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Biomedical subjects

M Mai

Publications and source records attributed to M Mai.

At least 55 records · Page 3Linked to original sources
PubMed1998

Significance of platelet-derived endothelial cell growth factor in the angiogenesis of human gastric cancer.

We have previously shown that platelet-derived endothelial cell growth factor (PD-ECGF) is associated with angiogenesis of human colon cancer; this factor is expressed at high levels in vascular tumors that express low levels of vascular endothelial growth factor (VEGF). In these colon cancers, the major source of PD-ECGF is the infiltrating cells. In this study, we examined the role of PD-ECGF in the angiogenesis of human gastric cancer. Immunostaining for PD-ECGF was done on 93 gastric cancers previously stained for VEGF, basic fibroblast growth factor, and factor VIII-related antigen (specific for endothelial cells). To determine the cell type expressing PD-ECGF, double staining was done using antibodies to both PD-ECGF and CD68 (specific for macrophages). PD-ECGF was expressed more frequently in infiltrating cells (positive CD68 staining; 53.8%) than in tumor epithelium (9.7%; P < 0.0001). Infiltrating cells simultaneously stained positive for both PD-ECGF and CD68. An association between PD-ECGF expression in infiltrating cells, VEGF expression in tumor epithelium, and vessel count was observed in intestinal-type gastric cancer but not in diffuse-type gastric cancer. Vessel count was greater in tumors with high expression of both PD-ECGF and VEGF than in those with high expression of either factor alone (P = 0.002). Multiple angiogenic factors expressed by both tumor cells and infiltrating cells may play a role in the regulation of angiogenesis in intestinal-type gastric cancer.

Adult↗
PubMed1998

Amplification of c-erbB-2 in gastric cancer: detection in formalin-fixed, paraffin-embedded tissue by fluorescence in situ hybridization.

A total of 396 adenocarcinomas of the stomach were examined immunohistochemically using antibodies specific for the internal domain of human c-erbB-2 protein. Forty of these (consisting of 35 well-differentiated and 5 undifferentiated types) overexpressed c-erbB-2, as evidenced by cytoplasmic membrane staining; these tumors were further examined by fluorescence in situ hybridization using a cosmid probe for 17q11.2-12 (c-erbB-2 locus) on formalin-fixed, paraffin-embedded tissues. This technique enabled us not only to detect c-erbB-2 amplification on a cell-by-cell basis, but also to compare the gene amplification with the protein expression, observe topographical distribution, and establish quantitative pictures of the amplification in vivo condition. In all 40 tumors, we observed gene amplification and found that the cancer cell with the amplification corresponded to the cells overexpressing c-erbB-2. In eight mucosal carcinomas, signals were coalesced to one or two clusters, indicating that the amplified gene resided in a homogeneous staining region (HSR). Among 32 carcinomas invading beyond muscularis mucosae, approximately half were mostly composed of cells with the amplification; the others had populations of tumor cells with and without amplification, which were sometimes in separate zones or areas and sometimes mixed together. In 22 cancers, the amplified genes were exclusively in HSR; however, cancer cells with multiple scattered signals-suggesting that the amplified genes were translocated to other chromosomes-were found exclusively in 6 tumors and concurrently with HSR in 4 tumors. These findings suggest that: (a) the amplification produces c-erbB-2 in the HSR form generally early in the carcinogenesis of gastric adenocarcinomas; and (b) in the process of cancer development, the amplified gene is lost in some cancer cells by uneven segregation of HSR in mitosis, whereas in others, it is kept in HSR or translocated to other chromosomal positions, thereby preserving overexpression of c-erbB-2 protein.

Adenocarcinoma↗
PubMed1998

Amplification of c-myc, K-sam, and c-met in gastric cancers: detection by fluorescence in situ hybridization.

Gene amplifications of c-myc, K-sam, and c-met were examined in cancer nuclei isolated from 154 primary gastric adenocarcinomas by fluorescence in situ hybridization (FISH) using cosmid probes for 8q24 (c-myc locus) and 7q31 (c-met), as well as a DNA probe for K-sam synthesized by PCR. The results were compared with those of Southern blot analysis. Dual-color FISH using gene locus and chromosome-specific probes detected gene amplifications of c-myc in 24 tumors (15.5%), c-met in 6 tumors (3.9%), and K-sam in 3 tumors (2.9%). The six tumors with c-myc amplification had also been found to have amplified c-erbB-2 in our previous study, and coamplification of c-myc and c-met was found in two other tumors. This technique also differentiated the amplified genes on the homogeneous staining region (HSR) and on double minute chromosomes (DMs) in metaphase spreads and interphase nuclei of cell lines established from poorly differentiated adenocarcinomas, KATO III, SNU 16, and HSC 39. Examination of FISH images of these cell lines suggested that the high-level amplifications of c-myc found in primary tumors occurred mainly on DM in four tumors and on HSR in one, and those of K-sam occured on DM in two tumors and on HSR in one. No high-level amplification of c-met was found. These high-level amplifications were also detected in formalin-fixed, paraffin-embedded tissues from primary gastric tumors and metastatic lymph nodes, in some of which heterogeneity of gene amplification was demonstrated within the same tumor. We conclude that FISH is an important tool for examining the proto-oncogene aberrations in intact cells in solid tumors.

Blotting, Southern↗
PubMed1997

Streptococcal preparation OK-432 is a potent inducer of IL-12 and a T helper cell 1 dominant state.

Streptococcal preparation OK-432 is a bacterial immunopotentiator extensively used in Japan for adjuvant cancer therapy. Using a C57BL/6 mouse model, OK-432 was found to induce multiple cytokines including the Th1 polarizing cytokine IL-12. Expression of IL-12 protein by murine splenocytes was restricted to macrophages and B cells and led to high levels of IFN-gamma production from both CD4+ and CD8+ T cells. Of the Th2 cytokines IL-4 and IL-10, only IL-10 protein was detected and originated primarily from the adherent cell population. Its expression was delayed relative to IL-12. A similar pattern of cytokine induction was observed from human PBMCs. OK-432-driven IFN-gamma production was inhibited by anti-IL-12 Ab, anti-IL-2 Ab, anti-TNF-alpha Ab, and anti-IL-2R alpha Ab, suggesting that IFN-gamma production from Th1 cells is induced by the cooperation action of these cytokines through the IL-2R alpha pathway. When compared with another widely used immunopotentiator bacillus Calmette-Guérin (BCG), OK-432 was a stronger IL-12 and IFN-gamma inducer. Furthermore, the mechanism of IFN-gamma induction by OK-432 differed from BCG in that coincident granulocyte-macrophage CSF and IL-1 expression played little to no role. These results suggest that OK-432 is a potent multicytokine inducer, specifically a strong inducer of IL-12, and that OK-432 may exert its antitumor effect by promoting a Th1-dominant state.

Adjuvants, Immunologic↗
PubMed1997

Effects of early and late antihypertensive treatment on extracellular matrix proteins and mononuclear cells in uninephrectomized SHR.

The efficacy of an early and late treatment with the angiotensin converting enzyme inhibitor lisinopril or the angiotensin II receptor blocker ICI D8731 was investigated in uninephrectomized spontaneously hypertensive rats (SHR). Rats that underwent uninephrectomy (UNX) at six weeks of age were randomly assigned to receive no treatment, lisinopril shortly after UNX, lisinopril starting 16 weeks after UNX, ICI D8731 shortly after UNX, and ICI D8731 starting 16 weeks after UNX. Blood pressure was normalized with both treatments. After six months inulin clearance was not significant different, while proteinuria and prevalence of interstitial fibrosis were significantly reduced in all treatment groups. Immunohistochemical studies revealed an interstitial, periglomerular and perivascular increase of extracellular matrix proteins in all rats, but a markedly reduced expression of collagen I, IV and fibronectin after early and late treatment compared to untreated controls. We found a significant reduction of infiltrating macrophages and T-lymphocytes in all treated animals compared to untreated controls after 2, 4 and 6 months. Especially early treatment was associated with lower numbers of infiltrating cells. Both treatments reduced proliferation of tubular and interstitial cells. There were no striking differences with regard to nephroprotection between the ACE inhibitor and angiotensin II receptor blocker. These findings show that both treatments have beneficial effects on kidney structure and function. They suggest that both ACE inhibition and angiotensin II blockade decrease renal cell proliferation and suppress the infiltration of mononuclear cells that may trigger expression of extracellular matrix proteins and progressive nephrosclerosis.

Angiotensin Receptor Antagonists↗
PubMed1997

Small-bowel obstruction during enzymatic treatment of gastric bezoar.

A 66-year-old woman had a sudden onset of small-bowel obstruction during enzymatic treatment for gastric persimmon bezoar. Oral enzymatic therapy is the most effective method of treatment for large phytobezoars when endoscopic extraction is not possible. However, this report suggests that a further endoscopic intervention may be necessary in case the dissolved bezoars cause small-bowel obstruction during this form of therapy.

Aged↗
PubMed1997

Prevalence of head-shaking nystagmus in patients according to their diagnostic classification in a dizziness unit.

OBJECTIVE: In a previous publication, the authors documented the prevalence and characteristics of head-shaking nystagmus (HSN) in over 1300 consecutive dizzy patients during formal electronystagmography (ENG) at the combined Otologic Function Unit (OFU) of the Toronto and Mount Sinai Hospitals. This companion study was done to prospectively analyze a subgroup of 300 patients with known clinical diagnoses belonging to the senior author (J.R.). METHODS: The prevalence of HSN in this series of patients with a known diagnosis is prospectively compared to the presence of HSN in a series of normal controls. RESULTS: Results indicate that HSN is seen significantly (p < .05) in those patients with peripheral vestibular dysfunction and that the more globally the peripheral vestibular disorder involves end-organ (i.e., Meniere's) or primary afferent-neuron function (i.e., vestibular neuronitis), the more likely HSN will be present. CONCLUSION: We further comment on the usefulness of the head-shake test and its clinical relevance in the bedside examination of the dizzy patient.

Adolescent↗
PubMed1997

Amplification of the c-erbB-2 (HER-2/neu) gene in gastric cancer cells. Detection by fluorescence in situ hybridization.

Amplification of the c-erbB-2 gene was examined in 120 gastric adenocarcinomas by dual-color fluorescence in situ hybridization (FISH) using probes for centromere 17 and the 17q11.2-12. The results were compared with Southern blot analysis and immunohistochemistry of c-erbB-2 overexpression. FISH was successful in 105 tumors, and the amplification was found in 19 tumors. FISH on 17 tumors revealed high-level amplification; in 15, the predominant cancer populations had amplified c-erbB-2 gene with the signals forming one or two clusters, indicating that the amplified gene was present in homogeneously staining regions. In two tumors, most cancer cells had multiple scattered c-erbB-2 signals, indicating that the amplicon was within double-minute chromosomes. The other two tumors had a few additional copies of the c-erbB-2 gene. Seventeen tumors had increased numbers of the gene probably due to polysomy 17, and sixty-nine tumors had no aberrations of chromosome 17. Immunohistochemically, distinct membrane staining was found only in the 17 tumors with the high-level amplification. It is concluded that, in gastric adenocarcinomas, high-level amplification produces the c-erbB-2 gene principally in homogeneously staining region form and occasionally in double-minute form and is thought to control the over-expression of the protein in the cytoplasmic membrane.

Adenocarcinoma↗
PubMed1997

Does p53 overexpression cause metastases in early invasive colorectal adenocarcinoma?

OBJECTIVE: To find out whether p53 overexpression correlates with metastatic potential and other adverse prognostic factors in early invasive colorectal carcinoma and whether measurement of the expression of p53 protein could be helpful in the choice of treatment (endoscopic/local or radical resection). DESIGN: Retrospective study. SETTING: University hospital, Japan. SUBJECTS: Overexpression of p53 protein in the primary tumour was examined immunohistochemically in 50 patients with early invasive colorectal cancer. MAIN OUTCOME MEASURES: Differences in p53 overexpression between subgroups. RESULTS: Abnormal accumulation of nuclear p53 was detected in the primary tumour of 20 patients (40%) with early invasive colorectal cancer. We found p53-positive cells in 7 (78%) of 9 that had metastasised to regional lymph nodes or distant organs, or both, and in 13 (32%) of 41 that had not metastasised (p = 0.02). p53 Immunoreactivity was also present in 10 (71%) of 14 superficial (type II) lesions compared with 10 (28%) of 36 protruding (type I) ones (p = 0.009) and in 12 (57%) of 21 moderately differentiated adenocarcinomas compared with 8 (28%) of 29 well-differentiated adenocarcinomas (p = 0.045). There was no significant correlation between p53 overexpression and the depth of tumour invasion or angiolymphatic involvement. The p53-positive metastasising tumours had features that corresponded to those of early carcinoma arising de novo. CONCLUSION: Our results seem to support the postulate that p53 overexpression in early invasive colorectal carcinomas is associated with an increase in their metastatic potential.

Adenocarcinoma↗
PubMed1997

[Correlations between risk factors for metastasis in early tumors of the large intestine].

UNLABELLED: Intramucosal colorectal cancers (Tis) are treated by local excision. Controversies remain as to the management of patients with the submucosally invasive colorectal cancers (EIC). The decision for radical surgery or local excision depends on an estimate of the risk of metastases. AIM: To estimate correlations between the risk factors for metastases in EIC and to evaluate the tests that identify the metastasising EICs. In the study, we investigated the relationships between selected prognostic factors (the gross appearance, depth of submucosal invasion, vessel invasion, grade, presence of adenoma component, and p53 overexpression) and the frequency of metastases in 64 EICs. STATISTICAL ANALYSIS: Fisher's exact test and log-linear analysis. Tests' evaluation: sensitivity, specificity, predictive values. The metastases were detected in 11 tumours (17%). The metastases were found with the significantly (p < 0.05) higher frequency in moderately differentiated adenocarcinomas, in tumours with massive invasion, with vessel invasion, and with the p53 overexpression. The only interaction was between the grade and the depth of invasion. No other interaction between the risk factors was found with the multivariate analysis. The evaluation of the depth of invasion was characterised by the highest sensitivity in detecting metastases, and by the highest negative predictive value. The highest specificity and the positive predictive value were found for the evaluation of vessel invasion. The massive submucosal invasion, vessel invasion, moderately differentiated characteristics, and the p53 overexpression seem to be the independent risk factors for metastases in EIC. The evaluation of these factors should be helpful as prognostic tests and for the proper choice of the treatment modality for the patients with EIC.

Adenocarcinoma↗
PubMed1997

Combined analysis of microsatellite instability and K-ras mutation increases detection incidence of normal samples from colorectal cancer patients.

Microsatellite instability (MI) and K-ras oncogene mutation have been widely used as biomarkers of genetic changes in colorectal cancer (CRC). Each of these biomarkers was independently found in normal-appearing colonic mucosa at stages preceding the development of CRC, albeit at a relatively low incidence. To assess the potential value of combined MI and K-ras mutation analysis in the detection of normal-appearing colonic mucosa samples taken from patients with CRC, we have chosen to analyze multiple (3-7) normal colonic mucosa samples and the respective colorectal tumor tissues from 20 patients with CRC. As a control, we have used 54 normal mucosa samples obtained from 9 autopsies of patients without CRC. In at least 1 of 5 loci analyzed, MI was found in 8 of 20 patients via analysis of multiple normal-appearing colonic mucosa samples from each patient. Combined analysis of MI and mutant ras alleles in normal-appearing colonic mucosa samples enabled the identification of 11 of 20 patients with CRC. None of the 54 normal colonic mucosa samples obtained from 9 patients without CRC were found to carry mutant ras or MI. The ability to detect 55% of patients with CRC via the analysis of normal mucosa samples provides an important advance in our approach toward early detection of individuals who may be at risk to develop this tumor type.

Aged↗
PubMed1996

Inhibition of metastasis in human gastric cancer cells transfected with tissue inhibitor of metalloproteinase 1 gene in nude mice.

BACKGROUND: Tissue inhibitors of metalloproteinases (TIMPs) act as negative regulators of matrix metalloproteinases (MMPs) that degrade extracellular matrix. We evaluated the metastatic ability of the highly metastatic human gastric cell line KKLS, and that of cells transfected with exogenous TIMP-1 gene by the orthotopic transplantation model in nude mice. METHODS: KKLS was derived from human gastric cancer. Expression of mRNA for tissue inhibitor of metalloproteinase-1 (TIMP-1) was almost undetectable in KKLS cells. KKLS cells were transfected with exogenous TIMP-1 gene by the Chen-Okay-ama method. Two clones (KTCLs) that expressed different levels of TIMP-1 and neomycin-resistant KKLS (K-neo) were obtained. The KKLS cells and these transfectants were orthotopically transplanted into nude mice (murine stomach) and metastasis in the murine liver was detected. As a method of detecting metastasis, we used a DNA fragment (human beta-globin gene) specific to human tumor cells that have metastasized into the murine liver by polymerase chain reaction (PCR). RESULTS: Differences in tumor growth in the murine stomach were not observed between KKLS cells, K-neo cells, and the two transfectants expressing the different TIMP-1 levels (low, KTCL-1; high, KTCL-14). The KKLS cells and K-neo cells had undergone liver metastasis, as shown by PCR amplification of the human beta-globin gene fragment from the murine liver samples, since Week 1 after transplantation and the metastasis had grown exponentially; however, although KTCL-1 cells and KTCL-14 cells had undergone liver metastasis since Week 2, the metastasis had not grown. The average intensities of the amplified gene fragments from K-neo cells, KTCL-1 cells, and KTCL-14 cells in Week 4 after transplantation were 100%, 45%, and 18%, respectively, of the parenteral KKLS cells. CONCLUSIONS: TIMP-1 was suggested to act as a negative regulator of the metastasis. The present data is thought to be especially important because the mice in this study underwent orthotopic transplantation with a metastatic model.

Animals↗
PubMed1996

Enhanced production of matrix metalloproteinases and activation of matrix metalloproteinase 2 (gelatinase A) in human gastric carcinomas.

We examined the production and tissue localization of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in gastric carcinoma tissues. MMP-1 (tissue collagenase), MMP-9 (gelatinase B) and TIMP-2 were immunolocalized in carcinoma cells and MMP-2 (gelatinase A) on tumor cell membranes, whereas no or little immunostaining for MMP-3 (stromelysin-1) and TIMP-1 was seen in carcinoma cells. Stromal cells in carcinoma tissue were also positively stained for these MMPs and TIMPs. MMP-2 immunostaining was observed exclusively on advanced gastric carcinoma cells and correlated with vascular invasion by tumor cells. Sandwich enzyme immunoassays revealed enhanced production of MMP-1, MMP-2, MMP-3, MMP-9 and TIMP-1 by carcinoma tissues. Gelatinolytic activities were significantly higher in carcinoma samples than in normal controls. Using gelatin zymography, active forms of MMP-2 and MMP-9 were more frequently detected in carcinoma tissue, and the activation rate of the zymogen of MMP-2 (proMMP-2), but not that of proMMP-9, correlated well with degree of local invasion and lymphatic permeation. Our data indicate an enhanced production of 4 MMPs in gastric carcinoma tissue and suggest that activation of pro-MMP-2 may be a key step for spreading of gastric carcinoma cells.

Enzyme Activation↗
PubMed1996

Numerical chromosome alterations in colorectal carcinomas detected by fluorescence in situ hybridization. Relationship to 17p and 18q allelic losses.

This study concerns DNA ploidy, numerical changes of chromosomes 7, 8, 10, 17 and 18, and allelic losses at chromosomes 17p13.3 (flanking the p53 gene) and 18q21 (location of the DCC gene) in 31 freshly resected colorectal tumours. Cytological smears were used to determine DNA ploidy by image analysis, and chromosome numbers by fluorescence in situ hybridization (FISH) using chromosome-specific pericentromeric alpha-satellite DNA probes. Allelic losses were assessed by Southern blotting and by the polymerase chain reaction loss of heterozygosity method. Approximately 50% of the tumours were aneuploid. There was heterogeneity with respect to chromosome numbers, but gains and losses of chromosomes, or both, were detected in all carcinomas examined, including 10 that were nonaneuploid by image analysis. Trisomy 7 was found in 74% of the tumours, and monosomy of chromosome 18 in 32%. Allelic loss at chromosome 17p13.3 was evident in 13 of 26 informative cases, and only one case exhibited monosomy 17. In comparison monosomy 18 was found in 10 cases; 7 of them corresponded to approximately half of the cases with allelic loss within the DCC gene, and the other three were noninformative. These findings indicate that the loss of one chromosome 18 is an important mechanism producing allelic deletion of the DCC gene in colorectal carcinomas. Our data also suggest that monosomy 18 is a useful indicator for studying colorectal cancer progression on a cell by cell basis.

Aneuploidy↗
PubMed1996

Association between preoperative plasma CEA levels and the prognosis of gastric cancer following curative resection. Tumor Marker Committee, Japanese Foundation for Multidisciplinary Treatment of Cancer, Tokyo, Japan.

A large-scale retrospective study was undertaken to evaluate the association between preoperative plasma carcinoembryonic antigen (CEA) levels and the prognosis of 2768 gastric cancer patients who underwent curative gastrectomy between 1983 and 1984 at 66 leading medical institutions in Japan Postoperative follow-up was at least 5 years. Preoperative plasma CEA levels were also analysed against other prognostic factors. Preoperative plasma CEA levels showed strong correlations to the degree of lymph node metastasis (P < 0.001), TNM stage (P = 0.004) and the histopathology of the gastric cancer (P < 0.001). Preoperative CEA levels were also evaluated against survival, after being adjusted for the effect of clinically important factors by multivariate analysis. Patients with lower preoperative plasma CEA levels survived significantly longer than patients with higher CEA levels (P = 0.0001). This analysis demonstrates that curatively resected gastric cancer patients with higher preoperative plasma CEA levels have a poorer prognosis than those with lower levels, despite the adjustment for the effects of major prognostic factors.

Adolescent↗
PubMed1996

Experimental studies on the role of intercellular adhesion molecule-1 and lymphocyte function-associated antigen-1 in hypertensive nephrosclerosis.

T helper cells and macrophages infiltrate into the renal cortical interstitium during the course of hypertensive nephrosclerosis. To investigate the mechanisms of mononuclear cell infiltration, we examined the expression of the intercellular adhesion molecule-1 (ICAM-1) and its counterpart lymphocyte function-associated antigen-1 (LFA-1) in the progression of hypertensive renal injury. We studied nonclipped kidneys of two-kidney, one clip renovascular hypertensive and sham-operated control rats immunohistochemically at 4, 7, 14, and 28 days after clipping (n = 5 per group and time point). Systolic pressure was significantly elevated by day 7 (154 +/- 4 versus 117 +/- 6 mm Hg in sham, P < .05). The development of hypertension resulted in a progressive increase of ICAM-1 expression in the perivascular and interstitial areas of the renal cortex and on proximal tubular brush borders. Only a few glomeruli showed augmented ICAM-1 staining. Increased ICAM-1 was associated with an accumulation of LFA-1-positive mononuclear cells in the perivascular region (day 14: 15 +/- 4 versus 2 +/- 0.2 cells/mm2 in sham, P < .005) and intertubular region (127 +/- 11 versus 32 +/- 3 cells per millimeter squared in sham, P < .005). The maximum was obtained at day 14 and remained elevated until day 28. In addition, the number of interstitial LFA-1-positive infiltrating cells was related to the degree of interstitial and tubular ICAM-1 expression and correlated with blood pressure (r = .75, P < .001, n = 18). Our data suggest that ICAM-1 is involved in the recruitment of macrophages/lymphocytes via specific interaction of ICAM-1 and LFA-1 in this model of hypertensive target-organ damage.

Animals↗
PubMed1996

[Comparative study on biological difference between gastric cancer and colorectal cancer].

In this study, we investigated the clinico-pathologic characteristics of patients with adenocarcinoma of the stomach and those with colorectal carcinoma to compare early progression patterns of both tumors. Histologically, gastric and colorectal adenocarcinomas showed similar progression patterns, including the incidence of submucosal invasion, lymphatic infiltration and lymph node metastasis. One striking finding was in gross appearance in born tumors. In contrast to most gastric well differentiated adenocarcinoma (DTA), which showed superficial growth, colorectal DTAs mainly showed polypoid growth. However, the superficial-type colorectal DTAs invaded the submucosal layer more frequently than did polypoid DTAs and gastric DTAs. These findings indicate that superficial-type colorectal DTAs grow more rapidly and aggressively than do polypoid DTAs and gastric DTAs. In order to elucidate growth rates between gastric cancer and colorectal cancer with hepatic metastasis doubling time was measured by exponential growth of tumor marker (CEA or AFP). The doubling time of liver metastases calculated from tumor markers was 26.6 +/- 10.8 days for stomach cancer and 57.8 +/- 35.4 days for colorectal cancer; accordingly doubling time for gastric cancer was approximately half of that for colonic cancer. However, there were no other factors (age, sex, site, histologic type in stomach, tumor marker production, etc.) influencing doubling time.

Adenocarcinoma↗