Pub Date : 2023-10-17eCollection Date: 2023-01-01DOI: 10.3389/or.2023.11429
Sarita Kumari
Cervical cancer remains a leading cause of cancer related morbidity and mortality in low/low-middle income countries. Lack of screening is the leading cause of cases being diagnosed in advanced stages and screening is still opportunistic in a majority of these countries. Hospital visits during pregnancy provides a window of opportunity to screen these susceptible women and reduce the burden of disease. Screening women during pregnancy is not practiced widely due to concerns of pregnancy loss, bleeding and a lack of clear information among patients as well as healthcare professionals.
{"title":"Screening for Cervical Cancer in Pregnancy.","authors":"Sarita Kumari","doi":"10.3389/or.2023.11429","DOIUrl":"https://doi.org/10.3389/or.2023.11429","url":null,"abstract":"<p><p>Cervical cancer remains a leading cause of cancer related morbidity and mortality in low/low-middle income countries. Lack of screening is the leading cause of cases being diagnosed in advanced stages and screening is still opportunistic in a majority of these countries. Hospital visits during pregnancy provides a window of opportunity to screen these susceptible women and reduce the burden of disease. Screening women during pregnancy is not practiced widely due to concerns of pregnancy loss, bleeding and a lack of clear information among patients as well as healthcare professionals.</p>","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"17 ","pages":"11429"},"PeriodicalIF":3.6,"publicationDate":"2023-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10616242/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71425619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-09-20eCollection Date: 2023-01-01DOI: 10.3389/or.2023.11471
John Nemunaitis, Laura Stanbery, Adam Walter, Rodney Rocconi, Philip Stephens
Therapeutic options for advanced-stage ovarian cancer patients are limited in those subjects with homologous recombination proficient molecular profiles. A recent review of the existing literature demonstrates evidence of enhanced relapse-free survival and overall survival associated with treatment with Vigil in the Phase 2b trial in the HRP population. Homologous recombination (HR) is a genetic rearrangement in which molecular information is exchanged between two similar molecules of double-stranded or single-stranded nucleic acids [1]. The purpose of HR is to maintain genome stability by performing high-fidelity repair of complex DNA damage such as DNA doublestrand breaks and interstrand crosslinks [2–4]. Homologous recombination is responsible for double-stranded DNA breaks and interstrand crosslink damage repair through the use of sister chromatids as a repair template. BRCA1/2 are critically important proteins in this pathway. HR deficiency (D) is the result of germline or somatic genetic alterations in HR genes (i.e., BRCA 1 or 2) [5]. Dysfunctional HR genes cause genome-wide errors and can lead to tumorigenesis [6, 7]. Tumors that are not HRD are considered HR proficient (P) and contain no functional genetic alterations in HR pathway genes, like BRCA1/2, resulting in faithful DNA repair, thereby reducing the mutation burden. While the HR pathway is responsible for repairing double-stranded breaks, the base excision repair pathway repairs single-stranded DNA breaks. Poly (ADP-ribose) polymerase proteins (PARPs) are essential proteins in this pathway. When PARPs are inhibited, single-stranded breaks are converted to double-stranded breaks during DNA replication. Synthetic lethality occurs in cells treated with a PARP inhibitor that have a BRCAmutation or are HRD. Alterations in HR pathway genes, especially mutations in BRCA1/2, can be germline and confer familial risk for breast, ovarian, prostate, and pancreatic cancer [8] or somatic. For patients who demonstrate negative germline testing, somatic HR molecular status is assessed by NGS and is most commonly evaluated by Myriad’s MyChoice CDx-testing. This involves the analysis of BRCA 1 and 2 gene mutation status, loss of heterozygosity (LOH), telomeric allelic imbalance (TAI), and largescale state transition score (LST) to determine a genomic instability score (GIS) [9]. Each is weighted and scored using a proprietary algorithm to determine the level of genomic instability. A GIS ≥42 in BRCA 1 or 2 negative patients defines HRD status. A GIS score <42 defines HRP status [10]. BRCA 1 or 2 mutations or HRDmolecular profile tumors are a sensitive ovarian cancer population to PARP inhibitor therapy [10–14] and are associated with a better prognosis in patients receiving platinumbased chemotherapy and/or bevacizumab [15]. However, ovarian cancer patients with HRP molecular status have a worse prognosis with standard-of-care therapy involving PARPIs, Edited by: Angela Cappello, University of Rome
{"title":"Rationale for the Use of Homologous Recombination Proficient Molecular Profile as a Biomarker for Therapeutic Targeting in Ovarian Cancer.","authors":"John Nemunaitis, Laura Stanbery, Adam Walter, Rodney Rocconi, Philip Stephens","doi":"10.3389/or.2023.11471","DOIUrl":"10.3389/or.2023.11471","url":null,"abstract":"Therapeutic options for advanced-stage ovarian cancer patients are limited in those subjects with homologous recombination proficient molecular profiles. A recent review of the existing literature demonstrates evidence of enhanced relapse-free survival and overall survival associated with treatment with Vigil in the Phase 2b trial in the HRP population. Homologous recombination (HR) is a genetic rearrangement in which molecular information is exchanged between two similar molecules of double-stranded or single-stranded nucleic acids [1]. The purpose of HR is to maintain genome stability by performing high-fidelity repair of complex DNA damage such as DNA doublestrand breaks and interstrand crosslinks [2–4]. Homologous recombination is responsible for double-stranded DNA breaks and interstrand crosslink damage repair through the use of sister chromatids as a repair template. BRCA1/2 are critically important proteins in this pathway. HR deficiency (D) is the result of germline or somatic genetic alterations in HR genes (i.e., BRCA 1 or 2) [5]. Dysfunctional HR genes cause genome-wide errors and can lead to tumorigenesis [6, 7]. Tumors that are not HRD are considered HR proficient (P) and contain no functional genetic alterations in HR pathway genes, like BRCA1/2, resulting in faithful DNA repair, thereby reducing the mutation burden. While the HR pathway is responsible for repairing double-stranded breaks, the base excision repair pathway repairs single-stranded DNA breaks. Poly (ADP-ribose) polymerase proteins (PARPs) are essential proteins in this pathway. When PARPs are inhibited, single-stranded breaks are converted to double-stranded breaks during DNA replication. Synthetic lethality occurs in cells treated with a PARP inhibitor that have a BRCAmutation or are HRD. Alterations in HR pathway genes, especially mutations in BRCA1/2, can be germline and confer familial risk for breast, ovarian, prostate, and pancreatic cancer [8] or somatic. For patients who demonstrate negative germline testing, somatic HR molecular status is assessed by NGS and is most commonly evaluated by Myriad’s MyChoice CDx-testing. This involves the analysis of BRCA 1 and 2 gene mutation status, loss of heterozygosity (LOH), telomeric allelic imbalance (TAI), and largescale state transition score (LST) to determine a genomic instability score (GIS) [9]. Each is weighted and scored using a proprietary algorithm to determine the level of genomic instability. A GIS ≥42 in BRCA 1 or 2 negative patients defines HRD status. A GIS score <42 defines HRP status [10]. BRCA 1 or 2 mutations or HRDmolecular profile tumors are a sensitive ovarian cancer population to PARP inhibitor therapy [10–14] and are associated with a better prognosis in patients receiving platinumbased chemotherapy and/or bevacizumab [15]. However, ovarian cancer patients with HRP molecular status have a worse prognosis with standard-of-care therapy involving PARPIs, Edited by: Angela Cappello, University of Rome","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"17 ","pages":"11471"},"PeriodicalIF":3.6,"publicationDate":"2023-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10547877/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41145596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-09-13eCollection Date: 2023-01-01DOI: 10.3389/or.2023.10676
Soňa Argalácsová, Michal Vočka, Otakar Čapoun, Lukáš Lambert
Between 25% and 33% of patients after radical prostatectomy experience a relapse of the disease. The risk of relapse increases in patients with risk factors up to 50%-80%. For a long time, adjuvant radiotherapy has been considered the standard of care. Four large prospective trials, that compared adjuvant and salvage radiotherapy in patients with biochemical relapse, showed the superiority of the adjuvant approach in biochemical and local relapse-free survival, but no consistent benefit in long-term endpoints (i.e., metastasis-free survival, overall survival, or carcinoma-specific survival) at the expense of increased urinary and bowel toxicity. Three large international studies comparing adjuvant and salvage radiotherapy paved the way toward early salvage radiotherapy. However, the optimal threshold of the PSA level (range of 0.2-0.5 ng/mL) for initiating early salvage radiotherapy remains unresolved and still poses a challenge in everyday clinical practice when balancing the need for early radiotherapy and the associated toxicity. Imprecise stratification of biochemical relaps patients according to the risk of clinical relapse drives efforts to find additional molecular biomarkers that would improve the timing of the salvage therapy.
{"title":"Timing of Early Salvage Therapy for Patients With Biochemical Relapse of Prostate Carcinoma.","authors":"Soňa Argalácsová, Michal Vočka, Otakar Čapoun, Lukáš Lambert","doi":"10.3389/or.2023.10676","DOIUrl":"https://doi.org/10.3389/or.2023.10676","url":null,"abstract":"<p><p>Between 25% and 33% of patients after radical prostatectomy experience a relapse of the disease. The risk of relapse increases in patients with risk factors up to 50%-80%. For a long time, adjuvant radiotherapy has been considered the standard of care. Four large prospective trials, that compared adjuvant and salvage radiotherapy in patients with biochemical relapse, showed the superiority of the adjuvant approach in biochemical and local relapse-free survival, but no consistent benefit in long-term endpoints (i.e., metastasis-free survival, overall survival, or carcinoma-specific survival) at the expense of increased urinary and bowel toxicity. Three large international studies comparing adjuvant and salvage radiotherapy paved the way toward early salvage radiotherapy. However, the optimal threshold of the PSA level (range of 0.2-0.5 ng/mL) for initiating early salvage radiotherapy remains unresolved and still poses a challenge in everyday clinical practice when balancing the need for early radiotherapy and the associated toxicity. Imprecise stratification of biochemical relaps patients according to the risk of clinical relapse drives efforts to find additional molecular biomarkers that would improve the timing of the salvage therapy.</p>","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"17 ","pages":"10676"},"PeriodicalIF":3.6,"publicationDate":"2023-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10522833/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41159608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Both cancer and metabolic disease have become the prevalent health risks in modern societies worldwide. Cancer is a complex set of illnesses with many definitions. About 15% of cancers are caused by infections, and 10% carry a hereditary burden. The remaining 70%–75% cancers are associated with a variety of processes, often associated with metabolic syndrome and chronic inflammation. This review examines the role of metabolic dysfunction and chronic inflammation in cancer development. I propose a novel concept of a switch, in which our intelligent body uses its sophisticated set of subsystems and sensors to pragmatically anticipate and combat metabolic dysfunction as its’ most direct and dire threat first, while temporarily accepting cancer as a state that in any other circumstances would be considered detrimental, and utilizing cancer as an additional tool to lower glucose levels. Once metabolic dysfunction has been resolved this switch is reversed, and cancer growth will be impaired.
{"title":"Cancer—A Pragmatic Switch to Combat Metabolic Syndrome?","authors":"John A. Claras","doi":"10.3389/or.2023.10573","DOIUrl":"https://doi.org/10.3389/or.2023.10573","url":null,"abstract":"Both cancer and metabolic disease have become the prevalent health risks in modern societies worldwide. Cancer is a complex set of illnesses with many definitions. About 15% of cancers are caused by infections, and 10% carry a hereditary burden. The remaining 70%–75% cancers are associated with a variety of processes, often associated with metabolic syndrome and chronic inflammation. This review examines the role of metabolic dysfunction and chronic inflammation in cancer development. I propose a novel concept of a switch, in which our intelligent body uses its sophisticated set of subsystems and sensors to pragmatically anticipate and combat metabolic dysfunction as its’ most direct and dire threat first, while temporarily accepting cancer as a state that in any other circumstances would be considered detrimental, and utilizing cancer as an additional tool to lower glucose levels. Once metabolic dysfunction has been resolved this switch is reversed, and cancer growth will be impaired.","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"17 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2023-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46295461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This work presents the history of the recognition of principal regulatory capacities of estrogen hormones having been mistakenly regarded as breast cancer promoting agents for more than 120 years. Comprehensive analysis of the results of clinical, epidemiological, immunological and molecular studies justified that endogenous estrogens are the principal regulators of embryonic development, survival and reproduction via orchestrating appropriate expression and even edition of all genes in mammalians. Medical use of chemically modified synthetic estrogens caused toxic complications; thromboembolic events and increased cancer risk in female organs as they proved to be endocrine disruptors deregulating estrogen receptors (ERs) rather than their activators. Synthetic estrogen treatment exhibits ambiguous correlations with cancer risk at different sites, which may be attributed to an inhibition of the unliganded activation of estrogen receptors (ERs) coupled with compensatory liganded activation. The principle of estrogen induced breast cancer led to the introduction of antiestrogen therapies against this tumor; inhibition of the liganded activation of estrogen receptors and aromatase enzyme activity. The initial enthusiasm turned into disappointment as the majority of breast cancers proved to be primarily resistant to antiestrogens. In addition, nearly all patients showing earlier good tumor responses to endocrine therapy, later experienced secondary resistance leading to metastatic disease and fatal outcome. Studying the molecular events in tumors responsive and unresponsive to antiestrogen therapy, it was illuminated that a complete inhibition of liganded ER activation stimulates the growth of cancers, while a successful compensatory upregulation of estrogen signal may achieve DNA restoration, tumor regression and patient's survival. Recognition of the principal role of endogenous estrogens in gene expression, gene edition and DNA repair, estrogen treatment and stimulation of ER expression in patients may bring about a great turn in medical practice.
{"title":"Rosetta Stone for Cancer Cure: Comparison of the Anticancer Capacity of Endogenous Estrogens, Synthetic Estrogens and Antiestrogens.","authors":"Zsuzsanna Suba","doi":"10.3389/or.2023.10708","DOIUrl":"https://doi.org/10.3389/or.2023.10708","url":null,"abstract":"<p><p>This work presents the history of the recognition of principal regulatory capacities of estrogen hormones having been mistakenly regarded as breast cancer promoting agents for more than 120 years. Comprehensive analysis of the results of clinical, epidemiological, immunological and molecular studies justified that endogenous estrogens are the principal regulators of embryonic development, survival and reproduction <i>via</i> orchestrating appropriate expression and even edition of all genes in mammalians. Medical use of chemically modified synthetic estrogens caused toxic complications; thromboembolic events and increased cancer risk in female organs as they proved to be endocrine disruptors deregulating estrogen receptors (ERs) rather than their activators. Synthetic estrogen treatment exhibits ambiguous correlations with cancer risk at different sites, which may be attributed to an inhibition of the unliganded activation of estrogen receptors (ERs) coupled with compensatory liganded activation. The principle of estrogen induced breast cancer led to the introduction of antiestrogen therapies against this tumor; inhibition of the liganded activation of estrogen receptors and aromatase enzyme activity. The initial enthusiasm turned into disappointment as the majority of breast cancers proved to be primarily resistant to antiestrogens. In addition, nearly all patients showing earlier good tumor responses to endocrine therapy, later experienced secondary resistance leading to metastatic disease and fatal outcome. Studying the molecular events in tumors responsive and unresponsive to antiestrogen therapy, it was illuminated that a complete inhibition of liganded ER activation stimulates the growth of cancers, while a successful compensatory upregulation of estrogen signal may achieve DNA restoration, tumor regression and patient's survival. Recognition of the principal role of endogenous estrogens in gene expression, gene edition and DNA repair, estrogen treatment and stimulation of ER expression in patients may bring about a great turn in medical practice.</p>","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"17 ","pages":"10708"},"PeriodicalIF":3.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10154579/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9432539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Carissa Ikka Pardamean, Digdo Sudigyo, Arif Budiarto, Bharuno Mahesworo, Alam Ahmad Hidayat, James W Baurley, Bens Pardamean
Once an infrequent disease in parts of Asia, the rate of colorectal cancer in recent decades appears to be steadily increasing. Colorectal cancer represents one of the most important causes of cancer mortality worldwide, including in many regions in Asia. Rapid changes in socioeconomic and lifestyle habits have been attributed to the notable increase in the incidence of colorectal cancers in many Asian countries. Through published data from the International Agency for Cancer Research (IARC), we utilized available continuous data to determine which Asian nations had a rise in colorectal cancer rates. We found that East and South East Asian countries had a significant rise in colorectal cancer rates. Subsequently, we summarized here the known genetics and environmental risk factors for colorectal cancer among populations in this region as well as approaches to screening and early detection that have been considered across various countries in the region.
{"title":"Changing Colorectal Cancer Trends in Asians: Epidemiology and Risk Factors.","authors":"Carissa Ikka Pardamean, Digdo Sudigyo, Arif Budiarto, Bharuno Mahesworo, Alam Ahmad Hidayat, James W Baurley, Bens Pardamean","doi":"10.3389/or.2023.10576","DOIUrl":"https://doi.org/10.3389/or.2023.10576","url":null,"abstract":"<p><p>Once an infrequent disease in parts of Asia, the rate of colorectal cancer in recent decades appears to be steadily increasing. Colorectal cancer represents one of the most important causes of cancer mortality worldwide, including in many regions in Asia. Rapid changes in socioeconomic and lifestyle habits have been attributed to the notable increase in the incidence of colorectal cancers in many Asian countries. Through published data from the International Agency for Cancer Research (IARC), we utilized available continuous data to determine which Asian nations had a rise in colorectal cancer rates. We found that East and South East Asian countries had a significant rise in colorectal cancer rates. Subsequently, we summarized here the known genetics and environmental risk factors for colorectal cancer among populations in this region as well as approaches to screening and early detection that have been considered across various countries in the region.</p>","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"17 ","pages":"10576"},"PeriodicalIF":3.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10241074/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9589920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In this review, we discuss the effectiveness of drug delivery system based on metal nanoparticles, and also, describe the problems associated with their delivery to tumor cells. Throughout recent years, more reports have appeared in the literature that demonstrate promising results for the treatment of various types of cancer using metal-based nanoparticles. Due to their unique physical and chemical properties, metal nanoparticles are effectively being used for the delivery of drug to the tumor cells, for cancer diagnosis and treatment. They can also be synthesized allowing the control of size and shape. However, the effectiveness of the metal nanoparticles for cancer treatment largely depends on their stability, biocompatibility, and ability to selectively affect tumor cells after their systemic or local administration. Another major problem associated with metal nanoparticles is their ability to overcome tumor tissue barriers such as atypical blood vessel structure, dense and rigid extracellular matrix, and high pressure of tumor interstitial fluid. The review also describes the design of tumor drug delivery systems that are based on metal nanoparticles. The mechanism of action of metal nanoparticles on cancer cells is also discussed. Considering the therapeutic safety and toxicity of metal nanoparticles, the prospects for their use for future clinical applications are being currently reviewed.
{"title":"Challenges and Opportunities Associated With Drug Delivery for the Treatment of Solid Tumors.","authors":"Teona Paresishvili, Zurab Kakabadze","doi":"10.3389/or.2023.10577","DOIUrl":"https://doi.org/10.3389/or.2023.10577","url":null,"abstract":"<p><p>In this review, we discuss the effectiveness of drug delivery system based on metal nanoparticles, and also, describe the problems associated with their delivery to tumor cells. Throughout recent years, more reports have appeared in the literature that demonstrate promising results for the treatment of various types of cancer using metal-based nanoparticles. Due to their unique physical and chemical properties, metal nanoparticles are effectively being used for the delivery of drug to the tumor cells, for cancer diagnosis and treatment. They can also be synthesized allowing the control of size and shape. However, the effectiveness of the metal nanoparticles for cancer treatment largely depends on their stability, biocompatibility, and ability to selectively affect tumor cells after their systemic or local administration. Another major problem associated with metal nanoparticles is their ability to overcome tumor tissue barriers such as atypical blood vessel structure, dense and rigid extracellular matrix, and high pressure of tumor interstitial fluid. The review also describes the design of tumor drug delivery systems that are based on metal nanoparticles. The mechanism of action of metal nanoparticles on cancer cells is also discussed. Considering the therapeutic safety and toxicity of metal nanoparticles, the prospects for their use for future clinical applications are being currently reviewed.</p>","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"17 ","pages":"10577"},"PeriodicalIF":3.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10497757/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10321420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-10-11eCollection Date: 2022-01-01DOI: 10.3389/or.2022.10654
Handoko, Melva Louisa, Tiara Bunga Mayang Permata, Soehartati A Gondhowiardjo
A great deal of progress has been made on understanding nasopharyngeal cancer in recent decades. Genomic, transcriptomic, and proteomic studies have enabled us to gain a deeper understanding on the biology of nasopharyngeal cancer, and though this new information is elaborate and detailed, an overall picture of the driver of nasopharyngeal cancer that includes all this information is lacking. This review will focus on providing a broad overview, with plausible and simple language, on nasopharyngeal carcinogenesis based on current updated information. This will help readers to gain a broad understanding, which may be necessary to provide common ground for further research on nasopharyngeal cancer.
{"title":"Deciphering Driver of Nasopharyngeal Cancer Development.","authors":"Handoko, Melva Louisa, Tiara Bunga Mayang Permata, Soehartati A Gondhowiardjo","doi":"10.3389/or.2022.10654","DOIUrl":"10.3389/or.2022.10654","url":null,"abstract":"<p><p>A great deal of progress has been made on understanding nasopharyngeal cancer in recent decades. Genomic, transcriptomic, and proteomic studies have enabled us to gain a deeper understanding on the biology of nasopharyngeal cancer, and though this new information is elaborate and detailed, an overall picture of the driver of nasopharyngeal cancer that includes all this information is lacking. This review will focus on providing a broad overview, with plausible and simple language, on nasopharyngeal carcinogenesis based on current updated information. This will help readers to gain a broad understanding, which may be necessary to provide common ground for further research on nasopharyngeal cancer.</p>","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"16 ","pages":"10654"},"PeriodicalIF":3.1,"publicationDate":"2022-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9756839/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10460150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-09-27eCollection Date: 2022-01-01DOI: 10.3389/or.2022.10605
Alexander A Tzanis, Christos Iavazzo, Alexandros Hadjivasilis, Hara Tsouvali, George Α Antoniou, Stavros A Antoniou
Objective: To investigate whether neoadjuvant chemotherapy (NACT) confers superior outcomes compared to primary debulking surgery (PDS) in patients with stage III and IV epithelial ovarian, tubal or peritoneal cancer as well as in patients with high tumour load. Methods: We searched the electronic databases PubMed, Cochrane Central Register of Controlled trials, and Scopus from inception to March 2021. We considered randomised controlled trials (RCTs) comparing NACT with PDS for women with epithelial ovarian cancer (EOC) stages III and IV. The primary outcomes were overall survival and progression-free survival. Secondary outcomes were optimal cytoreduction rates, peri-operative adverse events, and quality of life. Results: Six RCTs with a total of 1901 participants were included. Meta-analysis demonstrated similar overall survival (HR = 0.96, 95% CI [0.86-1.07]) and progression-free survival (HR = 0.98, 95% CI [0.89-1.08]) between NACT and PDS. Subgroup analyses did not demonstrate higher survival for stage IV patients (HR = 0.88, 95% CI [0.71-1.09]) nor for patients with metastatic lesions >5 cm (HR = 0.86, 95% CI [0.69-1.08]) treated with NACT, albeit with some uncertainty due to imprecision. Similarly, no survival benefit was observed in the subgroup of patients with metastatic lesions >10 cm (HR = 0.94, 95% CI [0.78-1.12]). NACT was associated with significantly higher rates of complete cytoreduction (RR = 2.34, 95% CI [1.48-3.71]). Severe peri-operative adverse events were less frequent in the NACT arm (RR = 0.34, 95% CI [0.16-0.72]. Conclusion: Patients with stage III and IV epithelial ovarian cancer undergoing NACT or PDS have similar overall survival. NACT is likely associated with higher rates of complete cytoreduction and lower risk of severe adverse events and peri-operative death.
{"title":"Neoadjuvant Chemotherapy Versus Primary Debulking Surgery in FIGO Stage III and IV Epithelial Ovarian, Tubal or Peritoneal Cancer: A Systematic Review and Meta-Analysis.","authors":"Alexander A Tzanis, Christos Iavazzo, Alexandros Hadjivasilis, Hara Tsouvali, George Α Antoniou, Stavros A Antoniou","doi":"10.3389/or.2022.10605","DOIUrl":"10.3389/or.2022.10605","url":null,"abstract":"<p><p><b>Objective:</b> To investigate whether neoadjuvant chemotherapy (NACT) confers superior outcomes compared to primary debulking surgery (PDS) in patients with stage III and IV epithelial ovarian, tubal or peritoneal cancer as well as in patients with high tumour load. <b>Methods:</b> We searched the electronic databases PubMed, Cochrane Central Register of Controlled trials, and Scopus from inception to March 2021. We considered randomised controlled trials (RCTs) comparing NACT with PDS for women with epithelial ovarian cancer (EOC) stages III and IV. The primary outcomes were overall survival and progression-free survival. Secondary outcomes were optimal cytoreduction rates, peri-operative adverse events, and quality of life. <b>Results:</b> Six RCTs with a total of 1901 participants were included. Meta-analysis demonstrated similar overall survival (HR = 0.96, 95% CI [0.86-1.07]) and progression-free survival (HR = 0.98, 95% CI [0.89-1.08]) between NACT and PDS. Subgroup analyses did not demonstrate higher survival for stage IV patients (HR = 0.88, 95% CI [0.71-1.09]) nor for patients with metastatic lesions >5 cm (HR = 0.86, 95% CI [0.69-1.08]) treated with NACT, albeit with some uncertainty due to imprecision. Similarly, no survival benefit was observed in the subgroup of patients with metastatic lesions >10 cm (HR = 0.94, 95% CI [0.78-1.12]). NACT was associated with significantly higher rates of complete cytoreduction (RR = 2.34, 95% CI [1.48-3.71]). Severe peri-operative adverse events were less frequent in the NACT arm (RR = 0.34, 95% CI [0.16-0.72]. <b>Conclusion:</b> Patients with stage III and IV epithelial ovarian cancer undergoing NACT or PDS have similar overall survival. NACT is likely associated with higher rates of complete cytoreduction and lower risk of severe adverse events and peri-operative death.</p>","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":"16 ","pages":"10605"},"PeriodicalIF":3.6,"publicationDate":"2022-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9756845/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10460152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Akhila Reddy, Camila Conde, Christopher Peterson, Kenneth M Nugent
Radon is an established human lung carcinogen naturally released as an odorless, colorless gas from soil and rocks. It is a major environmental source of ionizing radiation and can cause oxidative damage to DNA, increasing the risk of lung cancer. Although the association between radon and lung cancer is well established, the association between radon and other cancers is not. Based on reported studies, there is no consistent evidence indicating an association between radon and non-solid and solid cancers, but limited literature, heterogenous study design, and confounding variables preclude definitive conclusions. More research is needed to evaluate the association between residential radon and non-lung cancers, particularly with regard to skin cancer, central nervous system (CNS) cancer, renal, and stomach cancer, in which existing literature suggests potential associations with residential radon may exist. However, the literature largely demonstrates that lung cancer is the primary concern associated with residential radon exposure; the lack of association with nonlung cancers could reflect the lack of studies which have an adequate sample size, establish accurate levels of radon exposure, and control for confounders. These results should be considered in residential radon mitigation efforts which should focus on smokers with high radon exposures.
{"title":"Residential radon exposure and cancer","authors":"Akhila Reddy, Camila Conde, Christopher Peterson, Kenneth M Nugent","doi":"10.4081/oncol.2022.558","DOIUrl":"https://doi.org/10.4081/oncol.2022.558","url":null,"abstract":"Radon is an established human lung carcinogen naturally released as an odorless, colorless gas from soil and rocks. It is a major environmental source of ionizing radiation and can cause oxidative damage to DNA, increasing the risk of lung cancer. Although the association between radon and lung cancer is well established, the association between radon and other cancers is not. Based on reported studies, there is no consistent evidence indicating an association between radon and non-solid and solid cancers, but limited literature, heterogenous study design, and confounding variables preclude definitive conclusions. More research is needed to evaluate the association between residential radon and non-lung cancers, particularly with regard to skin cancer, central nervous system (CNS) cancer, renal, and stomach cancer, in which existing literature suggests potential associations with residential radon may exist. However, the literature largely demonstrates that lung cancer is the primary concern associated with residential radon exposure; the lack of association with nonlung cancers could reflect the lack of studies which have an adequate sample size, establish accurate levels of radon exposure, and control for confounders. These results should be considered in residential radon mitigation efforts which should focus on smokers with high radon exposures.","PeriodicalId":19487,"journal":{"name":"Oncology Reviews","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2022-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41459897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}