelines of the European Association of Urologists [12]; and (5) received a second mCRPC prostate biopsy. Cases were excluded if (1) there was no residual tumor on the second biopsy, (2) the patient was treated before the first biopsy, or (3) the second biopsy showed features of t-NEPC. Each patient in this study was her own control. All data were collected in accordance with the guidelines of the Ethics Committee of the authors’ institution.
Prostate biopsies were performed using a standard ultrasound-guided transperineal prostate biopsy technique. The first and second parts of the biopsy were reviewed independently by two urologist pathologists. Differences in histology, Gleason score (GS), and CgA expression between the initial and second biopsy specimens from each patient were assessed.
Standard immunohistochemical staining for CgA (ZSGB-Bio, Beijing, China, ZA0507, 1:200 dilution) was performed with negative and positive controls. Unequivocally strong cytoplasmic staining was considered positive staining. The percentage of CgA expression was estimated based on the number of positively stained tumor cells relative to the total tumor cells in each needle biopsy sample, and the average percentage of CgA-positive cells in all samples was the final fraction. of CgA. Cases with CgA expression > 1% were reported based on our preliminary analysis and published studies [13, 14, 15]. Two experienced pathologists reviewed the slides independently.
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Data on clinical and pathological variables were summarized using descriptive statistics. Percentages of CgA expression in different GS and ISUP/WHO 2016 grade groups were compared using one-way ANOVA. Overall survival (OS) was defined as the time from HSPC to death (OS
They were analyzed using the Kaplan-Meier method with the log-rank test. The chi-square test was used to determine the baseline differences between cases with and without CgA expression in the first and second cases.
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