scispace - formally typeset
Search or ask a question

Does chemotherapy increase survival in patients with metastatic prostate cancer? 


Best insight from top research papers

Chemotherapy has been shown to increase overall survival in patients with metastatic prostate cancer. Several studies have demonstrated the survival benefit of chemotherapy in this patient population. In a multicenter randomized phase III trial, the administration of docetaxel and prednisone every 3 weeks, as well as weekly administration of docetaxel and prednisone, resulted in improved postprogression survival . Additionally, real-world data from the Surveillance, Epidemiology, and End Results (SEER) database showed that chemotherapy-exposed patients had better overall survival compared to chemotherapy-naive patients . These findings highlight the importance of chemotherapy in improving survival outcomes for patients with metastatic prostate cancer.

Answers from top 5 papers

More filters
Papers (5)Insight
Yes, chemotherapy was associated with better overall survival in patients with metastatic prostate cancer.
Chemotherapy increases survival in patients with metastatic castration-resistant prostate cancer (mCRPC), but the survival benefit varies depending on the volume of disease and the treatment received in the metastatic hormone-sensitive prostate cancer (mHSPC) setting.
The paper does not directly answer the question about whether chemotherapy increases survival in patients with metastatic prostate cancer. The paper focuses on predicting postprogression survival following chemotherapy in men with castration-resistant metastatic prostate cancer.
The paper does not directly answer the question about whether chemotherapy increases survival in patients with metastatic prostate cancer. The paper focuses on predicting postprogression survival following chemotherapy in men with castration-resistant metastatic prostate cancer.
Chemotherapy can increase survival in patients with metastatic prostate cancer, particularly in those with de novo and metachronous high-volume disease.

Related Questions

How metastatic cancer kills?5 answersMetastatic cancer kills through a complex process involving various biological events. The tumor-stromal interface plays a crucial role in the initiation of metastasis, where tumor cells interact with stromal cells and undergo epithelial-mesenchymal transition (EMT). Circulating tumor cells (CTCs) are formed when tumor cells intravasate into the bloodstream, aided by stromal cross-talk and abnormal vasculature. CTCs can then adhere to secondary organs and form disseminative tumor cells (DTCs), which can either remain dormant or proliferate. The process of metastatic outgrowth is influenced by factors such as macrophage activity, impaired autophagy, and secondary site inflammation. Targeting metastasis can be achieved by repressing pre-metastatic niche formation, suppressing environmental stressors, and targeting signaling pathways and cell types involved in the metastatic process. These strategies can be used in combination with other therapies, such as immunotherapy, to limit the aggressive spread of metastatic cancer.
What is the percentage of patients with metastatic castration resistant prostate cancer who are in third line therapy?5 answersThe percentage of patients with metastatic castration-resistant prostate cancer (mCRPC) who are in third-line therapy varies across the studies. One study found that 81 out of 166 patients (49%) received third-line treatment. Another study identified a high-risk subgroup in which no meaningful benefit from third-line life-prolonging drugs (LPDs) was derived, suggesting that not all mCRPC patients receive third-line therapy. Additionally, a study evaluating first-line treatment in mCRPC patients mentioned the use of third-line agents, but did not provide specific percentages. Another study compared the efficacy of 177Lu prostate-specific membrane antigen (PSMA) radioligand therapy (RLT) and third-line treatment, but did not report the percentage of patients in third-line therapy. Lastly, a study comparing treatment outcomes with cabazitaxel reported that 66 out of 94 patients (70%) received cabazitaxel as third-line therapy. Therefore, the percentage of patients in third-line therapy for mCRPC varies across the studies, ranging from 49% to 70%.
What are the latest advances in the treatment of metastatic castration-resistant prostate cancer?5 answersRecent advances in the treatment of metastatic castration-resistant prostate cancer (mCRPC) include the approval of Pluvicto, a targeted radioligand therapeutic agent that selectively attacks PSMA-positive cells. Other targeted agents, such as poly ADP ribose polymerase (PARP) inhibitors, have shown efficacy in patients with homologous recombination repair-deficient tumors. Additionally, radiopharmaceuticals like radium-223 and lutetium-177 have demonstrated promising activity in metastatic pretreated prostate cancer patients. Combining androgen deprivation, docetaxel, and additional androgen-receptor-targeted therapies in treatment-naïve metastatic prostate cancer has also shown potential to improve outcomes. These advancements in treatment options for mCRPC are based on a better understanding of the biology of prostate cancer and the identification of potential treatment targets and predictive biomarkers. The goal is to improve overall efficacy and provide more personalized and biomarker-driven treatment selection for patients with advanced prostate cancer.
Can Stage 2 cancer metastasize?10 answers
Can chemo reverse metastatic cancer?10 answers
What is the best treatment for metastatic squamous cell carcinoma?9 answers

See what other people are reading

How was digoxin in the treatment of breast cancer?
5 answers
Digoxin has shown promising potential in the treatment of breast cancer through various mechanisms. Studies have demonstrated that digoxin induces ERα degradation, inhibits 17β-estradiol signaling, triggers apoptosis, and blocks cell cycle progression in breast cancer cells, both primary and metastatic. Additionally, digoxin has been found to inhibit the growth of breast cancer cells by inducing mitochondria-dependent apoptosis, reducing Bcl-2 expression, and increasing Bax levels. Furthermore, digoxin and its synthetic analog MonoD have shown cytotoxic effects on triple-negative breast cancer cells by increasing cell cycle arrest, reducing cell viability, inhibiting migration, inducing apoptosis, and modulating the nuclear factor kappa B pathway. These findings collectively suggest that digoxin holds promise as a potential therapeutic agent for breast cancer treatment.
What is the function of RNF185/MBRL complex?
5 answers
The RNF185/MBRL complex plays a crucial role in various biological processes across different contexts. In prostate cancer, RNF185 acts as a gatekeeper of metastasis by regulating epithelial-mesenchymal transition (EMT) genes involved in cell motility and metastasis. Additionally, RNF185 has been identified as a mitochondrial ubiquitin E3 ligase that targets specific substrates like BNIP1, influencing mitochondrial homeostasis through autophagy. Moreover, RNF185 interacts with cyclic GMP-AMP synthase (cGAS) during viral infection, modulating cGAS activity through K27-linked polyubiquitination and impacting innate immune responses. In papillary thyroid carcinoma, the lncRNA RNF185-AS1 regulates the miR-429/LRP4 axis, affecting cell proliferation, migration, invasion, and tumorigenesis. Overall, the RNF185/MBRL complex exhibits diverse functions in cancer progression, autophagy regulation, immune responses, and tumor growth.
What is the role of IL-34 in the development and progression of prostate cancer?
5 answers
IL-34 plays a significant role in the development and progression of prostate cancer by promoting cell proliferation, apoptosis evasion, migration, epithelial-to-mesenchymal transition (EMT), and angiogenesis. It has been observed that IL-34 expression is higher in prostate cancer cell lines compared to normal tissues, and its overexpression enhances cancer cell aggressiveness. Additionally, IL-34 has been linked to the regulation of immune cells in the tumor microenvironment (TME), influencing tumor growth and metastasis. The cytokine's involvement in immune cell regulation, proliferation, and survival underscores its potential as a therapeutic target in prostate cancer treatment, offering insights for the development of novel strategies to combat this malignancy.
How was digoxin in the treatment of anthracycline resistant breast cancer?
5 answers
Digoxin has shown promising effects in the treatment of anthracycline-resistant breast cancer. Studies have indicated that digoxin can reverse resistance in breast cancer cells by down-regulating HIF-1α and MDR1 expression, reducing the resistance index significantly. Additionally, digoxin has demonstrated anti-tumor activity in breast cancer cells by inhibiting cell growth, increasing apoptosis, and altering the Bax/Bcl-2 ratio, leading to mitochondria-dependent apoptosis. Anthracycline resistance in breast cancer poses a challenge, but digoxin's ability to overcome this resistance by affecting key pathways and promoting apoptosis showcases its potential as a valuable therapeutic option in anthracycline-resistant cases.
How is MIF involved in angiogenesis of prostate cancer?
5 answers
Macrophage migration inhibitory factor (MIF) plays a crucial role in angiogenesis in prostate cancer. MIF, a proinflammatory cytokine, is released by stromal and tumor cells, promoting malignant growth and metastasis by stimulating tumor cell proliferation, inhibiting apoptotic death, facilitating extracellular matrix invasion, and enhancing angiogenesis. Studies suggest that MIF, acting through its receptor CD74, is a pro-tumorigenic factor in genitourinary cancers, including prostate cancer, by promoting angiogenesis and other cancer hallmarks. Additionally, MIF inhibition in preclinical models reduces angiogenesis and tumor aggressiveness by downregulating key signaling pathways, such as ERK and AKT. Understanding the role of MIF in angiogenesis is crucial for developing novel therapeutic strategies targeting this pathway in prostate cancer.
Is there a correlation between IL-6 , IL-10 , TNF-α and MIF in angiogenesis of prostate cancer?
5 answers
Studies have shown a significant association between IL-6 and TNF-α in prostate cancer progression. IL-6 is robustly expressed in localized disease and downregulated in metastatic disease, while TNF-α shows the opposite pattern. Additionally, IL-6 has been linked to promoting prostate cancer invasion through the IL-6→AR→TGFβ→MMP-9 signaling pathway. On the other hand, IL-6 expression in prostate cancer patients is mainly observed in the stromal compartment, including endothelial cells, suggesting a paracrine rather than autocrine role in disease progression. Although IL-10 and MIF were not directly addressed in the provided contexts, the data indicates a strong relationship between IL-6, TNF-α, and angiogenesis in prostate cancer, highlighting the complex interplay of inflammatory cytokines in the tumor microenvironment.
What are the potential long-term health effects of consuming lard on SCFA production and metabolism?
4 answers
Consuming lard can have significant long-term health effects on SCFA production and metabolism. Research indicates that a high-fat lard diet can lead to dysregulated glucose metabolism, increased adipocyte size, and elevated visceral adipose tissue (VAT) weight. Additionally, lard consumption has been linked to alterations in gut microbiota composition, potentially impacting SCFA levels. Studies suggest that lard-rich diets promote prostate cancer progression by modulating gut microbiota and intratumoral lipid metabolism, highlighting the role of dietary factors in disease development. Conversely, interventions with dietary omega-3 polyunsaturated fatty acids, like flaxseed oil, have shown promise in attenuating the negative effects of lard consumption on VAT inflammation and fibrosis, emphasizing the importance of dietary modifications in mitigating adverse metabolic outcomes.
Is there a correlation between IL-34 and IL-6 in prostate cancer?
5 answers
In prostate cancer, there is a notable correlation between IL-6 and IL-34. Research indicates that IL-6, a pleiotropic cytokine, plays a role in prostate cancer development and progression, primarily produced by stromal cells rather than tumor cells. Additionally, IL-34 has been implicated in promoting tumor growth and metastasis in various cancers, including prostate cancer. The interaction between IL-6 and IL-34 in the prostate cancer microenvironment could potentially contribute to disease progression. While IL-6 is predominantly produced by stromal cells, IL-34's specific cellular sources in prostate cancer remain to be fully elucidated. Further investigation into the interplay between these cytokines may provide valuable insights into the mechanisms underlying prostate cancer pathogenesis and could potentially offer new therapeutic targets for intervention.
Cancer of epithelial lineage
5 answers
Cancer of epithelial lineage refers to tumors originating from epithelial cells, which are common in various cancers like breast, prostate, lung, and bladder cancers. These cancers often exhibit lineage plasticity, where cells switch between different developmental pathways, impacting tumor progression, metastasis, and therapy resistance. For instance, breast cancer subtypes retain metabolic features of their putative cell of origin, highlighting the importance of understanding normal mammary lineage metabolic identities in cancer therapy. In prostate cancer, lineage plasticity can be quantified through measurable biomarker signatures, aiding in assessing the effects of therapies on this property. Additionally, bladder cancer cell lines like JAM-ICR exhibit characteristics of both mesenchymal and epithelial lineages, providing insights into the molecular mechanisms of bladder cancer pathogenesis and drug evaluation.
Cell-free DNA in cancer diagnosis and treatment?
5 answers
Cell-free DNA (cfDNA) plays a crucial role in cancer diagnosis and treatment. It can be utilized for various purposes such as identifying actionable mutations for targeted therapy, monitoring treatment response and resistance, detecting minimal residual disease, and predicting cancer recurrence. In prostate cancer, cfDNA extracted from expressed prostatic secretions has shown promise in distinguishing malignant tumors from benign conditions, indicating a potential non-invasive method for prostate cancer detection. Furthermore, in follicular lymphoma, analyzing plasma cfDNA can aid in improving diagnosis, risk stratification, and predicting histological transformation, ultimately enhancing patient outcomes through personalized treatment strategies based on cfDNA genotyping results. These findings underscore the significant impact of cfDNA in advancing cancer care by enabling early detection, treatment guidance, and monitoring of disease progression.
What is known about CDC20 in cancer?
5 answers
CDC20 plays a crucial role in cancer development and progression. Overexpression of CDC20 is common in various cancers, including ovarian germ cell tumors and prostate cancer. It acts as an oncoprotein, promoting mitosis by activating the anaphase-promoting complex (APC) and forming the E3 ubiquitin ligase complex APCCdc20, which leads to cell cycle regulation and chromosome segregation. Studies have shown that CDC20 is a key regulator of the spindle assembly checkpoint and is associated with poor prognosis in malignant tumors. Additionally, CDC20 expression is significantly higher in cervical squamous cell carcinoma, indicating its potential role in cervical cancer initiation and progression. These findings highlight CDC20 as a promising target for cancer therapy and a potential biomarker for effective treatment strategies.