Journal articles on the topic 'Cancer tumer'
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Blaich, Günter, Hella Raade, and Manfred Metzler. "Modification of 7,8–benzoflavone metabolism in hamster liver and kidney microsomes by hepatic tumer inducing treatments." Carcinogenesis 11, no. 1 (1990): 95–101. http://dx.doi.org/10.1093/carcin/11.1.95.
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Parsons, Heather A., Timothy Blewett, Xiangying Chu, Sainetra Sridhar, Katheryn Santos, Kan Xiong, Vandana Abramson, et al. "Abstract PD11-06: PD11-06 Circulating tumor DNA association with residual cancer burden after neoadjuvant therapy in triple negative breast cancer in TBCRC 030." Cancer Research 83, no. 5_Supplement (March 1, 2023): PD11–06—PD11–06. http://dx.doi.org/10.1158/1538-7445.sabcs22-pd11-06.
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Abstract Background. Patients (pts) with early triple negative breast cancer (eTNBC) are at increased risk of breast cancer recurrence and death. Recent studies have focused on escalation of therapy, with current treatment standard of at least five drugs – and associated toxicities - for eTNBC. Though presence of residual disease after neoadjuvant therapy (NAT) as measured by residual cancer burden (RCB) helps guide addition of adjuvant treatment, more effective tools to tailor therapy are limited. Persistence of circulating tumor DNA (ctDNA) in the setting of residual disease is associated with high risk of distant recurrence. However, more sensitive minimal residual disease (MRD) assays are needed to potentially guide optimization of systemic therapy. Methods. TBCRC 030 is a phase II randomized study of 12 weeks of NAT single agent cisplatin or paclitaxel for stage II-III TNBC, followed by surgery. The primary objective of the parent study was to correlate baseline biomarker for homologous recombination deficiency and RCB by study arm. From this group, responders (RCB 0/1) and non-responders (RCB 2/3) from both study arms who did not receive additional NAT prior to surgery were selected for analysis from the study cohort, matched on baseline nodal status and tumor size. As a post hoc study amendment, available pts were followed for event free survival (EFS). Plasma samples were collected prior to treatment initiation (W0), at three weeks (W3), and at twelve weeks, prior to surgery (W12). Whole genome sequencing (WGS) was performed on primary tumor tissue to identify somatic mutations and design for each pt a tumor-informed, ctDNA assay tracking up to 1000 mutations to detect MRD. Detection limit was computed for each tested sample as previously described. For each sample assayed, we report tumor fraction (TFx) when MRD was detected and the detection limit at 90% power when MRD was not detected. Results. Of 139 study pts, 68 had complete tissue and plasma samples and no receipt of additional NAT. Of these, 22 were responders. These responders, and 22 matched non-responders were identified for analysis. Data from 22 pts – 11 responders, 11 non-responders - are described here; full analysis on all 44 pts will be presented at the meeting. Personalized ctDNA assays were designed targeting 434 to 1000 variants (median 1000) and applied to 66 plasma samples. At W0, 100% (22/22) were positive for ctDNA; 73% (16/22) and 55% (12/22) were positive at W3, and W12, respectively. In pts with T1-T2 tumors median TFx was 4.1e-3(7.8e-6, 3.4e-2) and 4.7e-1(4.3e-2, 9.0e-1) in pts with T3-T4 tumors. TFx decreased from W0 to W3 and from W0 to W12 in responders (Table 1). By W12, ctDNA had cleared in 7/8 pts with RCB 0, 1/3 with RCB 1, 2/8 with RCB 2, and 0/3 with RCB 3. Overall, ctDNA levels were broad with median TFx of 1.5e-3 (range 2.9e-6 to 0.90). Detection limit at 90% power for all tested samples was a median of 8.8e-6 (range 9.9e-7 to 6.8e-3). To investigate whether ctDNA persistence after NAT was associated with BC recurrence, we analyzed a separate group of all 8 pts with known recurrence and with complete data and samples. All pts had persistent ctDNA at W12 (median TFx 6.8e-3, [2.9e-6 to 6.6e-2]). Conclusions. After 3 weeks of NAT for eTNBC, ctDNA TFx decreased, with a 3900-fold change in responders and 18-fold change in non-responders. By W3, TFx for most pts with RCB 0/1 were below the 1 in 10,000 limit of detection for many currently available assays, emphasizing the need for sensitive tests to potentially guide therapy. Additional studies will determine if ctDNA-guided approaches in eTNBC can improve pt outcomes. Table 1: Tumer Fraction and Tumer Fraction Fold Change by Response to Neoadjuvant Therapy Citation Format: Heather A. Parsons, Timothy Blewett, Xiangying Chu, Sainetra Sridhar, Katheryn Santos, Kan Xiong, Vandana Abramson, Ashka Patel, Ju Cheng, Adam M. Brufsky, Justin Rhoades, Jeremy Force, Ruolin Liu, Tiffany A. Traina, Lisa Carey, Mothaffar Rimawi, Ahmed Elkhanany, Vered Stearns, Jennifer M. Specht, Harold Burstein, Antonio C. Wolff, Eric Winer, Nabihah Tayob, Ian Krop, Todd Golub, Erica L. Mayer, Viktor Adalsteinsson. PD11-06 Circulating tumor DNA association with residual cancer burden after neoadjuvant therapy in triple negative breast cancer in TBCRC 030 [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr PD11-06.
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Cho, Bong Jun, Hans H. Kim, David J. Lee, Eun Jung Choi, Yeo Hyun Hwang, Sun Ha Chun, and In Ah Kim. "MicroRNA-21 inhibitor potentiates anti-tumor effect of radiation therapy in vitro and in vivo." Tumor Microenvironment and Therapy 2, no. 1 (January 10, 2014): 1–13. http://dx.doi.org/10.2478/tumor-2014-0001.
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AbstractMicroRNA-21 (miR-21) plays important roles in carcinogenesis and is highly expressed in diverse human cancers. We evaluated the potential of targeting miRNA-21 to overcome the radioresistance of human cancer cells having an activated EGFR2-associated signaling and also aimed to elucidate the mechanisms of radiosensitization, and the effect on epithelial- mesenchymal transition (EMT). Ectopic overexpression of miR-21 up-regulated EGFR/HER2-associated signaling and increased radioresistance of a panel of human cancer cells (U251, U87, and A549 cells). In contrast, a specific inhibitor of miR-21 attenuated this signaling and radiosensitized a panel of human cancer cells. Inhibition of miR-21 was associated with persistent γH2AX foci formation. Inhibition of miR-21 decreased the typical features of EMT, such as invasion and migration and vascular tube formation. Treatment with anti-miR-21 decreased tumor burden in nude mice bearing intracranial U251 xenografts compared to controls. Combined treatment of anti-miR-21 and radiation further decreased tumor burden compared to each treatment alone. In summary, miR-21 is an important onco-miR, which confers radioresistance and diverse features of EMT. Inhibition of miR-21 could be a potential strategy for improving the efficacy of radiation therapy via unique modulation of pro-survival signaling implicated in radiation response and EMT.
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Lavekar, G. S. "Arbud-Tumor-Cancer- a concise integrative review." Journal of Clinical Oncology Reports 1, no. 1 (January 20, 2023): 01–05. http://dx.doi.org/10.58489/2836-5062/001.
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The Cancerous diseases will cause 10 million deaths in 2020 and may increase in coming years (1). Since ancient times Cancer-Arbud has been considered a mega disease and critical for treatment. A review is presenting the conception, description and treatment modalities as described in ayurveda, a short review is presented in this article.
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GARCÍA CEBRIÁN, MARÍA JOSÉ, MONIKA BAUDEN, ROLAND ANDERSSON, STEFAN HOLDENRIEDER, and DANIEL ANSARI. "Paradoxical Role of HMGB1 in Pancreatic Cancer: Tumor Suppressor or Tumor Promoter?" Anticancer Research 36, no. 9 (September 9, 2016): 4381–90. http://dx.doi.org/10.21873/anticanres.10981.
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SK, Deshmukh. "Immune Cells in the Tumor Microenvironment and Cancer Stem Cells: Interplay for Tumor Progression." Journal of Embryology & Stem Cell Research 2, no. 2 (2018): 1–2. http://dx.doi.org/10.23880/jes-16000109.
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Fejzić, Hanifa. "Tumor marker CA 15-3 in breast cancer patients." Acta Medica Academica 44, no. 1 (June 2, 2015): 39–46. http://dx.doi.org/10.5644/ama2006-124.125.
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Singh, Dr Ravi Pratap. "HLA A24 Associated Tumor Immunity in HER2/neu Positive Breast Cancer." Recent Advances in Pathology & Laboratory Medicine 3, no. 2 (August 21, 2017): 13–16. http://dx.doi.org/10.24321/2454.8642.201702.
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Li, Lin, Mengyuan Li, Zehang Jiang, and Xiaosheng Wang. "ARID1A Mutations Are Associated with Increased Immune Activity in Gastrointestinal Cancer." Cells 8, no. 7 (July 4, 2019): 678. http://dx.doi.org/10.3390/cells8070678.
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Because traditional treatment strategies for advanced gastrointestinal (GI) cancers often have a limited therapeutic effect, immunotherapy could be a viable approach for the therapy of advanced GI cancers, considering the recent success of immunotherapy in treating various refractory malignancies, including the DNA mismatch repair-deficient GI cancers. However, only a subset of cancer patients currently respond to immunotherapy. Thus, it is important to identify useful biomarkers for predicting cancer immunotherapy response. The tumor suppressor gene ARID1A has a high mutation rate in GI cancers and its deficiency is correlated with the microsatellite instability (MSI) genomic feature of cancer. We investigated the correlation between ARID1A mutations and tumor immunity using three GI cancer genomics datasets by the bioinformatic approach, and found that diverse antitumor immune signatures were more highly enriched in ARID1A-mutated GI cancers than in ARID1A-wildtype GI cancers. The elevated immune activity in ARID1A-mutated GI cancers was associated with the higher tumor mutation burden and lower tumor aneuploidy level, as well as a higher proportion of MSI cancers in this GI cancer subtype. Moreover, we found that ARID1A-mutated GI cancers more highly expressed PD-L1 than ARID1A-wildtype GI cancers. The elevated antitumor immune signatures and PD-L1 expression could contribute to the more active immunotherapeutic responsiveness and better survival prognosis in ARID1A-mutated GI cancers than in ARID1A-wildtype GI cancers in the immunotherapy setting, as evidenced in three cancer cohorts receiving immunotherapy. Thus, the ARID1A mutation could be a useful biomarker for identifying GI cancer patients responsive to immunotherapy.
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Nenciu, Adina-Elena, C. G. Nenciu, R. Fodoroiu, Florica Șandru, and M. C. Dumitrașcu. "TUMOR MARKERS IN OVARIAN CANCER." Journal of Surgical Sciences 7, no. 2 (September 1, 2020): 79–84. http://dx.doi.org/10.33695/jss.v7i2.356.
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Even if today’s society is rapidly evolving there is still much that can be done. This applies in theoncological field. One of the main female health problems worldwide is represented by thegynecological cancers. Ovarian cancer is the main cause of mortality among women withgynecological cancers. Although its prevalence is lover compared to breast, uterine or cervicalcancer, the mortality and morbidity rates are significantly higher. The first step in the managementof ovarian cancer is represented by regular screening and rapid diagnosis. One of the most importanttolls is represented by serological markers dosage in order to estimate the type of tumor before thegynecological specific intervention. There is a real need to identify correctly the ovarian cancer asearly as possible in order to obtain the favorable prognosis that comes with the diagnosis in earlystage. Most of the ovarian cancers (above 90%) are represented by carcinomas which are frequentlydiagnosed in advanced stages. The roles of the biomarkers are to indicate the malignancy of anovarian tumor and to predict the relapse risk. The aim of this paper is to update the indicationsregarding the usage of serological markers in ovarian cancers and the importance of using them forour patients.
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Kashyap, Poonam. "Ovarian tumor: a review." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 10, no. 9 (August 26, 2021): 3657. http://dx.doi.org/10.18203/2320-1770.ijrcog20213510.
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Ovarian cancers are the 7th most common cancers in women. It is found more commonly in elderly age group. The survival depends on the stage of diagnosis and many of the patients present in advanced disease when the prognosis becomes dismal. The dilemma is to differentiate them from benign disease so that the unwanted laparotomies could be saved. Biomarkers and radiological classification may play a role in differentiating benign from malignant and deciding on the management. There is no screening method to diagnose ovarian cancers and the patient presents with nonspecific complaints missing them in early stages. Optimal cytoreduction is required for better overall survival, progression free survival and response to adjuvant chemotherapy. Those women having history of breast, ovary, endometrial, colorectal cancers should be screened for malignancies and genetic testing is advised. Surgery is the mainstay of treatment followed by chemotherapy. Risk reducing salpingoophorectomy can be offered to women having BRCA1 and BRCA2 mutation carriers after they complete their family. The area of target therapies is the most recent and promising in treatment of ovarian cancer. They are coming in forefront when chemotherapy toxicity, drug resistance are big hurdles in treatment of ovarian cancer. With recent advances and understanding of the biology of ovarian cancer have led to clinical trials of targeted agents. The angiogenesis inhibitors and polyadenosine diphosphate-ribose polymerase (PARP) inhibitors are the most developed.
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Da Gama Duarte, Jessica, Luke T. Quigley, Anna Rachel Young, Masaru Hayashi, Mariko Miyazawa, Alex Lopata, Nunzio Mancuso, Mikio Mikami, Andreas Behren, and Els Meeusen. "Identification of Tumor Antigens in Ovarian Cancers Using Local and Circulating Tumor-Specific Antibodies." International Journal of Molecular Sciences 22, no. 20 (October 18, 2021): 11220. http://dx.doi.org/10.3390/ijms222011220.
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Ovarian cancers include several disease subtypes and patients often present with advanced metastatic disease and a poor prognosis. New biomarkers for early diagnosis and targeted therapy are, therefore, urgently required. This study uses antibodies produced locally in tumor-draining lymph nodes (ASC probes) of individual ovarian cancer patients to screen two separate protein microarray platforms and identify cognate tumor antigens. The resulting antigen profiles were unique for each individual cancer patient and were used to generate a 50-antigen custom microarray. Serum from a separate cohort of ovarian cancer patients encompassing four disease subtypes was screened on the custom array and we identified 28.8% of all ovarian cancers, with a higher sensitivity for mucinous (50.0%) and serous (40.0%) subtypes. Combining local and circulating antibodies with high-density protein microarrays can identify novel, patient-specific tumor-associated antigens that may have diagnostic, prognostic or therapeutic uses in ovarian cancer.
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Margul, Daniel, Camilla Yu, and Mariam M. AlHilli. "Tumor Immune Microenvironment in Gynecologic Cancers." Cancers 15, no. 15 (July 28, 2023): 3849. http://dx.doi.org/10.3390/cancers15153849.
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Gynecologic cancers have varying response rates to immunotherapy due to the heterogeneity of each cancer’s molecular biology and features of the tumor immune microenvironment (TIME). This article reviews key features of the TIME and its role in the pathophysiology and treatment of ovarian, endometrial, cervical, vulvar, and vaginal cancer. Knowledge of the role of the TIME in gynecologic cancers has been rapidly developing with a large body of preclinical studies demonstrating an intricate yet dichotomous role that the immune system plays in either supporting the growth of cancer or opposing it and facilitating effective treatment. Many targets and therapeutics have been identified including cytokines, antibodies, small molecules, vaccines, adoptive cell therapy, and bacterial-based therapies but most efforts in gynecologic cancers to utilize them have not been effective. However, with the development of immune checkpoint inhibitors, we have started to see the rapid and successful employment of therapeutics in cervical and endometrial cancer. There remain many challenges in utilizing the TIME, particularly in ovarian cancer, and further studies are needed to identify and validate efficacious therapeutics.
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Duval, Adrian, Cheryl Jeanneret, Tania Santoro, and Olivier Dormond. "mTOR and Tumor Cachexia." International Journal of Molecular Sciences 19, no. 8 (July 30, 2018): 2225. http://dx.doi.org/10.3390/ijms19082225.
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Cancer cachexia affects most patients with advanced forms of cancers. It is mainly characterized by weight loss, due to muscle and adipose mass depletion. As cachexia is associated with increased morbidity and mortality in cancer patients, identifying the underlying mechanisms leading to cachexia is essential in order to design novel therapeutic strategies. The mechanistic target of rapamycin (mTOR) is a major intracellular signalling intermediary that participates in cell growth by upregulating anabolic processes such as protein and lipid synthesis. Accordingly, emerging evidence suggests that mTOR and mTOR inhibitors influence cancer cachexia. Here, we review the role of mTOR in cellular processes involved in cancer cachexia and highlight the studies supporting the contribution of mTOR in cancer cachexia.
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Zhang, Chunfeng, Chenyu Hu, Kunqi Su, Kun Wang, Xiaojuan Du, Baocai Xing, and Xiaofeng Liu. "The Integrative Analysis of Thrombospondin Family Genes in Pan-Cancer Reveals that THBS2 Facilitates Gastrointestinal Cancer Metastasis." Journal of Oncology 2021 (November 10, 2021): 1–19. http://dx.doi.org/10.1155/2021/4405491.
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Recent cancer studies have found that the thrombospondin (THBS) family, including THBS1, THBS2, THBS3, THBS4, and THBS5, play vital roles in the development and progression of human cancers. However, their relationships with tumor stage, prognosis, and tumor immunity in pan-cancer have not been systematically reported. In the present study, we employed versatile public databases to assess the expression and mutations of different THBSs in pan-cancer and performed functional experiments to analyze the roles of THBS2 in gastrointestinal cancer metastasis. Our findings indicate that THBS genes are frequently mutated in various cancers and the dysregulation of THBS family members is associated with the progression of some cancers such as gastric cancer, colon cancer, and lung cancer. Further analyses indicate that THBS genes are associated with cancer hallmarks such as cell cycle and epithelial-mesenchymal transition (EMT). Importantly, thrombospondins, especially THBS1 and THBS2, are correlated with the immune cell infiltration level in gastrointestinal cancers. Our experiments further verified that THBS2 participates in tumor metastasis by enhancing EMT. Therefore, the overall analyses reveal that THBSs might offer us potential chances for tumor diagnosis and therapy.
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Shahriar, Mohammad Hasan, Mohammad Kamal, Tariqul Islam, Muhammad Rakibuz-Zaman, and Habibul Ahsan. "Tumor Burden in Bangladesh: A Pathology-Based Tumor Registry Overview." Journal of Global Oncology 3, no. 2_suppl (April 2017): 34s. http://dx.doi.org/10.1200/jgo.2017.009548.
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Abstract 15 Background: Cancer is a public health concern in both developed and developing countries. Appropriate prevention and surveillance of cancer deserves urgent attention as incidence of the disease is expected to double in the next 20 to 25 years in most developing nations. Given the dearth of basic cancer-related data in Bangladesh and feasibility considerations, Bangabandhu Sheikh Mujib Medical University, in collaboration with University of Chicago, has continued a pathology-based tumor registry in Bangladesh for the last 4 years (from 2012 to present) at Bangabandhu Sheikh Mujib Medical University. We undertook this work to assess the incidence and prevalence of major cancers in Bangladesh according to a histopathology-based cancer registry by establishing a functional network among pathologists working at different government and private sectors as well as to collect tissue and paraffin blocks from patients. Methods: Basic epidemiologic and socioeconomic data were obtained via questionnaire from all patients (N = 13,040 patients; collected from 2012 to 2014) who came to the department laboratory for diagnostic purposes. Histopathologic and/or cytopathologic data were obtained from the department database. Results: Middle-aged (30 to 50 years) adults are more vulnerable (62%) than other extreme age groups to the development of different tumors, including cancer. Women (61.11%) are more prone to develop tumors than men (39.89%). Low socioecomic status (86.73%) and poor education level (less than grade 5; 69.48%) have a key impact on the development of tumors in Bangladesh. In terms of occupation, housewife (49%) is the most vulnerable group compared with all others. Skin tumor (55.6%) is the most common benign tumor among men, and breast tumor (33.28%) among women. In the case of malignancy, uterine malignancy (23.38%) is the most common in women, and mouth and oral cavity cancer (11.7%) in men. The uterus (13.18%) is the most common tumor site, followed by breast (10.69%), among all cases. Conclusion: Although such an effort underestimates the true occurrence of cancers in this population, these data are valuable for formulating any plan or program for epidemiology, prevention, and treatment of cancers at the local and/or national level. AUTHORS' DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST No COIs from the authors.
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Akolkar, Dadasaheb, Darshana Patil, Raymond Page, Timothy Crook, Sewanti Limaye, Vineet Datta, Stefan Schuster, et al. "Circulating ensembles of tumor-associated cells in gastrointestinal cancers." Journal of Clinical Oncology 38, no. 4_suppl (February 1, 2020): 808. http://dx.doi.org/10.1200/jco.2020.38.4_suppl.808.
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808 Background: CEA and CA19-9 are non-specific markers for Gastrointestinal (GI) cancers. Molecular analysis of fecal blood is of limited utility in colorectal cancers. A non-invasive pan-GI-cancer blood-based test with high specificity and sensitivity is an unmet medical need. Considering that unprovoked thromboembolism is a significant risk in multiple cancers, we hypothesized that circulating thrombotic emboli in peripheral blood could comprise cancer cells and would serve as a reliable biomarker for detection of GI cancers. Methods: We obtained 15ml of blood from 7481 individuals, including 181 cases of Esophageal cancer, 125 cases of Gastric cancer, 448 cases of colorectal cancer and from 6727 asymptomatic individuals with age related elevated risk who underwent evaluation of serum CA19-9 and AFP. Peripheral blood mononuclear cells (PBMC) were isolated by centrifugation and further processes for negative enrichment and harvesting of circulating tumor cell clusters which were characterized by immunostaining. Circulating Ensembles of Tumor Associated Cells (C-ETACs) were defined as clusters of 3 or more cells which were positive for EpCAM and CK, irrespective of CD45 status. Results: C-ETACs were detected in 86.7% of esophageal cancers, 94.4% of gastric cancers and 91.3% of colorectal cancers respectively irrespective of extent (stage / metastatic status) of disease and prior treatments. Overall sensitivity among 754 cancer patients was 90.7%. Among the asymptomatic individuals, C-ETACs were detected in 31 / 366 (8.5%) individuals with elevated CEA and 10 / 152 (6.2%) individuals with elevated CA19-9. C-ETACs were detected in 160 / 5333 (2.9%) of the asymptomatic individuals who had no abnormal findings in any of the said markers. Conclusions: C-ETACs were ubiquitously detected in cancers of Oesophagus, Stomach and Colorectum regardless of stage and treatment status, and pose significant latent risk of thromboembolism and metastasis/recurrence. The relative undetectability of C-ETACs in the asymptomatic cohort indicates causative connection with malignancies and are suitable for screening for these cancers.
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Heit, John A., Tanya M. Petterson, Randolph S. Marks, Kent R. Bailey, and L. Joseph Melton. "The Risk of Venous Thromboembolism (VTE) among Cancer Patients by Tumor Site: A Population-Based Study." Blood 104, no. 11 (November 16, 2004): 2596. http://dx.doi.org/10.1182/blood.v104.11.2596.2596.
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Abstract Active cancer is an independent VTE risk factor (overall 6- to 9-fold increased risk) and accounts for almost 20% of all VTE in the community, but which cancer patients are at risk for VTE is largely unknown. Reportedly, VTE risk varies by tumor site, and cancer of the ovary, pancreas, colon, stomach, lung, prostate, and kidney convey particularly high VTE risk. Objective: To estimate VTE risk by tumor site. Methods: We enumerated observed cancers by tumor site for Olmsted County, MN active cancer patients with incident VTE over the seven-year period, 1991–1997 (n=152). We used 1991–1997 State Surveillance, Epidemiology, and End Results (SEER) data for Iowa to estimate the expected age-specific prevalence of cancer by tumor site in Olmsted County. VTE risk ratios (RR) for each tumor site were estimated by dividing the observed number of cancers by the expected number (calculated as the product of the SEER prevalence and the number of incident VTE cases in the age stratum). Results: For our population of 1991–1997 VTE cases, all tumor sites had RR > 5.0 (range 5.2 to 37.3, all p-values<0.05). Compared to published overall VTE odds ratios of 6–9 for active cancer compared to no cancer, the RR for some tumor sites were particularly increased. A Chi-squared test of heterogeneity of the RR across sites was highly significant (p-value<0.001). Three rare cancer sites - pancreatic cancer, lymphoma, and brain cancer - had unusually high RR (all RR>25). The high number of VTE cases with lymphoma was not due to catheter-related arm vein thrombosis. Liver, leukemia, other gastrointestinal (esophagus, small intestine, gallbladder, other biliary) and other gynecologic (primarily cervical) cancers had over twice the baseline risk (i.e., RR>17.0). On the other hand, the RR for many common cancers (breast, colorectal, ovary, lung, prostate) were essentially the same as the overall baseline risk (all had 9.5<RR<12.0). Conclusions: In contrast to previous reports, pancreas, lymphoma, brain, liver, leukemia, other gastrointestinal, and other gynecologic cancers have the highest VTE risk. Prior estimates of VTE risk by tumor site may have been biased by studies of prevalent cancers among patients hospitalized in tertiary care centers.
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Tsuneo, Ishida. "Highly Bactericidal Silver () against Bacteria and Anti-Cancer Activity of Ag+ ions for Regulation of Cancer/Tumor Cell Growth." Cancer Medicine Journal 1, no. 1 (August 31, 2018): 24–36. http://dx.doi.org/10.46619/cmj.2018.1-1004.
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Since highly bactericidal silver (I) ions against bacteria have been obtained, as highly accurate results, prospect effects of silver (I) ions for regulation of cancer and tumor cell growth can be expected to occur even at apoptotic conditions. This mini-review article is reported that as an availability for most highly bactericidal effect of Ag+ ions, the regulation of cancer cell growth may be able to be achieved by Ag+ ions-mediated hydrolyzing and degrading functions. Bactericidal effects of silver (I) ions on bacteriolyses of bacterial cell walls by activation of peptidoglycan (PGN) autolysins and silver ion-mediated cancer cell hydrolyzing and degrading activity by endolysins have been analyzed. Bacteriolysis against Staphylococcus aureus (S. aureus) PGN cell wall by Ag+ ions is caused by the inhibition of PGN elongation due to regulation of PGN synthetic transglycosylase (TG) and transpeptidase (TP), and the enhancement of activation of PGN autolysins of amidases. On the other hand, bacteriolysis and destruction against Escherichia coli (E. coli) cell wall by Ag+ ions are caused by the destruction of outer membrane structure due to degradative enzymes of lipoproteins at N- and Cterminals, and by the inhibition of PGN elongation owing to inactivation of PGN TP synthetic enzyme endopeptidase and enhancement of the activations of PGN hydrolases and autolysins of amidase, peptidase, and carboxypeptidase. Ag+ ions-mediated cancerous cell hydrolyzing enzyme that binds to and degrades intact cancer cells of the producing organism are classified as autolysins or endolysins (phage lysin), resulting that the hydrolase activity is an essential as regulator of cancer and tumor cell growth and hydrolase activation may be promoted the apoptosis and the necrosis of cancer cells, and subsequently lead to cancer cell death by this hydrolase. Thus, highly bactericidal Ag+ ions against bacteria and effect of Ag+ ions for cancer cell growth regulation or cell death can be able to realize at the same time. Silver ions induced ROS generations such as O2 - , H2O2,･OH, OH- producing in bacterial and tumorous cells occur and lead to oxidative stress. DNA damages may be due to linear coordinated Ag+ complex formations by Ag+ substitution within double and triple hydrogen bonds in DNA base pairs.
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Bošković, Bogdan. "Antibiotics that target mitochondria effectively eradicate cancer stem cells, across multiple tumor types: Treating cancer like an infectious disease." Acta Medica Academica 44, no. 1 (June 2, 2015): 85–86. http://dx.doi.org/10.5644/ama2006-124.134.
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Kazbarienė, Birutė. "Tumor and immunity." Medicina 45, no. 2 (February 10, 2009): 162. http://dx.doi.org/10.3390/medicina45020021.
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System of organism defense is an important complex of interrelated cellular, molecular, genetic, and other components, which regulate homeostasis of host. Experimental and clinical data show that immune system functions are significant, but also a complicated question in cancer development. It is very important to investigate and understood how immune system coordinates the response to cancer cells. Our understanding about innate and adaptive immunity functions and interaction with transformed cells is constantly changing. Different responses of these system components can promote, reduce, or inhibit tumor development. It is established that malignant cells develop into invasive cancer with interaction with tumor microenvironment, which is influenced by inflammation. Clinical and experimental studies have revealed the link between inflammation and cancer risk. Many cancers develop in the sites of inflammation. Activation of humoral and cellular immunity may predispose to neoplastic or cancer development. Despite the scientific progress, understanding of the immune system mechanisms responding to malignance remains insufficient.
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Cohen, Ivan J., and Ronald Blasberg. "Impact of the Tumor Microenvironment on Tumor-Infiltrating Lymphocytes: Focus on Breast Cancer." Breast Cancer: Basic and Clinical Research 11 (January 1, 2017): 117822341773156. http://dx.doi.org/10.1177/1178223417731565.
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Immunotherapy is revolutionizing cancer care across disciplines. The original success of immune checkpoint blockade in melanoma has already been translated to Food and Drug Administration–approved therapies in a number of other cancers, and a large number of clinical trials are underway in many other disease types, including breast cancer. Here, we review the basic requirements for a successful antitumor immune response, with a focus on the metabolic and physical barriers encountered by lymphocytes entering breast tumors. We also review recent clinical trials of immunotherapy in breast cancer and provide a number of interesting questions that will need to be answered for successful breast cancer immunotherapy.
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Gupta, Brinda, Sharon Wu, Sai-Hong Ignatius Ou, Sourat Darabi, Kathryn Finch Mileham, Nishant Gandhi, Benjamin Adam Weinberg, et al. "NRG1 fusions in solid tumors." Journal of Clinical Oncology 41, no. 16_suppl (June 1, 2023): 3132. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.3132.
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3132 Background: NRG1 fusions are rare but actionable genomic drivers that occur across a growing number of tumor types. NRG1 has an EGF-like domain that serves as a ligand for ErbB (HER3) receptors, thereby inducing heterodimerization, usually with HER2, and subsequent activation of relevant downstream signaling pathways. Agents targeting the HER2/HER3 pathway have shown early clinical promise in NRG1 fusion-positive cancers: currently zenocutuzumab has FDA Fast Track Designation for tumors harboring NRG1-fusions. Here, we update the incidence and characterization of NRG1 fusions across tumor types. Methods: Samples were submitted for clinical molecular profiling at Caris Life Sciences via Caris MI Tumor Seek (Phoenix, AZ). Gene fusion detection was performed on mRNA isolated from a formalin-fixed paraffin-embedded tumor sample using the Illumina NovaSeq platform (Illumina, Inc., San Diego, CA) and Agilent SureSelect Human All Exon V7 bait panel (Agilent Technologies, Santa Clara, CA). All NRG1 fusions with ≥ 3 junction reads were identified for manual review and for characterization of fusion class, intact functional domains, domain prediction, breakpoints, frame retention and co-occurring alterations by next-generation sequencing. Results: In an analysis of 169,273 tumor specimens, 261 unique tumors with an NRG1 fusion were identified for an overall incidence of 0.154% across tumors. NRG1 fusions were most frequently detected in NSCLC, breast cancer, ovarian cancer, pancreatic ductal adenocarcinoma, colorectal cancer, cholangiocarcinoma, prostate cancer, bladder and urothelial cancers, esophagogastric cancers and less commonly, prostate cancer, soft tissue sarcoma, anal cancer, salivary gland cancers, head and neck cancer, small intestine cancer, small cell lung cancer, endometrial cancer, thyroid cancer, neuroendocrine cancer, high grade glioma, and melanoma. The highest incidence was in breast cancer (0.301%), followed by cholangiocarcinoma (0.263%), NSCLC (0.232%), carcinoma of unknown primary (0.215%), pancreatic ductal adenocarcinoma (0.190%), ovarian cancer (0.174%), bladder cancer (0.148%), esophageal cancer (0.145%) and vulvar cancers (0.145%). There were 153 unique NRG1 fusion partners. The most common fusion partner was CD74 (12.37%), followed by SLC3A2 (8.13%), ATP1B1 (4.59%), and RBPMS (4.24%). Conclusions: NRG1 fusions are rare but actionable genomic events with significant heterogeneity of tumor type and fusion partner.
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Liou, Geou-Yarh. "Inflammatory Cytokine Signaling during Development of Pancreatic and Prostate Cancers." Journal of Immunology Research 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/7979637.
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Inflammation is essential for many diseases including cancer. Activation and recruitment of immune cells during inflammation result in a cytokine- and chemokine-enriched cell environment, which affects cancer development. Since each type of cancer has its unique tumor environment, effects of cytokines from different sources such as tumor-infiltrating immune cells, stromal cells, endothelial cells, and cancer cells on cancer development can be quite complex. In this review, how immune cells contribute to tumorigenesis of pancreatic and prostate cancers through their secreted cytokines is discussed. In addition, the cytokine signaling that tumor cells of pancreatic and prostate cancers utilize to benefit their own survival is delineated.
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Srinivasan, Ajay, Dadasaheb B. Akolkar, Pradip Fulmali, Pooja Fulmali, Navin Srivastava, Darshana Patil, Revati Patil, et al. "Circulating ensembles of tumor-associated cells in genitourinary cancers." Journal of Clinical Oncology 38, no. 6_suppl (February 20, 2020): 718. http://dx.doi.org/10.1200/jco.2020.38.6_suppl.718.
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718 Background: Detection of genitourinary cancers is based on histopathological analysis of tumor tissue obtained by invasive biopsies following manifestation of clinical or radiological symptoms. There is presently no non-invasive blood-based test with high specificity and sensitivity for detection of genitourinary cancers. Considering that unprovoked thromboembolism is a significant risk in multiple cancers, we hypothesized that tumor derived circulating emboli in peripheral blood could comprise cancer cells and would serve as a reliable biomarker for detection of genitourinary cancers. These Circulating Ensembles of Tumor Associated Cells (C-ETACs) are defined as clusters of 3 or more cells of tumorigenic origin (EpCAM+, CK+ and CD45±). Methods: We obtained 15ml of blood from 8828 individuals, including 103 cases of Renal cancer, 79 cases of bladder cancer, 153 cases of prostate cancers as well as from 8493 asymptomatic individuals with age related elevated risk and were negative in various screening investigations (CEA, AFP, CA19-9, CA125, PSA, LDCT, Mammography, PAP Smear). PBMC were isolated by centrifugation. C-ETACs were enriched, harvested and characterized by immunofluorescence staining for EpCAM, CK, CD45 as well as organ specific markers for renal, bladder and prostate cancers. Results: C-ETACs were detected in 87 (84.5%) of 103 renal cancers, 71 (89.9%) of 79 bladder cancers and 138 (90.2%) of 153 prostate cancers respectively irrespective of extent (stage / metastatic status) of disease and prior treatments. Overall sensitivity among 335 cancer patients was 88.4%. Among the 8493 asymptomatic individuals, C-ETACs were detected in 255 individuals (97% specificity). Conclusions: C-ETACs were ubiquitously detected in cancers of Kidney, Bladder and Prostate regardless of stage and treatment status, and pose significant latent risk of metastasis/recurrence. The relative undetectability of C-ETACs in the asymptomatic cohort indicates causative connection with malignancies and are hence suitable for screening for these cancers.
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Athar, M., and Raja Radhika Raman. "Correlating MRI and histological tumor thickness in the assessment of tongue cancer." Asian Pacific Journal of Health Sciences 7, no. 1 (March 30, 2020): 22–27. http://dx.doi.org/10.21276/apjhs.2020.7.1.5.
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Chen, Chaoran, Yueming Ding, Huiyang Liu, Mengyao Sun, Honggang Wang, and Dongdong Wu. "Flubendazole Plays an Important Anti-Tumor Role in Different Types of Cancers." International Journal of Molecular Sciences 23, no. 1 (January 4, 2022): 519. http://dx.doi.org/10.3390/ijms23010519.
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Flubendazole, belonging to benzimidazole, is a broad-spectrum insect repellent and has been repurposed as a promising anticancer drug. In recent years, many studies have shown that flubendazole plays an anti-tumor role in different types of cancers, including breast cancer, melanoma, prostate cancer, colorectal cancer, and lung cancer. Although the anti-tumor mechanism of flubendazole has been studied, it has not been fully understood. In this review, we summarized the recent studies regarding the anti-tumor effects of flubendazole in different types of cancers and analyzed the related mechanisms, in order to provide the theoretical reference for further studies in the future.
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Weidemann, Sören, Natalia Gorbokon, Maximilian Lennartz, Claudia Hube-Magg, Christoph Fraune, Christian Bernreuther, Till Clauditz, et al. "Abstract 3303: High homogeneity of mesothelin expressionin primary and metastatic ovarian cancer." Cancer Research 83, no. 7_Supplement (April 4, 2023): 3303. http://dx.doi.org/10.1158/1538-7445.am2023-3303.
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Abstract Background: Mesothelin is a glycosylphosphatidylinositol-anchored cell surface protein of widely unknown function that may play a role in tumor growth control. Because mesothelin is overexpressed in a variety of human cancer types including ovarian cancers, it represents an attractive target for novel therapies employing adaptive T-cell transfer in these tumors. However, tumor heterogeneity is a challenge for targeted therapies. Methods: To study the extent of heterogeneity of mesothelin overexpression in primary ovarian cancers and their peritoneal and lymph node metastases, a tissue microarray (TMA) was constructed from multiple sites of 220 ovarian cancers and analyzed by immunohistochemistry. One tissue core each was taken from up to 18 different tumor blocks per cancer, resulting in a total of 2,460 tissue spots from 423 tumor sites (188 primary cancers, 162 peritoneal carcinosis and 73 lymph node metastases). Results: Positive mesothelin expression was found in 2,041 of the 2,342 (87%) arrayed tissue spots and in 372 of the 392 (95%) tumor sites that were interpretable for mesothelin immunohistochemistry. Intratumoral heterogeneity was found in 23% of 168 primary cancer sites interpretable for mesothelin and decreased to 12% in 154 peritoneal carcinosis and to 6% in 71 lymph node metastases (p<0.0001). Heterogeneity between the primary tumor and matched peritoneal carcinosis was found in 16% of 102 cancers with interpretable mesothelin results. In these cancers, the mesothelin status switched from positive in the primary tumor to negative in the peritoneal carcinosis (3 cancers) in or vice versa (2 cancers), or a mixture of positive and negative peritoneal carcinoses was found (11 cancers). No such switch was seen between the mesothelin-interpretable primary tumors and their nodal metastases of 59 cancers, and only one mesothelin-positive tumor had a mixture of positive and negative lymph node metastases. Conclusions: Our data demonstrate that mesothelin expression is frequent and highly homogeneous in ovarian cancer and prompt for future anti-mesothelin therapy studies in this tumor type. Citation Format: Sören Weidemann, Natalia Gorbokon, Maximilian Lennartz, Claudia Hube-Magg, Christoph Fraune, Christian Bernreuther, Till Clauditz, Frank Jacobsen, Kristina Jansen, Barbara Schmalfeldt, Linn Wölber, Peter Paluchowski, Enikö Berkes, Uwe Heilenkötter, Guido Sauter, Ria Uhlig, Waldemar Wilczak, Stefan Steurer, Ronald Simon, Till Krech, Andreas Marx, Eike Burandt. High homogeneity of mesothelin expressionin primary and metastatic ovarian cancer [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 3303.
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Nadhan, Revathy, Srishti Kashyap, Ji Hee Ha, Muralidharan Jayaraman, Yong Sang Song, Ciro Isidoro, and Danny N. Dhanasekaran. "Targeting Oncometabolites in Peritoneal Cancers: Preclinical Insights and Therapeutic Strategies." Metabolites 13, no. 5 (April 30, 2023): 618. http://dx.doi.org/10.3390/metabo13050618.
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Peritoneal cancers present significant clinical challenges with poor prognosis. Understanding the role of cancer cell metabolism and cancer-promoting metabolites in peritoneal cancers can provide new insights into the mechanisms that drive tumor progression and can identify novel therapeutic targets and biomarkers for early detection, prognosis, and treatment response. Cancer cells dynamically reprogram their metabolism to facilitate tumor growth and overcome metabolic stress, with cancer-promoting metabolites such as kynurenines, lactate, and sphingosine-1-phosphate promoting cell proliferation, angiogenesis, and immune evasion. Targeting cancer-promoting metabolites could also lead to the development of effective combinatorial and adjuvant therapies involving metabolic inhibitors for the treatment of peritoneal cancers. With the observed metabolomic heterogeneity in cancer patients, defining peritoneal cancer metabolome and cancer-promoting metabolites holds great promise for improving outcomes for patients with peritoneal tumors and advancing the field of precision cancer medicine. This review provides an overview of the metabolic signatures of peritoneal cancer cells, explores the role of cancer-promoting metabolites as potential therapeutic targets, and discusses the implications for advancing precision cancer medicine in peritoneal cancers.
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Looi, Chin-King, Ling-Wei Hii, Siew Ching Ngai, Chee-Onn Leong, and Chun-Wai Mai. "The Role of Ras-Associated Protein 1 (Rap1) in Cancer: Bad Actor or Good Player?" Biomedicines 8, no. 9 (September 7, 2020): 334. http://dx.doi.org/10.3390/biomedicines8090334.
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Metastasis is known as the most life-threatening event in cancer patients. In principle, the immune system can prevent tumor development. However, dysfunctional T cells may fail to eliminate the tumor cells effectively and provide additional survival advantages for tumor proliferation and metastasis. Constitutive activation of Ras-associated protein1 (Rap1) has not only led to T cell anergy, but also inhibited autophagy and supported cancer progression through various oncogenic events. Inhibition of Rap1 activity with its negative regulator, Rap1GAP, impairs tumor progression. However, active Rap1 reduces tumor invasion in some cancers, indicating that the pleiotropic effects of Rap1 signaling in cancers could be cancer-specific. All in all, targeting Rap1 signaling and its regulators could potentially control carcinogenesis, metastasis, chemoresistance and immune evasion. Rap1GAP could be a promising therapeutic target in combating cancer.
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Holm, Johanna, Keith Humphreys, Jingmei Li, Alexander Ploner, Abbas Cheddad, Mikael Eriksson, Sven Törnberg, Per Hall, and Kamila Czene. "Risk Factors and Tumor Characteristics of Interval Cancers by Mammographic Density." Journal of Clinical Oncology 33, no. 9 (March 20, 2015): 1030–37. http://dx.doi.org/10.1200/jco.2014.58.9986.
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Purpose To compare tumor characteristics and risk factors of interval breast cancers and screen-detected breast cancers, taking mammographic density into account. Patients and Methods Women diagnosed with invasive breast cancer from 2001 to 2008 in Stockholm, Sweden, with data on tumor characteristics (n = 4,091), risk factors, and mammographic density (n = 1,957) were included. Logistic regression was used to compare interval breast cancers with screen-detected breast cancers, overall and by highest and lowest quartiles of percent mammographic density. Results Compared with screen-detected breast cancers, interval breast cancers in nondense breasts (≤ 20% mammographic density) were significantly more likely to exhibit lymph node involvement (odds ratio [OR], 3.55; 95% CI, 1.74 to 7.13) and to be estrogen receptor negative (OR, 4.05; 95% CI, 2.24 to 7.25), human epidermal growth factor receptor 2 positive (OR, 5.17; 95% CI, 1.64 to 17.01), progesterone receptor negative (OR, 2.63; 95% CI, 1.58 to 4.38), and triple negative (OR, 5.33; 95% CI, 1.21 to 22.46). In contrast, interval breast cancers in dense breasts (> 40.9% mammographic density) were less aggressive than interval breast cancers in nondense breasts (overall difference, P = .008) and were phenotypically more similar to screen-detected breast cancers. Risk factors differentially associated with interval breast cancer relative to screen-detected breast cancer after adjusting for age and mammographic density were family history of breast cancer (OR, 1.32; 95% CI, 1.02 to 1.70), current use of hormone replacement therapy (HRT; OR, 1.84; 95% CI, 1.38 to 2.44), and body mass index more than 25 kg/m2 (OR, 0.49; 95% CI, 0.29 to 0.82). Conclusion Interval breast cancers in women with low mammographic density have the most aggressive phenotype. The effect of HRT on interval breast cancer risk is not fully explained by mammographic density. Family history is associated with interval breast cancers, possibly indicating disparate genetic background of screen-detected breast cancers and interval breast cancers.
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Chen, Chao-Yi, Yi-Feng Yang, Paul C. Wang, Liang Shan, Stephen Lin, Po-Jung Chen, Yi-Jung Chen, et al. "Simvastatin Attenuated Tumor Growth in Different Pancreatic Tumor Animal Models." Pharmaceuticals 15, no. 11 (November 14, 2022): 1408. http://dx.doi.org/10.3390/ph15111408.
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Newly diagnosed pancreatic cancer increases year by year, while the prognosis of pancreatic cancer has not been very good. Statin drugs were found to have protective effects against a variety of cancers, but their association with pancreatic cancer remains to be clarified. This study used different pancreatic cancer cell lines and in different animal models to confirm the relationship between simvastatin and pancreatic cancer. Flow cytometry and luciferase-based bioluminescent images were used to investigate the cell cycle and tumor growth changes under simvastatin treatment. Simvastatin decreased the MIA PaCa-2 cells, PANC-1 cells, and BxPC-3 cell viability significantly and may arrest the cell cycle in the G0 phase. During in vivo study, subcutaneously implanted simvastatin pre-treated pancreatic cancer cells and intraperitoneally treated simvastatin continuously demonstrated a slower tumor growth rate and decreased the tumor/body weight ratio significantly. In intravenous implant models, implanted simvastatin-pre-treated BxPC-3 cells and cells treated along with simvastatin significantly decreased the tumor growth curve. Implanting the simvastatin-pre-treated pancreatic cells in the subcutaneous model showed better growth inhibition than the intravenous model. These results suggest simvastatin treatment may relate to different signaling pathways in local growth and metastasis. Pancreatic cancer cells presented different growth patterns in different animal-induced models, which could be important for clinical reference when it comes to the relationship of long-term statin use and pancreatic cancer.
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Li, Mengyuan, Zhixian Liu, and Xiaosheng Wang. "Exploration of the Combination of PLK1 Inhibition with Immunotherapy in Cancer Treatment." Journal of Oncology 2018 (December 2, 2018): 1–13. http://dx.doi.org/10.1155/2018/3979527.
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Background. PLK1 overexpression is oncogenic and is associated with poor prognosis in various cancers. However, the current PLK1 inhibitors have achieved limited clinical successes. On the other hand, although immunotherapies are demonstrating efficacy in treating many refractory cancers, a substantial number of patients do not respond to such therapies. The potential of combining PLK1 inhibition with immunotherapy for cancer treatment is worthy of exploration. Methods. We analyzed the associations of PLK1 expression with tumor immunity in 33 different cancer types. Moreover, we analyzed the associations of the drug sensitivities of PLK1 inhibitors with tumor immunity in cancer cell lines. Furthermore, we explored the mechanism underlying the significant associations between PLK1 and tumor immunity. Finally, we experimentally verified some findings from bioinformatics analysis. Results. The cancers with higher PLK1 expression levels tended to have lower immune activities, such as lower HLA expression and decreased B cells, NK cells and tumor-infiltrating lymphocytes infiltration. On the other side, elevated tumor immunity likely increased the sensitivity of cancer cells to PLK1 inhibitors. The main mechanism underlying the associations between PLK1 and tumor immunity may lie in the aberrant cell cycle and p53 pathways in cancers. Conclusions. Our findings implicate that the PLK1 inhibition and immunotherapy combination may achieve a synergistic antitumor efficacy.
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Pauletto, Eleonora, Nils Eickhoff, Nuno Padrão, Christine Blattner, and Wilbert Zwart. "TRIMming Down Hormone-Driven Cancers: The Biological Impact of TRIM Proteins on Tumor Development, Progression and Prognostication." Cells 10, no. 6 (June 16, 2021): 1517. http://dx.doi.org/10.3390/cells10061517.
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The tripartite motif (TRIM) protein family is attracting increasing interest in oncology. As a protein family based on structure rather than function, a plethora of biological activities are described for TRIM proteins, which are implicated in multiple diseases including cancer. With hormone-driven cancers being among the leading causes of cancer-related death, TRIM proteins have been described to portrait tumor suppressive or oncogenic activities in these tumor types. This review describes the biological impact of TRIM proteins in relation to hormone receptor biology, as well as hormone-independent mechanisms that contribute to tumor cell biology in prostate, breast, ovarian and endometrial cancer. Furthermore, we point out common functions of TRIM proteins throughout the group of hormone-driven cancers. An improved understanding of the biological impact of TRIM proteins in cancer may pave the way for improved prognostication and novel therapeutics, ultimately improving cancer care for patients with hormone-driven cancers.
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Malekghasemi, Somaiyeh, Jafar Majidi, Amir Baghbanzadeh, Jalal Abdolalizadeh, Behzad Baradaran, and Leili Aghebati-Maleki. "Tumor-Associated Macrophages: Protumoral Macrophages in Inflammatory Tumor Microenvironment." Advanced Pharmaceutical Bulletin 10, no. 4 (August 9, 2020): 556–65. http://dx.doi.org/10.34172/apb.2020.066.
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Tumor microenvironment consists of malignant and non-malignant cells. The interaction of these dynamic and different cells is responsible for tumor progression at different levels. The non-malignant cells in TME contain cells such as tumor-associated macrophages (TAMs), cancer associated fibroblasts, pericytes, adipocytes, T cells, B cells, myeloid-derived suppressor cells (MDSCs), tumor-associated neutrophils (TANs), dendritic cells (DCs) and Vascular endothelial cells. TAMs are abundant in most human and murine cancers and their presence are associated with poor prognosis. The major event in tumor microenvironment is macrophage polarization into tumor-suppressive M1 or tumor-promoting M2 types. Although much evidence suggests that TAMS are primarily M2-like macrophages, the mechanism responsible for polarization into M1 and M2 macrophages remain unclear. TAM contributes cancer cell motility, invasion, metastases and angiogenesis. The relationship between TAM and tumor cells lead to used them as a diagnostic marker, therapeutic target and prognosis of cancer. This review presents the origin, polarization, role of TAMs in inflammation, metastasis, immune evasion and angiogenesis as well as they can be used as therapeutic target in variety of cancer cells. It is obvious that additional substantial and preclinical research is needed to support the effectiveness and applicability of this new and promising strategy for cancer treatment.
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Shao, Ting, Xiling Jiang, Guochang Bao, Chunsheng Li, and Changgang Guo. "Comprehensive Analysis of the Oncogenic Role of Targeting Protein for Xklp2 (TPX2) in Human Malignancies." Disease Markers 2022 (October 18, 2022): 1–13. http://dx.doi.org/10.1155/2022/7571066.
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Mitosis and spindle assembly require the microtubule-associated protein Xenopus kinesin-like protein 2 (TPX2). Although TPX2 is highly expressed in several malignant tumor forms, little is known about its role in cancer. In this study, we performed the gene set enrichment analysis of TPX2 in 33 types of cancers and an extensive pan-cancer bioinformatic analysis using prognosis, tumor mutational burdens, microsatellite instability, tumor microenvironment, and immune cell infiltration data. According to the differential expression study, TPX2 was found to be overexpressed across all studied cancer types. Based on the survival analysis, increased TPX2 expression was associated with a poor prognosis for most cancers. The TPX2 expression level was confirmed to correlate with the clinical stage, microsatellite instability, and tumor mutational burden across all cancer types. Furthermore, TPX2 expression has been linked to tumor microenvironments and immune cell infiltration, particularly in bladder urothelial carcinoma, liver hepatocellular carcinoma, lung adenocarcinoma, stomach adenocarcinoma, and uterine corpus endometrial carcinoma. Finally, the gene set enrichment analysis implicated TPX2 in the regulation of aminoacyl tRNA biosynthesis, which is the most important tumor cell cycle signaling pathway. This comprehensive pan-cancer analysis shows that TPX2 is a prognostic molecular biomarker for most cancers and suggests its potential as an effective therapeutic target for the treatment of these diseases.
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Sun, Qingrong, Md Nazim Uddin, Mengyuan Li, Xiaosheng Wang, and Maode Lai. "Computational Identification of Tumor Suppressor Genes Based on Gene Expression Profiles in Normal and Cancerous Gastrointestinal Tissues." Journal of Oncology 2020 (July 22, 2020): 1–12. http://dx.doi.org/10.1155/2020/2503790.
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Cancer prevails in various gastrointestinal (GI) organs, such as esophagus, stomach, and colon. However, the small intestine has an extremely low cancer risk. It is interesting to investigate the molecular cues that could explain the significant difference in cancer incidence rates among different GI tissues. Using several large-scale normal and cancer tissue genomics datasets, we compared the gene expression profiling between small intestine and other GI tissues and between GI cancers and normal tissues. We identified 17 tumor suppressor genes (TSGs) which showed significantly higher expression levels in small intestine than in other GI tissues and significantly lower expression levels in GI cancers than in normal tissues. These TSGs were mainly involved in metabolism, immune, and cell growth signaling-associated pathways. Many TSGs had a positive expression correlation with survival prognosis in various cancers, confirming their tumor suppressive function. We demonstrated that the downregulation of many TSGs was associated with their hypermethylation in cancer. Moreover, we showed that the expression of many TSGs inversely correlated with tumor purity and positively correlated with antitumor immune response in various cancers, suggesting that these TSGs may exert their tumor suppressive function by promoting antitumor immunity. Furthermore, we identified a transcriptional regulatory network of the TSGs and their master transcriptional regulators (MTRs). Many of MTRs have been recognized as tumor suppressors, such as HNF4A, ZBTB7A, p53, and RUNX3. The TSGs could provide new molecular cues associated with tumorigenesis and tumor development and have potential clinical implications for cancer diagnosis, prognosis, and treatment.
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Wendel, Jillian, Xiyin Wang, and Shannon Hawkins. "The Endometriotic Tumor Microenvironment in Ovarian Cancer." Cancers 10, no. 8 (August 7, 2018): 261. http://dx.doi.org/10.3390/cancers10080261.
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Women with endometriosis are at increased risk of developing ovarian cancer, specifically ovarian endometrioid, low-grade serous, and clear-cell adenocarcinoma. An important clinical caveat to the association of endometriosis with ovarian cancer is the improved prognosis for women with endometriosis at time of ovarian cancer staging. Whether endometriosis-associated ovarian cancers develop from the molecular transformation of endometriosis or develop because of the endometriotic tumor microenvironment remain unknown. Additionally, how the presence of endometriosis improves prognosis is also undefined, but likely relies on the endometriotic microenvironment. The unique tumor microenvironment of endometriosis is composed of epithelial, stromal, and immune cells, which adapt to survive in hypoxic conditions with high levels of iron, estrogen, and inflammatory cytokines and chemokines. Understanding the unique molecular features of the endometriotic tumor microenvironment may lead to impactful precision therapies and/or modalities for prevention. A challenge to this important study is the rarity of well-characterized clinical samples and the limited model systems. In this review, we will describe the unique molecular features of endometriosis-associated ovarian cancers, the endometriotic tumor microenvironment, and available model systems for endometriosis-associated ovarian cancers. Continued research on these unique ovarian cancers may lead to improved prevention and treatment options.
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Kim, Nari, Yousun Ko, Youngbin Shin, Jisuk Park, Amy Junghyun Lee, Kyung Won Kim, and Junhee Pyo. "Comprehensive Analysis for Anti-Cancer Target-Indication Prioritization of Placental Growth Factor Inhibitor (PGF) by Use of Omics and Patient Survival Data." Biology 12, no. 7 (July 7, 2023): 970. http://dx.doi.org/10.3390/biology12070970.
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The expression of the placental growth factor (PGF) in cancer cells and the tumor microenvironment can contribute to the induction of angiogenesis, supporting cancer cell metabolism by ensuring an adequate blood supply. Angiogenesis is a key component of cancer metabolism as it facilitates the delivery of nutrients and oxygen to rapidly growing tumor cells. PGF is recognized as a novel target for anti-cancer treatment due to its ability to overcome resistance to existing angiogenesis inhibitors and its impact on the tumor microenvironment. We aimed to integrate bioinformatics evidence using various data sources and analytic tools for target-indication identification of the PGF target and prioritize the indication across various cancer types as an initial step of drug development. The data analysis included PGF gene function, molecular pathway, protein interaction, gene expression and mutation across cancer type, survival prognosis and tumor immune infiltration association with PGF. The overall evaluation was conducted given the totality of evidence, to target the PGF gene to treat the cancer where the PGF level was highly expressed in a certain tumor type with poor survival prognosis as well as possibly associated with poor tumor infiltration level. PGF showed a significant impact on overall survival in several cancers through univariate or multivariate survival analysis. The cancers considered as target diseases for PGF inhibitors, due to their potential effects on PGF, are adrenocortical carcinoma, kidney cancers, liver hepatocellular carcinoma, stomach adenocarcinoma, and uveal melanoma.
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Roik, Elena. "Abstract IA015: The Alaska Native Tumor Registry: Fifty years of cancer surveillance data for Alaska Native people." Cancer Epidemiology, Biomarkers & Prevention 32, no. 1_Supplement (January 1, 2023): IA015. http://dx.doi.org/10.1158/1538-7755.disp22-ia015.
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Abstract Background: Cancer is the leading cause of death among Alaska Native (AN) people. Indigenous people throughout the Circumpolar North experience different patterns of cancer incidence and mortality. The Alaska Native Tumor Registry (ANTR) was established for cancer surveillance among Alaska Native and American Indian (ANAI) people living in Alaska, with data available going back to 1969. Every 5 years, the ANTR releases a comprehensive report on cancer among AN people; latest study provides 50 years of cancer surveillance data. Methods: Cancer data were collected by the ANTR a population-based central cancer registry that records information on AN people. The ANTR has been collecting cancer information according to NCI SEER Program standards since 1969, and has been a full member of the SEER Program since 1999. Five-year annual-average age-adjusted incidence rates were calculated for time-periods ranging 1969–2018. AN data was compared with data for US whites (SEER 9). Mortality rates were calculated for 1994–2018 using data from the National Center for Health Statistics. Results: An estimated 144,274 Alaska Native/American Indian people resided in Alaska in 2015, comprising 19.5% of the Alaskan population. During 2014–2018, there were 2,401 cases of invasive cancer among AN people. The most commonly diagnosed cancers were colorectal (405 cases, 17% of all cancers), lung (373 cases, 16 cancers), and female breast (340 cases, 14% of all cancers). The majority of cancers (40%) were diagnosed at local stage, with 24% diagnosed at regional stage, and 30% at distant stage. However, the pattern varied by cancer site. Among colorectal cancers, just over one third were diagnosed at local and regional stages each, with one quarter diagnosed at distant stage. Over half of lung cancers were diagnosed at distant stage. Among the leading cancers, lung cancer mortality was 1.3 times higher among AN people, and colorectal cancer 2.8 times higher among AN people. Female breast cancer mortality rates were not significantly different between AN people and US White population. Conclusion: Lung cancer was the leading cause of cancer death, followed by colorectal and female breast cancers. These leading cancers are screenable, and preventable through lifestyle modifications. These data provide important information to support cancer prevention and control among AN people. Cancer surveillance has been a valuable tool throughout the Circumpolar North to support reducing the burden of cancer among Indigenous populations. Citation Format: Elena Roik. The Alaska Native Tumor Registry: Fifty years of cancer surveillance data for Alaska Native people [abstract]. In: Proceedings of the 15th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2022 Sep 16-19; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2022;31(1 Suppl):Abstract nr IA015.
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Shin, Eunah, and Ja Seung Koo. "Cell Component and Function of Tumor Microenvironment in Thyroid Cancer." International Journal of Molecular Sciences 23, no. 20 (October 20, 2022): 12578. http://dx.doi.org/10.3390/ijms232012578.
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Thyroid cancer is the most common cancer in the endocrine system. Most thyroid cancers have good prognosis, but some of them are resistant to treatment or show aggressive behavior. Like other tumors, thyroid cancers harbor tumor microenvironment (TME) composed of cancer associated fibroblasts (CAF) and immune cells. Autoimmune lymphocytic thyroiditis can occur in the thyroid, and it may be associated with cancer development. TME is involved in tumor progression through various mechanisms: (1) CAF is involved in tumor progression through cell proliferation and extracellular matrix (ECM) remodeling; and (2) immune cells are involved in tumor progression through cell proliferation, angiogenesis, epithelial mesenchymal transformation (EMT), and immune suppression. These events are activated by various cytokines, chemokines, and metabolites secreted from cells that comprise TME. This review is focused on how CAF and immune cells, two important cell components of thyroid cancer TME, are involved in tumor progression, and will explore their potential as therapeutic targets.
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Lucarini, Valeria, Daniela Nardozi, Valentina Angiolini, Monica Benvenuto, Chiara Focaccetti, Raffaele Carrano, Zein Mersini Besharat, Roberto Bei, and Laura Masuelli. "Tumor Microenvironment Remodeling in Gastrointestinal Cancer: Role of miRNAs as Biomarkers of Tumor Invasion." Biomedicines 11, no. 6 (June 19, 2023): 1761. http://dx.doi.org/10.3390/biomedicines11061761.
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Gastrointestinal (GI) cancers are the most frequent neoplasm, responsible for half of all cancer-related deaths. Metastasis is the leading cause of death from GI cancer; thus, studying the processes that regulate cancer cell migration is of paramount importance for the development of new therapeutic strategies. In this review, we summarize the mechanisms adopted by cancer cells to promote cell migration and the subsequent metastasis formation by highlighting the key role that tumor microenvironment components play in deregulating cellular pathways involved in these processes. We, therefore, provide an overview of the role of different microRNAs in promoting tumor metastasis and their role as potential biomarkers for the prognosis, monitoring, and diagnosis of GI cancer patients. Finally, we relate the possible use of nutraceuticals as a new strategy for targeting numerous microRNAs and different pathways involved in GI tumor invasiveness.
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Shirai, Katsuyuki, Akiko Nakagawa, Takanori Abe, Masahiro Kawahara, Jun-ichi Saitoh, Tatsuya Ohno, and Takashi Nakano. "Use of FDG-PET in Radiation Treatment Planning for Thoracic Cancers." International Journal of Molecular Imaging 2012 (May 14, 2012): 1–9. http://dx.doi.org/10.1155/2012/609545.
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Radiotherapy plays an important role in the treatment for thoracic cancers. Accurate diagnosis is essential to correctly perform curative radiotherapy. Tumor delineation is also important to prevent geographic misses in radiotherapy planning. Currently, planning is based on computed tomography (CT) imaging when radiation oncologists manually contour the tumor, and this practice often induces interobserver variability. F-18 fluorodeoxyglucose positron emission tomography (FDG-PET) has been reported to enable accurate staging and detect tumor extension in several thoracic cancers, such as lung cancer and esophageal cancer. FDG-PET imaging has many potential advantages in radiotherapy planning for these cancers, because it can add biological information to conventional anatomical images and decrease the inter-observer variability. FDG-PET improves radiotherapy volume and enables dose escalation without causing severe side effects, especially in lung cancer patients. The main advantage of FDG-PET for esophageal cancer patients is the detection of unrecognized lymph node or distal metastases. However, automatic delineation by FDG-PET is still controversial in these tumors, despite the initial expectations. We will review the role of FDG-PET in radiotherapy for thoracic cancers, including lung cancer and esophageal cancer.
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Zheng, Haosheng, Guojie Long, Yuzhen Zheng, Xingping Yang, Weijie Cai, Shiyun He, Xianyu Qin, and Hongying Liao. "Glycolysis-Related SLC2A1 Is a Potential Pan-Cancer Biomarker for Prognosis and Immunotherapy." Cancers 14, no. 21 (October 29, 2022): 5344. http://dx.doi.org/10.3390/cancers14215344.
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SLC2A1 plays a pivotal role in cancer glycometabolism. SLC2A1 has been proposed as a putative driver gene in various cancers. However, a pan-cancer analysis of SLC2A1 has not yet been performed. In this study, we explored the expression and prognosis of SLC2A1 in pan-cancer across multiple databases. We conducted genetic alteration, epigenetic, and functional enrichment analyses of SLC2A. We calculated the correlation between SLC2A1 and tumor microenvironment using the TCGA pan-cancer dataset. We observed high expression levels of SLC2A1 with poor prognosis in most cancers. The overall genetic alteration frequency of SLC2A1 was 1.8% in pan-cancer, and the SLC2A1 promoter was hypomethylation in several cancers. Most m6A-methylation-related genes positively correlated with the expression of SLC2A1 in 33 TCGA cancers. Moreover, SLC2A1 was mainly related to the functions including epithelial–mesenchymal transition, glycolysis, hypoxia, cell-cycle regulation, and DNA repair. Finally, SLC2A1 positively associated with neutrophils and cancer-associated fibroblasts in the tumor microenvironment of most cancers and significantly correlated with TMB and MSI in various cancers. Notably, SLC2A1 was remarkably positively correlated with PD-L1 and CTLA4 in most cancers. SLC2A1 might serve as an attractive pan-cancer biomarker for providing new insights into cancer therapeutics.
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Wang, Sheng-Fan, Kuo-Hung Huang, Wei-Chuan Tseng, Jeng-Fan Lo, Anna Fen-Yau Li, Wen-Liang Fang, Chian-Feng Chen, et al. "DNAJA3/Tid1 Is Required for Mitochondrial DNA Maintenance and Regulates Migration and Invasion of Human Gastric Cancer Cells." Cancers 12, no. 11 (November 20, 2020): 3463. http://dx.doi.org/10.3390/cancers12113463.
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Background: Gastric cancer is a common health issue. Deregulated cellular energetics is regarded as a cancer hallmark and mitochondrial dysfunction might contribute to cancer progression. Tid1, a mitochondrial co-chaperone, may play a role as a tumor suppressor in various cancers, but the role of Tid1 in gastric cancers remains under investigated. Methods: The clinical TCGA online database and immunohistochemical staining for Tid1 expression in tumor samples of gastric cancer patients were analyzed. Tid1 knockdown by siRNA was applied to investigate the role of Tid1 in gastric cancer cells. Results: Low Tid1 protein-expressing gastric cancer patients had a poorer prognosis and higher lymph node invasion than high Tid1-expressing patients. Knockdown of Tid1 did not increase cell proliferation, colony/tumor sphere formation, or chemotherapy resistance in gastric cancer cells. However, Tid1 knockdown increased cell migration and invasion. Moreover, Tid1 knockdown reduced the mtDNA copy number of gastric cancer cells. In addition, the Tid1-galectin-7-MMP-9 axis might be associated with Tid1 knockdown–induced cell migration and invasion of gastric cancer cells. Conclusions: Tid1 is required for mtDNA maintenance and regulates migration and invasion of gastric cancer cells. Tid1 deletion may be a poor prognostic factor in gastric cancers and could be further investigated for development of gastric cancer treatments.
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Kooshkaki, Omid, Afshin Derakhshani, Hossein Safarpour, Souzan Najafi, Parviz Vahedi, Oronzo Brunetti, Mitra Torabi, et al. "The Latest Findings of PD-1/PD-L1 Inhibitor Application in Gynecologic Cancers." International Journal of Molecular Sciences 21, no. 14 (July 16, 2020): 5034. http://dx.doi.org/10.3390/ijms21145034.
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Gynecologic cancers account for approximately 11% of the newly diagnosed cancers in women in the United States and for 18% globally. The presence of tumor-infiltrating lymphocytes (TILs) influences the clinical outcome of cancer patients and immune checkpoint inhibitors (ICIs), including anti programmed cell death protein-1 (anti-PD-1), anti-programmed death-ligand 1 (anti-PD-L1), and anticytotoxic T-lymphocyte antigen 4 (anti-CTLA-4), which have been approved for treating different types of malignancies. Antibodies targeting the PD-1/PD-L1 checkpoint have shown dynamic and durable tumor regressions, suggesting a rebalancing of the host–tumor interaction. There are several the US food and drug administration (FDA)-approved ICIs targeting PD-1, including pembrolizumab and nivolumab, as well as those targeting PD-L1, including avelumab, atezolizumab, and durvalumab for melanoma, renal cell cancer, colorectal cancer, head and neck cancer, cervix cancer, urothelial cancer, and lung cancer. Current pre-clinical and clinical studies assessing PD-1/PD-L1 inhibitors in several gynecologic cancers have reported significant antitumor activity. In this review, we investigate pre-clinical and clinical studies that describe the safety and efficacy of anti-PD-1/PD-L1 antibodies, with a particular focus on ongoing clinical trials, analyzing the oncological outcome and adverse effects of ICIs in gynecologic cancers.
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Choi, Jane Ru, Gül Kozalak, Ighli di Bari, Quratulain Babar, Zahra Niknam, Yousef Rasmi, and Kar Wey Yong. "In Vitro Human Cancer Models for Biomedical Applications." Cancers 14, no. 9 (May 3, 2022): 2284. http://dx.doi.org/10.3390/cancers14092284.
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Cancer is one of the leading causes of death worldwide, and its incidence is steadily increasing. Although years of research have been conducted on cancer treatment, clinical treatment options for cancers are still limited. Animal cancer models have been widely used for studies of cancer therapeutics, but these models have been associated with many concerns, including inaccuracy in the representation of human cancers, high cost and ethical issues. Therefore, in vitro human cancer models are being developed quickly to fulfill the increasing demand for more relevant models in order to get a better knowledge of human cancers and to find novel treatments. This review summarizes the development of in vitro human cancer models for biomedical applications. We first review the latest development in the field by detailing various types of in vitro human cancer models, including transwell-based models, tumor spheroids, microfluidic tumor-microvascular systems and scaffold-based models. The advantages and limitations of each model, as well as their biomedical applications, are summarized, including therapeutic development, assessment of tumor cell migration, metastasis and invasion and discovery of key cancer markers. Finally, the existing challenges and future perspectives are briefly discussed.
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Anderson, Kristin, Patricia Thompson, Betsy Wertheim, Lorena Martin, Ian K. Komenaka, Melissa Bondy, Adrian Daneri-Navarro, et al. "Family history and breast cancer subtype among women of Mexican descent." Journal of Clinical Oncology 32, no. 26_suppl (September 10, 2014): 41. http://dx.doi.org/10.1200/jco.2014.32.26_suppl.41.
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41 Background: A family history of breast cancer in a first-degree relative is associated with a 2-fold increase in breast cancer risk; however, breast cancer is a heterogeneous disease and there may be differences in risk profiles driven by tumor subtype or by racial/ethnic group. Methods: We assessed prevalence of familial breast cancer and its association with tumor subtype among 914 women with breast cancer of Mexican descent enrolled in the Ella Study, a case-only, binational (U.S.-Mexico) breast cancer study. Logistic regression was conducted to compare odds of triple negative breast cancers to non triple-negative breast cancers according to family history. Results: The prevalence of family history of breast cancer in a first- or second-degree relative was 24.1%, with 13.1% having an affected first-degree relative. Among participants who were diagnosed at age < 50, prevalence of family history of breast cancer in a first- or second-degree relative was 27.4%. After adjustment for age and country of residence, women with a first-degree relative with breast cancer were significantly more likely to be diagnosed with triple-negative breast cancers compared to non triple-negative breast cancers (OR = 1.98; 95% CI, 1.26-3.11). Similar results were seen for odds of triple-negative breast cancers compared to non-triple negative breast cancers for women with affected first- or second-degree relatives (OR=2.04; 95% CI, 1.40–2.98). The odds of triple-negative breast cancer compared to non-triple negative breast cancer was 1.93 (95% CI, 1.26–2.97) for women with first-degree relatives affected with breast or ovarian cancer. Conclusions: Findings suggest that familial cancers are most likely to be associated with triple negative subtype, supporting etiologic heterogeneity by tumor subtype in this population of Hispanic women. This association may be related to the prevalence of BRCA1 founder mutations in this population, which are strongly associated with triple-negative breast cancers. Identification of such differences in risk factors can help personalize screening and prevention approaches.
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Korbecki, Jan, Mateusz Bosiacki, Katarzyna Barczak, Ryta Łagocka, Dariusz Chlubek, and Irena Baranowska-Bosiacka. "The Clinical Significance and Role of CXCL1 Chemokine in Gastrointestinal Cancers." Cells 12, no. 10 (May 17, 2023): 1406. http://dx.doi.org/10.3390/cells12101406.
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One area of cancer research is the interaction between cancer cells and immune cells, in which chemokines play a vital role. Despite this, a comprehensive summary of the involvement of C-X-C motif ligand 1 (CXCL1) chemokine (also known as growth-regulated gene-α (GRO-α), melanoma growth-stimulatory activity (MGSA)) in cancer processes is lacking. To address this gap, this review provides a detailed analysis of CXCL1’s role in gastrointestinal cancers, including head and neck cancer, esophageal cancer, gastric cancer, liver cancer (hepatocellular carcinoma (HCC)), cholangiocarcinoma, pancreatic cancer (pancreatic ductal adenocarcinoma), and colorectal cancer (colon cancer and rectal cancer). This paper presents the impact of CXCL1 on various molecular cancer processes, such as cancer cell proliferation, migration, and invasion, lymph node metastasis, angiogenesis, recruitment to the tumor microenvironment, and its effect on immune system cells, such as tumor-associated neutrophils (TAN), regulatory T (Treg) cells, myeloid-derived suppressor cells (MDSCs), and macrophages. Furthermore, this review discusses the association of CXCL1 with clinical aspects of gastrointestinal cancers, including its correlation with tumor size, cancer grade, tumor–node–metastasis (TNM) stage, and patient prognosis. This paper concludes by exploring CXCL1’s potential as a therapeutic target in anticancer therapy.
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Meiliana, Anna, Nurrani Mustika Dewi, and Andi Wijaya. "Cancer Stem Cell Hypothesis: Implication for Cancer Prevention and Treatment." Indonesian Biomedical Journal 8, no. 1 (April 1, 2016): 21. http://dx.doi.org/10.18585/inabj.v8i1.190.
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BACKGROUND: Cancer is a disease of genomic instability, evasion of immune cells, and adaptation of the tumor cells to the changing environment. Genetic heterogeneity caused by tumors and tumor microenvironmental factors forms the basis of aggressive behavior of some cancer cell populations.CONTENT: Cancers arise in self-renewing cell populations and that the resulting cancers, like their normal organ counterparts, are composed of hierarchically organized cell populations. Self – renewing “cancer stem cells” (CSC) maintain tumor growth and generate the diverse populations constituting the tumor bulk. CSCs in multiple tumor types have been demonstrated to be relatively resistant to radiation and chemotherapy. The clinical relevance of these studies has been supported by neoadjuvant breast cancer trials that demonstrated increases in the proportions of CSCs after therapy. The CSC hypothesis has tremendously important clinical implications.SUMMARY: In summary, a large and accumulating body of evidence supports the CSC hypothesis, which has important implications for cancer prevention and therapy. The ultimate test of this hypothesis will require clinical trials demonstrating that targeting of these pathways reduces cancer incidence and improves outcomes for patients with cancer.KEYWORDS: Somatic mutation, tumor heterogeneity, metastasis, epithelial-mesenchymal transition, CSC niche