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Male breast cancer (MBC) is uncommon, accounting for less than 1% of all breast cancers. Secondary breast cancers among childhood cancer survivors have been well described in the literature, but less is known about MBC.
Rare cancers collectively account for a significant proportion of the overall cancer burden in Japan. We aimed to describe and examine the incidence of each rare cancer and the temporal changes using the internationally agreed rare cancer classification. Cancer cases registered in regional population-based cancer registries from 2011 to 2015 and the National Cancer Registry (NCR) from 2016 to 2018 were classified into 18 families, 68 Tier-1 cancer groupings, and 216 single cancer entities based on the RARECAREnet list. Crude incidence rates and age-standardized incidence rates (ASR) were calculated for Tier-1 and Tier-2 cancers. The annual percent change and the 95% and 99% confidence limits for annual ASR for each of the 68 Tier-1 cancers were estimated using the log-linear regression of the weighted least squares method. The differences in ASRs between 2011 and 2018 were evaluated as an absolute change. A total of 5,640,879 cases were classified into Tier-1 and Tier-2 cancers. The ASRs of 18 out of 52 Tier-1 cancers in the rare cancer families increased, whereas the ASR for epithelial tumors of gallbladder decreased. The ASRs of 6 out of the 16 Tier-1 cancers in the common cancer families increased, whereas those of epithelial tumors of stomach and liver decreased. There was no significant change in the incidence of the other 40 Tier-1 cancers. The incidence of several cancers increased due to the dissemination of diagnostic concepts, improved diagnostic techniques, changes in coding practice, and the initiation of the NCR.
Background Cancer survival has improved for the most common cancers. However, less improvement and lower survival has been observed in some groups perhaps due to differential access to cancer care including prevention, screening, diagnosis, and treatment. Methods To further understand contemporary relative cancer survival (one- and five- year), we used survival data from CDC’s National Program of Cancer Registries (NPCR) for cancers diagnosed during 2007–2016. We examined overall relative cancer survival by sex, race and ethnicity, age, and county-level metropolitan and non-metropolitan status. Relative cancer survival by metropolitan and non-metropolitan status was further examined by sex, race and ethnicity, age, and cancer type. Results Among persons with cancer diagnosed during 2007–2016 the overall one-year and five-year relative survival was 80.6% and 67.4%, respectively. One-year relative survival for persons living in metropolitan counties was 81.1% and 77.8% among persons living in non-metropolitan counties. We found that persons who lived in non-metropolitan counties had lower survival than those who lived in metropolitan counties, and this difference persisted across sex, race and ethnicity, age, and most cancer types. Conclusion Further examination of the differences in cancer survival by cancer type or other characteristics might be helpful for identifying potential interventions, such as programs that target screening and early detection or strategies to improve access to high quality cancer treatment and follow-up care, that could improve long-term outcomes. Impact This analysis provided a high-level overview of contemporary cancer survival in the United States.
The collection and evaluation of family health history in a clinical setting presents an opportunity to discuss cancer risk, tailor cancer screening recommendations, and identify people with an increased risk of carrying a pathogenic variant who may benefit from referral to genetic counseling and testing. National recommendations for breast and colorectal cancer screening indicate that men and women who have a first-degree relative affected with these types of cancers may benefit from talking to a healthcare provider about starting screening at an earlier age and other options for cancer prevention. The prevalence of reporting a first-degree relative who had cancer was assessed among adult respondents of the 2015 National Health Interview Survey who had never had cancer themselves (n = 27,999). We found 35.6% of adults reported having at least one first-degree relative with cancer at any site. Significant differences in reporting a family history of cancer were observed by sex, age, race/ethnicity, educational attainment, and census region. Nearly 5% of women under age 50 and 2.5% of adults under age 50 had at least one first-degree relative with breast cancer or colorectal cancer, respectively. We estimated that 5.8% of women had a family history of breast or ovarian cancer that may indicate increased genetic risk. A third of U.S. adults who have never had cancer report a family history of cancer in a first-degree relative. Furthermore, this finding underscores the importance of using family history to inform discussions about cancer risk and screening options between healthcare providers and their patients.
Abstract Rare cancers are a group of approximately 200 malignancies with extremely low incidences and with a wide variety of genotypes and phenotypes. Collectively, they are more common than any single malignancy. However, given the small numbers of individuals diagnosed with rare cancers, it is difficult to design clinical trials with sufficient patient numbers. Therefore, few effective anticancer drugs have been developed, and evidence‐based medicine is not always feasible for rare cancers. Consequently, their clinical outcomes are generally poorer. Cancer research requires adequate models that faithfully recapitulate molecular features and reproduce treatment responses of the original tumors. Such models allow us to focus on more efficacious drugs in the clinical studies. For rare cancers, patient‐derived cancer models are particularly important because the enrollment of sufficient patients is rarely attainable within a reasonable period of time. However, extremely few models are available for rare cancers. For example, cell lines and xenografts are available for only a limited number of histological subtypes of sarcomas; therefore, most sarcoma research is performed without such models, and a lack of adequate cancer models causes a lag in therapeutic development. The establishment of novel rare cancer models will dramatically facilitate rare cancer research and treatment development in the near future. This review focuses on the status of patient‐derived rare cancer models and discusses their pivotal problems and possibilities, using sarcomas as a representative rare cancer type. Multi‐institutional collaboration will help address the scarcity of patient‐derived rare cancer models.
Highlights: • LncRNA TP73-AS1 is identified with downregulation in bladder cancer tissues and cell lines. • Patients with low TP73-AS1 have shorter overall survival and progression-free survival. • Overexpression of TP73-AS1 can inhibit cell growth, migration, and invasion in vitro study. • Overexpression of TP73-AS1 inhibits metastasis of bladder cancer cell through inactivating EMT pathway. • We firstly reported the tumor suppressor function of TP73-AS1 in bladder cancer. Long noncoding RNAs (lncRNAs) have been identified to have more and more important roles in tumorigenesis and may be novel biomarker for cancer therapy. LncRNA TP73-AS1 is a novel identified lncRNA that has been demonstrated to be increased in several cancers, however, its function in bladder cancer remains unknown. The aim of this work was to examine the expression and role of lncRNA TP73-AS1 in bladder cancer. The expression levels of lncRNA TP73-AS1 in bladder cancer tissues and cell lines were determined by quantitative real-time PCR (qRT-PCR), and its clinical significance was assessed by statistical analysis. Moreover, by gain-of-function assay, the effect of TP73-AS1 on proliferation, cell cycle, apoptosis, migration and invasion was examined in bladder cancer cells. We identified that the expression level of TP73-AS1 was significantly down-regulated in bladder cancer tissues and cells compared to adjacent non-tumor tissues. Kaplan-Meier survival analysis found that patients with low TP73-AS1 expression level had shorter overall survival and progression-free survival than those with high TP73-AS1 expression. Moreover, we showed that overexpression of TP73-AS1 could inhibit cell growth, arrest cell cycle, reduce cell migration and invasion, and promote cell apotosis in vitro study. In addition, overexpression of TP73-AS1 diminished epithelial-mesenchymal transition (EMT) through inhibiting the expression of vimentin, snail, MMP-2, and MMP-9 and upregulating the expression levels of E-cadherin. Collectively, our findings for the first time elucidated that lncRNA TP73-AS1 may serve as a tumor suppressor participated in bladder cancer progression, which provided a promising therapy strategy for patients with bladder cancer.
BackgroundCancer is a complex, multiscale dynamical system, with interactions between tumor cells and non-cancerous host systems. Therapies act on this combined cancer-host system, sometimes with unexpected results. Systematic investigation of mechanistic computational models can augment traditional laboratory and clinical studies, helping identify the factors driving a treatment's success or failure. However, given the uncertainties regarding the underlying biology, these multiscale computational models can take many potential forms, in addition to encompassing high-dimensional parameter spaces. Therefore, the exploration of these models is computationally challenging. We propose that integrating two existing technologiesone to aid the construction of multiscale agent-based models, the other developed to enhance model exploration and optimizationcan provide a computational means for high-throughput hypothesis testing, and eventually, optimization.ResultsIn this paper, we introduce a high throughput computing (HTC) framework that integrates a mechanistic 3-D multicellular simulator (PhysiCell) with an extreme-scale model exploration platform (EMEWS) to investigate high-dimensional parameter spaces. We show early results in applying PhysiCell-EMEWS to 3-D cancer immunotherapy and show insights on therapeutic failure. We describe a generalized PhysiCell-EMEWS workflow for high-throughput cancer hypothesis testing, where hundreds or thousands of mechanistic simulations are compared against data-driven error metrics to perform hypothesis optimization.ConclusionsWhile key notational and computational challenges remain, mechanistic agent-based models and high-throughput model exploration environments can be combined to systematically and rapidly explore key problems in cancer. These high-throughput computational experiments can improve our understanding of the underlying biology, drive future experiments, and ultimately inform clinical practice.
Highlights: • Higher spherogenicity in ROS{sup low} fractions of thyroid cancer cell lines. • Flexibility of ROS levels. • Functional importance of ROS levels for cancer stemness. • Lower GSH levels and quiescent state for cellular oxidative phosphorylation/glycolysis in ROS{sup low} cells. Cancer stem cells (CSCs), a small fraction of a tumor mass, are proposed to be highly crucial for cancer initiation, recurrence and metastasis. We have recently found that aldehyde dehydrogenase (ALDH) 1A3 is a CSC marker in some thyroid cancer cell lines, whose functional activity is, however, not relevant for thyroid cancer stemness. Since previous studies on malignancies in other organs suggest that intracellular reactive oxygen species (ROS) might be a functional and targetable CSC marker, the present study was conducted to elucidate the significance of ROS as a functional CSC marker in thyroid cancer cell lines. We first found that ROS levels controlled spherogenicity; that is, ROS{sup low} cells were more spherogenic than ROS{sup high} cells. However, unlike typical CSCs in other cancers, CSC-like ROS{sup low} cells in thyroid cancer cells were plastic and were not accompanied by de-differentiation status (i.e., expression of stemness markers/thyroid-specific transcription factors) or chemo-/radio-resistance. The lower levels of ROS were functionally critical because a forced increase in ROS levels by L-buthionine-S,R-sulfoximine, an inhibitor of glutathione (GSH) synthesis, and irradiation suppressed spherogenicity. ROS levels were also correlated with the number of double strand DNA breaks determined by 53BP1 staining. Lower ROS levels appear to be a result of decreased mitochondrial oxidative phosphorylation and elevated GSH contents. Given the importance of CSC-targeted therapy for achieving long-term disease eradication by exhausting self-renewal and growth potential of cancer tissues, ROS may be a good candidate for CSC-targeted therapy in thyroid cancer.
Highlights: • Indirect effects of glucocorticoid treatment on cancer cells via CAFs are described. • Glucocorticoids decrease expression of MMP-2 by CAFs. • Glucocorticoids neutralize growth-promoting and pro-invasive effects of CAFs. • In vivo, glucocorticoid treatment inhibits tumor progression. Cancer-associated fibroblasts (CAFs) support cancer growth, invasion, and metastasis. Glucocorticoids (GCs), drugs often administered together with chemotherapy, are steroidal ligands of the glucocorticoid receptor (GR), a transcription factor which upon activation regulates expression of multiple genes involved in suppression of inflammation. We have previously shown that in dexamethasone (Dex)-treated CAFs derived from colon cancer, production and secretion of several factors related to cancer progression, such as tenascin C (TNC) and hepatocyte growth factor (HGF), were strongly suppressed. In this study we show that GCs can neutralize the cancer cell-promoting properties of CAFs. Conditioned medium from solvent-treated CAFs (CM{sup CTRL}) stimulates proliferation, motility and stretched morphotype of GR-deficient HCT8/E11 colon cancer cells. Yet, HCT8/E11 proliferation and stretched morphotype are impaired upon treatment with conditioned medium from Dex-treated CAFs (CM{sup DEX}), but HCT8/E11 cell migration is slightly increased under these conditions. Moreover, expression and potential activity of MMP-2 is also reduced in CM{sup DEX} compared with CM{sup CTRL}. These combined in vitro results concur with the results from in vivo chick chorioallantoic membrane assays, where the co-cultures of CAFs with colon cancer cells displayed impaired tumor formation and cancer cell invasion due to Dex administration. Combined, GC treatment influences cancer cell behavior indirectly through effects on CAFs.
Highlights: • Up-regulated ACBD3 is associated with clinicopathological featuresin breast cancer. • ACBD3 regulates the enrichment of BCSCs via Wnt/beta-catenin pathway. • ACBD3 may represent candidate therapeutic targets to enable the elimination of BCSCs. Acyl-CoA binding domain containing 3 (ACBD3) is involved in the maintenance of Golgi structure and function through its interaction with the integral membrane protein. However, the clinical significance and biological role of ACBD3 in breast cancer remain unclear. Herein, we found that the mRNA and protein levels of ACBD3 were markedly up-regulated in breast cancer cells and tissues. Immunohistochemical analysis of breast cancer tissues demonstrated that ACBD3 overexpression was significantly associated with advanced clinicopathological features. Univariate and multivariate analysis indicated that ACBD3 overexpression correlates with poor prognosis in breast cancer. Furthermore, overexpressing ACBD3 promoted, while silencing ACBD3 inhibited, self-renewal and tumorigenesis in breast cancer cells in vitro and in vivo respectively. Importantly, upregulating ACBD3 promoted the self-renewal and tumorigenesis of breast cancer cells via activating the Wnt/beta-catenin signaling, and the pro-self-renewal effect of ACBD3 in breast cancer was antagonized by the Wnt signaling inhibitor TCF4-siRNA and Lef1-siRNA.These findings indicate that ACBD3 may represent candidate therapeutic targets to enable the elimination of breast cancer stem cells, providing the preclinical proof-of-concept for the prevention and treatment of breast cancer.
Although a potential inverse association between vegetable intake and bladder cancer risk has been reported, epidemiological evidence is inconsistent. This research aimed to elucidate the association between vegetable intake and bladder cancer risk by conducting a pooled analysis of data from prospective cohort studies. Vegetable intake in relation to bladder cancer risk was examined by pooling individual-level data from 13 cohort studies, comprising 3203 cases among a total of 555,685 participants. Pooled multivariate hazard ratios (HRs), with corresponding 95% confidence intervals (CIs), were estimated using Cox proportional hazards regression models stratified by cohort for intakes of total vegetable, vegetable subtypes (i.e. non-starchy, starchy, green leafy and cruciferous vegetables) and individual vegetable types. In addition, a diet diversity score was used to assess the association of the varied types of vegetable intake on bladder cancer risk. The association between vegetable intake and bladder cancer risk differed by sex ( P -interaction = 0.011) and smoking status ( P -interaction = 0.038); therefore, analyses were stratified by sex and smoking status. With adjustment of age, sex, smoking, energy intake, ethnicity and other potential dietary factors, we found that higher intake of total and non-starchy vegetables were inversely associated with the risk of bladder cancer among women (comparing the highest with lowest intake tertile: HR = 0.79, 95% CI = 0.64–0.98, P = 0.037 for trend, HR per 1 SD increment = 0.89, 95% CI = 0.81–0.99; HR = 0.78, 95% CI = 0.63–0.97, P = 0.034 for trend, HR per 1 SD increment = 0.88, 95% CI = 0.79–0.98, respectively). However, no evidence of association was observed among men, and the intake of vegetable was not found to be associated with bladder cancer when stratified by smoking status. Moreover, we found no evidence of association for diet diversity with bladder cancer risk. Higher intakes of total and non-starchy vegetable are associated with reduced risk of bladder cancer for women. Further studies are needed to clarify whether these results reflect causal processes and potential underlying mechanisms.
Introduction: Leading cancer hospitals have increasingly shared their ‘brand’ with smaller hospitals through affiliations. Because each brand evokes a distinct reputation for the care provided, ‘brand-sharing’ has the potential to impact the public’s ability to differentiate the safety and quality within hospital networks. The general public was surveyed to determine the perceived similarities and differences in the safety and quality of complex cancer surgery performed at top cancer hospitals and their smaller affiliate hospitals. Methods: A national, web-based KnowledgePanel (GfK) survey of American adults was conducted. Respondents were asked about their beliefs regarding the quality and safety of complex cancer surgery at a large, top-ranked cancer hospital and a smaller, local hospital, both in the presence and absence of an affiliation between the hospitals. Results: A total of 1010 surveys were completed (58.1% response rate). Overall, 85% of respondents felt ‘motivated’ to travel an hour for complex surgery at a larger hospital specializing in cancer, over a smaller local hospital. However, if the smaller hospital was affiliated with a top-ranked cancer hospital, 31% of the motivated respondents changed their preference to the smaller hospital. When asked to compare leading cancer hospitals and their smaller affiliates, 47% of respondents felt that surgical safety, 66% felt guideline compliance, and 53% felt cure rates would be the same at both hospitals. Conclusions: Approximately half of surveyed Americans did not distinguish the quality and safety of surgical care at top-ranked cancer hospitals from their smaller affiliates, potentially decreasing their motivation to travel to top centers for complex surgical care.
Mitochondria are crucial regulators of the intrinsic pathway of cancer cell death. The high sensitivity of cancer cells to mitochondrial dysfunction offers opportunities for emerging targets in cancer therapy. Herein, magnetic nano-transducers, which convert external magnetic fields into physical stress, are designed to induce mitochondrial dysfunction to remotely kill cancer cells. Spindle-shaped iron oxide nanoparticles were synthesized to maximize cellular internalization and magnetic transduction. The magneto-mechanical transduction of nano-transducers in mitochondria enhances cancer cell apoptosis by promoting a mitochondrial quality control mechanism, referred to as mitophagy. Furthermore, in the liver cancer animal model, nano-transducers are infused into the local liver tumor via the hepatic artery. After treatment with a magnetic field, in vivo mitophagy-mediated cancer cell death was also confirmed by mitophagy markers, mitochondrial DNA damage assay, and TUNEL staining of tissues. This study is expected to contribute to the development of nanoparticle-mediated mitochondria-targeting cancer therapy and biological tools, such as magneto-genetics.
Highlights: • SUSD2 was one of Notch3 downstream genes in high grade serous ovarian cancer (HGSOC). • High expression of SUSD2 was associated with poor prognosis in HGSOC. • Over-expression of SUSD2 can promote ovarian cancer cells metastasis via inducing EMT. • SUSD2 down-regulating E-cadherin and promoting migration were triggered by EpCAM. • Over-expression of SUSD2 could confer ovarian cancer cells cisplatin resistance through enhancing autophagy. The activation of Notch3 is associated with potential progression of ovarian cancer, tumor invasion, metastasis and chemoresistance, which account for poor prognosis of high grade serous ovarian cancer (HGSOC). However, the underlying mechanisms of Notch3 are not yet very clear. Here we show that SUSD2 is one of Notch3-regulating genes and the elevated protein expression of SUSD2 in HGSOC. We also found that its high expression level was significantly correlated with worse overall survival, early recurrence and lymph nodes metastasis. Moreover, overexpression of SUSD2 in ovarian cancer cells promoted epithelial-mesenchymal transition (EMT) and the metastatic capacity of malignant cells. In contrast, silencing SUSD2 in aggressive ovarian cancer cells inhibited these processes both in vitro and in vivo. Mechanistically, we found SUSD2 promoted EMT through regulating the expression of EpCAM and EpCAM silencing reversed SUSD2-induced E-cadherin reduction and cells migration. Further experiments indicated a role of SUSD2 in conferring cisplatin resistance in ovarian cancer probably through enhancing autophagy in vitro. Collectively, these findings shed a new insight into the role of Notch3 downstream gene SUSD2 and provided a new therapeutic target for HGSOC.
Lung cancer is the most frequent cause of cancer-related deaths worldwide, but its molecular pathogenesis is poorly understood. The tumor suppressor candidate 3 (TUSC3) gene is located on chromosome 8p22 and is universally acknowledged as a cancer suppressor. However, our research has demonstrated that TUSC3 expression is significantly upregulated in non-small-cell lung cancer compared to benign controls. In this study, we analyzed the consequences of TUSC3 knockdown or overexpression on the biological functions of non-small-cell lung cancer cell lines. To identify the molecules and signaling pathways with which TUSC3 might interact, we completed immunoblotting, quantitative polymerase chain reaction, microarray, co-immunoprecipitation, and immunofluorescence assays. We demonstrated that TUSC3 knockdown leads to decreased proliferation, migration, and invasion, and reduced xenograft tumor growth of non-small-cell lung cancer cell lines, whereas opposite results were observed with overexpression of TUSC3. In addition, TUSC3 knockdown suppressed epithelial-mesenchymal transition by downregulating the expression of claudin-1, which plays an indispensable role in EMT progress. On the contrary, overexpression of TUSC3 significantly enhanced EMT progress by upregulating claudin-1 expression. Overall, our observations suggest that TUSC3 accelerates cancer growth and induces the epithelial-mesenchymal transition in non-small-cell lung cancer cells; we also identified claudin-1 as a target of TUSC3.
Quantification of variation in levels of spontaneously occurring cancer driver mutations (CDMs) was developed to assess clonal expansion and predict future risk of neoplasm development. Specifically, an error-corrected next-generation sequencing method, CarcSeq, and a mouse CarcSeq panel (analogous to human and rat panels) were developed and used to quantify low-frequency mutations in a panel of amplicons enriched in hotspot CDMs. Mutations in a subset of panel amplicons, Braf, Egfr, Kras, Stk11, and Tp53, were related to incidence of lung neoplasms at 2 years. This was achieved by correlating median absolute deviation (MAD) from the overall median mutant fraction (MF) measured in the lung DNA of 16-week-old male and female, B6C3F1 and CD-1 mice (10 mice/sex/strain) with percentages of spontaneous alveolar/bronchioloalveolar adenomas and carcinomas reported in bioassay control groups. A total of 1586 mouse lung mutants with MFs > x 10-4 were recovered. The ratio of nonsynonymous to synonymous mutations was used to assess the proportion of recovered mutations conferring a positive selective advantage. The greatest ratio was observed in what is considered the most lung tumor-sensitive model examined, male B6C3F1 mice. Of the recurrent, nonsynonymous mouse mutations recovered, 55.5% have been reported in human tumors, with many located in or around the mouse equivalent of human cancer hotspot codons. MAD for the same subset of amplicons measured in normal human lung DNA samples showed a correlation of moderate strength and borderline significance with age (a cancer risk factor), as well as age-related cumulative lung cancer risk, suggesting MAD may inform species extrapolation.
Purpose: Pathology reports are the primary source of information concerning the millions of cancer cases across the United States. Cancer registries manually process the pathology reports to extract the pertinent information including primary tumor site, behavior, histology, laterality, and grade. Processing a large volume of the pathology reports in a timely manner is a continuing challenge for cancer registries. The purpose of this study is to develop an information extraction pipeline to reliably and efficiently extract reportable information. Method: We have developed a novel inverse-regression (IR) based information extraction pipeline. The inverse-regression based supervised filter has been successfully applied to many application domains. However, its application to the information extraction from unstructured text is hindered primarily by the extreme high-dimensionality of n-gram representations of text. In this study, we attempt to overcome the obstacles by a novel bootstrapping strategy. First, we use an information-theoretic mutual information based filter to discard the excessive and redundant n-gram features. This step reduces the size and improves the condition number of the sample covariance matrix, thus reducing the computational cost and improving the numerical stability of the subsequent inverse-regression step. Then we use localized sliced inverse-regression (LSIR) to learn a low-dimensional discriminatory subspace for information inference. In particular, we use the k-nearest neighbors of an unlabeled pathology report in the learned representation to infer the desired information from the labeled data in a supervised manner. Results: The experiments were conducted on a set of de-identified pathology reports with human expert labels as the ground truth. Our pipeline consistently performed better than or comparable to the best performing state-of-the-art methods while reducing the training and inference times substantially. Conclusion: Our results demonstrate the potential of inverse-regression based information extraction pipeline for reliable and efficient information extraction from unstructured text. The information extracted from the pathology reports can be used along with clinical information, medical imaging, and genomic information to instigate discoveries in cancer research.
Background: Understanding the natural progression of untreated gastric cancer is critical for determining the disease prognosis as well as treatment options and timing. The aim of this study is to analyze the natural history of gastric cancer. Patients and Methods: We included patients with gastric cancer who had not received any treatment and were staged using endoscopy/endoscopic ultrasonography and computed tomography on at least two follow-up visits during intervals of nontreatment. Tumor volumes were also measured in addition to the staging. Survival of each stage at diagnosis was also analyzed. Results: A total of 101 patients were included. The mean follow-up period was 35.1 ± 34.4 months. The gastric cancer doubling time was 11.8 months for T1 and 6.2 months for T4. The progression time from early gastric cancer to advanced gastric cancer was 34 months. It decreased as the stages advanced: from 34 months between tumor-nodes-metastasis stage I and II to 1.8 months between stage III and IV. No variable was identified as a risk factor for cancer progression. The 5-year survival rates of untreated patients were 46.2% in stage I and 0% in stage II, stage III, and stage IV. Conclusions: The progression and doubling times of gastric cancer shorten as the stages advance. Objective data reported in this study can be a critical factor in determining treatment timing and screening interval.