tbuckley/cabot-search huggingface dataset:
Gastric Ulceration in Tumor-Bearing Rats
Authors: Peter Baillie, Florence K. Millar, Seoras D. Morrison, Arnold W. Pratt
Journal: JNCI Journal of the National Cancer Institute (1967)

Sprague-Dawley rats, in which the Walker carcinosarcoma 256 (1 of 2 lines) was transplanted, were fed ad libitum one of several diets (casein base, dried tumor base, chow, diluted evaporated milk), or were fed a restricted amount of the casein diet. These rats were examined for gastric ulcers. Normal (non-tumor-bearing) rats were fed ad libitum or were partially or totally deprived of food. In tumor-bearing rats fed ad libitum, ulcers developed in both the forestomach and in the glandular area of the stomach 21 or more days after tumor transplant with all diets fed except chow. Ulcer incidence increased with age of the tumor, but variability was great. In tumor-bearing rats partially deprived of food and killed 18 days after transplant, the ulcer incidence was significantly lower than in rats with spontaneous comparable intake killed 28 days after transplant. In normal rats totally deprived of food, the incidence of forestomach ulcers increased with the period of deprivation (3–7 days); glandular ulcers developed only after more than 6 days of deprivation. From the relation of ulcer incidence to tumor weight, food intake, carcass weight change, and adrenal weight, it appears that gastric ulceration in the tumor bearer requires a degree of food deficit, such as occurs with progressive tumor growth, in conjunction with some minimal stage of tumor development. No definitive cause for the ulceration has been found.
Payer current and future utilization of pathways: A research study.
Authors: Rhonda Greenapple
Journal: Journal of Clinical Oncology (2013)

273 Background: Clinical pathways are a growing payer management technique for controlling costs and standardizing care. Their use in other therapeutic areas has helped payers control costs and standardize care; however, use of pathways in oncology has not been assessed. Methods: There were a total of 49 respondents, including 19 Medical Directors and 30 Pharmacy Directors, covering 100 million lives in the US across all channels (Medicare, Commercial, and Medicaid). Approximately 39% of respondents were from small plans (covering less than 750,000 lives), 28% were from medium-sized plans (covering 750,000 – 2.5 million lives), and 33% of respondents represented large plans (covering more than 2.5 million lives). About 33% of respondents were from national plans, while 67% were from regional plans. Results: Only 39% of payers have actually implemented pathway programs in oncology. Of the payers surveyed that did not already have a clinical pathway, 59% said they are not currently implementing pathways. However, among those who are using pathways, a disproportionate share is commercial plans (42%) and Medicaid (40%), not Medicare (25%). Only 25% of Medicare-focused plans anticipate implementing clinical pathways in the future, while more than 40% of commercially-focused plans intend to do so. About half of plans (53%) anticipate that pathways also will be integrated into provider ratings, and a minority, (42%), see a role for pathways in product formulary placement or tier status. When payers have implemented pathways, the tumor types with the highest costs have been initial targets, with breast (84%), lung (63%), colorectal (63%), and prostate (37%) with the highest penetration of pathway implementation. Conclusions: Payers view clinical pathways as an important tool for reducing drug costs, especially with respect to tumor types that carry high treatment costs. Near-term strategies like step edits and coverage via the pharmacy vs. medical benefit will continue to play a significant role in oncology reimbursement decisions, but product companies need to understand how existing clinical pathway programs will impact provider access to products to more accurately forecast their future impact as the concept gains national traction.
Corrigendum to “Allo-transplantation of mesenchymal stem cells attenuates hepatic injury through IL1Ra dependent macrophage switch in a mouse model of liver disease” [J Hepatol 2015;63:1405–1412]
Authors: Kuei-Chuan Lee, Han-Chieh Lin, Yi-Hsiang Huang, Shih-Chieh Hung
Journal: Journal of Hepatology (2016)
최신 연구 소개 : 활성화된 간 성상세포에서의 TRAIL receptor- 2 발현 증가 및 TRAIL 유도 세포사멸 항진
Authors: 곽금연 ( Geun Youn Gwok ), 윤정환 ( Jung Hwan Yoon )
Journal: Clinical and Molecular Hepatology (2003)

요약: 최근 간섬유화의 resolution phase에서 활성화된 간 성상세포(hepatic stellate cell)의 수가 줄어드는 기전으로 세포사멸(apoptosis)가 중요한 역할을 담당함이 알려지고 있다. 이러한 사실은 활성화된 간 성상세포가 휴지기에 있을 때보다 세포사멸을 일으키는 자극에 더 민감하다는 것을 암시한다. 이미 다른 종류의 세포들이 휴지 상태보다 활성화된 상태에서 TRAIL (tumor necrosis factor-related apoptosis-inducing ligand)에 의한 세포사멸에 더 민감하다는 사실이 알려진 바 있기 때문에 본 연구자들은 이번 연구에서 점진적인 활성화 단계를 거치는 간 성상세포에서 단계별 TRAIL 사망 수용체(death receptor)의 발현과 TRAIL에 의한 세포 독성에 대한 민감도를 밝히고자 하였다. 자연적으로 불멸화된 인간 간 성상세포주인 LX-2 세포를 14일간 플라스틱 용기에서 배양하며 분석한 결과, 14일 후 간 성상세포 활성화의 지표인 α-smooth muscle actin (α-SMA)과 β-crystalline의 messenger RNA (mRNA)의 양이 각각 7배와 5배 증가하였으며, 같은 기간동안 TRAIL-R1/DR4와 TRAIL-R2/DR5 mRNA 발현은 각각 18배와 17.6배 증가하였다. 양적으로 보았을 때에는 TRAIL-R2/DR5의 발현이 TRAIL-R1/ DR4보다 103배 높았다. 아울러 TRAIL-R2/DR5 단백 발현과 TRAIL 유도 세포사멸에 대한 민감플라스틱 용기에서 활성화 과정을 거치는 동안 도에서도 동일한 양상의 변화가 관찰되었으며, 설치류의 간으로부터 일차배양한 간 성상세포 역시 유사한 변화를 보였다. 결론적으로 간 성상세포는 활성화되어감에 따라 TRAIL-R2/DR5 발현이 증가하고 TRAIL 유도 세포사멸에 민감해짐을 알 수 있었다. 따라서 임상적으로 TRAIL-R2/DR5 agonist가 생체 내에서 선택적으로 간 성상세포의 세포사멸을 유도하여 간섬유화를 줄이는데 유용하게 이용될 수 있을 것으로 기대된다. 해설: 간 성상세포는 비타민 A 대사에 관여하며 Disse강에 있을 때에는 대부분 비활성화 상태를 유지하지만 적절한 자극을 받게 되면 활성화된다. 이러한 세포 활성화에 따르는 간 성상세포의 기능 변화는 T-세포나 수지상 세포(dendritic cell)의 경우와 유사하여 세포가 활성화됨에 따라 사망 수용체 매개 세포사멸의 민감도가 증가하게 된다. 실제로 갓 배양한 간 성상세포에서는 Fas 매개 세포사멸이 잘 일어나지 않는 반면, 이들 세포가 활성화되면 Fas를 발현하게 되고 Fas 매개 세포사멸에 민감해진다는 보고가 있었으나,1 이러한 현상은 이후 다른 연구에서는 재현되지 못하였다.2 한편, 최근에 보고된 간 성상세포에서의 TRAIL 신호 전달에 대한 연구에 의하면, 상기한 바와 같이 사람 간 성상세포주에서 세포가 활성화됨에 따라 TRAIL-R2 단백 발현이 증가되고 이와 함께 TRAIL 매개 세포사멸에 대한 민감도도 증가된다는 것이 증명되었다.3 이와 같이 TRAIL을 이용하여 선택적으로 활성화된 간 성상세포에만 국한하여 세포사멸을 유도할 수 있다면 이는 이상적인 항 섬유화 치료 전략이 될 것이다. 단, TRAIL을 임상적으로 생체 내에서 이용할 수 있으려면 TRAIL이 간세포의 세포사멸을 일으키지 않아야 한다는 전제 조건을만족시켜야 한다. 일찍이 간세포에서는 사망 수용체인 Fas, TNF-R1 뿐만 아니라 TRAIL-R1/ R2도 발현된다는 사실이 알려졌다.4 Fas와 TNF- R1에 의한 간세포사멸은 agonistic anti-Fas antibody 및 TNF-α에 의해 유도되는 간독성에 관한 연구에서 잘 밝혀져 있으나,5,6 TRAIL에 의한 간세포사멸에는 아직까지 논란의 여지가 있다. 이와 관련된 몇가지 연구를 살펴보면, trimerizing leucine zipper에 결합시킨 유전자 재조합 TRAIL 리간드는 생쥐에서 간독성을 일으키지 않는 반면,7 polyhistidine을 붙인 유전자 재조합 TRAIL 리간드는 일차 배양한 사람 간세포에서 세포사멸을 일으키는 것이 알려졌다.8 하지만 간세포를 일차 배양하였을 때 역분화(dedifferentiation)가 빠르게 나타나는 점을 감안한다면 이러한 실험 결과를 생체에 적용시키기에는 무리가 있으며, 또한 TRAIL에 관련된 이러한 서로 상충되는 실험 결과가 재조합 TRAIL 제형의 차이에 의한 것일 수도 있다. 한편, 사람의 간세포에서는 TRAIL-R1과 TRAIL-R2의 mRNA가 모두 발현되지만 실제로 간세포 표면에 발현되는 TRAIL-R2 양은 매우 적으며, TRAIL-R2에 특이적인 agonist가 일차 배양한 사람의 간세포에서 세포사멸을 일으키지 못하였다는 보고도 있어,9 아직까지 간세포의 세포사멸 과정에 있어서 TRAIL을 통한 세포사멸 신호 전달은 Fas나 TNF-α를 통한 신호 전달에 비해 그 중요성이 떨어질 것으로 생각된다. 따라서 이론적으로는 TRAIL-R2 자극 물질 투여가 간세포에는 별다른 영향 없이 활성화된 간 성상세포에서만 선택적으로 세포사멸을 유도하여 간 섬유화 치료에 유용하게 이용될 수 있을 것으로 기대된다. 다
Abstract 9602: Cystathionine ?-lyase/hydrogen Sulfide Metabolism Regulates Endothelial Progenitor Cell Mediated Vasculogenesis During Ischemic Vascular Remodeling
Authors: Gopi K Kolluru, Shyamal C Bir, Xinggui Shen, John W Elrod, Rui Wang, David Lefer, Christopher G Kevil
Journal: Circulation (2013)

Introduction: H2S is a gaseous signaling molecule primarily produced in the vasculature by Cystathionine γ-lyase (CGL/CSE) enzyme, that regulates many biological functions including vasodilation, anti-inflammation, cytoprotection and angiogenesis. CSE genetic deficiency and subsequent reduction in H2S levels attenuates ischemic vascular remodeling. However, effects of CSE/H2S in relation to vasculogenesis have not been investigated. Objective: To investigate the effect of endothelial specific CSE (EC-CSE) transgenic overexpression in restoring blood flow and vasculogenesis in the ischemic hind limb model. Methods: Unilateral femoral artery ligation was performed in wild type (WT), CSE-/- and EC-CSE mice, treated with PBS or H2S donor, DATS (n=8-10, in each group). Tissue angiogenic and proliferation indices were determined by the ratios of CD31/DAPI and Ki67/DAPI staining respectively. Expression of CSE and SDF-1 in the ischemic and non-ischemic limbs was determined by immunohistochemistry; CSE and HIF-1α were measured by qRT-PCR; and ELISA to measure VEGF levels. Plasma and tissue sulfide levels were measured using the MBB/HPLC method. Flow cytometry was used to analyze bone marrow-derived, blood and skeletal muscle EPCs positive for CD34/FLK-1 staining. Results: Ischemic hind limb perfusion was significantly impaired in CSE-/- compared to WT mice, while blood flow was restored in DATS treated cohort groups and EC-CSE transgenic mice by day 14. Angiogenic and proliferation indices were decreased in CSE-/- mice, and restored by DATS treatment and in EC-CSE transgenic mice. These findings corresponded with significantly increased circulating EPCs at days 3, 5 and 7 upon DATS treatment and EC-CSE transgenic overexpression. Lastly, we observed that CSE/H2S induces EPC recruitment via SDF-1/VEGF mediated pathways that augments vasculogenesis and restoration of ischemic hind limb blood flow. Conclusion: Endothelial specific overexpression of CSE (EC-CSE) and exogenous H2S delivery reversed impaired blood flow in CSE-/- mice through EPC mediated revascularization during hind limb ischemia. Modulation of CSE mediated H2S induced revascularization might serve as a novel therapeutic approach for ischemic vascular remodeling.
Tumor efficacy of an oncolytic herpes simplex virus (NV1020) in patients with colorectal cancer metastatic to liver (mCRC)
Authors: R. S. Chari, S. S. Gambhir, S. Geevarghese, D. A. Geller, A. Iagaru, A. Mescheder, J. J. Nemunaitis, T. R. Reid, D. Y. Sze, K. Tanabe
Journal: Journal of Clinical Oncology (2008)

15014 Background: Dose-finding safety results are published for NV1020, a genetically engineered oncolytic Herpes simplex virus. Except for transient (<24 hr) viral syndrome no serious, or significant Grade 3/4, related toxicity was found. Using the optimal biological dose, tumor response data are now reported. Methods: Patients with measurable liver metastases from CRC relapsing after extensive chemotherapy received 4 doses of NV1020 (1 X108 pfu) by weekly hepatic artery infusion, followed by two more cycles of chemotherapy in a Phase 2 study. Follow-up involved scans every 3 months for 1 year (tumor response) and telephone calls thereafter (survival). Separate, blinded, independent radiologists interpreted CT (RECIST) and PET (EORTC) scans. Data were available to Dec 3, 2007. Results: 22 patients enrolled;1 was excluded (no liver mets). 100% had prior 5FU-based treatment; in addition 86% had oxaliplatin, 58% irinotecan, 43% both agents; 52% also had single targeted therapy, 24% ≥2 such agents. Mean time from primary resection was 95 (range: 26 - 223) weeks, mean CEA was 213 (range: 2 - 958) ng/mL, 52% had pulmonary lesions. After NV1020 9/18 (50%) and 7/17 (41%) showed stable disease (SD) on CT and PET, respectively. After 2 cycles of further chemotherapy (33% repeated prior drugs), CT showed 6/12 (50%) SD, PET 6/11 (55%) SD and 3/11 (27%) partial regression (PR). Clinical, CEA and KPS outcomes were concordant with scan findings. Kaplan-Meier analyses showed a median time to progression of 26 weeks (95% CI [14,46]) and median survival probability of 51 weeks (95% CI [30,65]). Conclusions: NV1020 stabilizes liver metastases in heavily pretreated mCRC. Relative to historical data, it may improve tumor response to salvage chemotherapy and extend overall survival. Considering also lack of toxicity, controlled clinical trials with NV1020 are justified. Author Disclosure Employment or Leadership Consultant or Advisory Role Stock Ownership Honoraria Research Expert Testimony Other Remuneration MediGene AG MediGene Inc
Ifosfamide and mitoxantrone as first-line chemotherapy for metastatic breast cancer.
Authors: J E Perez, M Machiavelli, B A Leone, A Romero, M G Rabinovich, C T Vallejo, A Bianco, J A Lacava, R Rodriguez, M A Cuevas
Journal: Journal of Clinical Oncology (1993)

PURPOSE A phase II trial was performed to evaluate the efficacy and toxicity of a combination of ifosfamide (IFX) and mitoxantrone (MXN) as first-line chemotherapy for metastatic breast carcinoma. PATIENTS AND METHODS Between January 1990 and August 1991, 48 patients with metastatic breast cancer were entered onto the study. Therapy consisted of IFX 2 g/m2 given as a 1-hour intravenous (IV) infusion on days 1 to 3; mesna 400 mg/m2 as an IV bolus immediately before and 4 hours after IFX administration and 2,000 mg orally 8 hours after IFX administration on days 1 to 3; and MXN 12 mg/m2 as an i.v. bolus on day 3. Cycles were repeated every 21 days until progressive disease (PD) or severe toxicity developed. RESULTS One patient was considered not assessable for response. Objective regression (OR) was observed in 28 of 47 patients (60%; 95% confidence interval, 46% to 74%). Six patients (13%) had a complete response (CR) and 22 (47%) had a partial response (PR). The median time to treatment failure for the whole group was 9 months (range, 1 to 28); median survival was 19 months (range, 2 to 28). There were no treatment-related deaths. The limiting toxicity was myelosuppression. Leukopenia occurred in 37 patients (77%) and was grade 3 or 4 in 19 patients (40%). Nausea and vomiting were observed in 38 patients (80%), mucositis in 16 patients (33%), and grade 2 hematuria in two patients (4%). Eight patients (16%) developed mild neurotoxicity. CONCLUSION The combination of IFX plus MXN is an active regimen against metastatic breast cancer with moderate toxicity that deserves further evaluation.
Weekly administration of gemcitabine plus docetaxel in advanced non-small cell lung cancer (NSCLC)
Authors: Y. Sun, J. Li, Y. Wu, L. Li, L. Gu, L. Zhang, J. Wang, X. Zhang
Journal: Journal of Clinical Oncology (2004)

7328 Background: Gemcitabine and docetaxel are both active and well tolerated in NSCLC treatment. Preliminary data with weekly schedules of gemcitabine combined docetaxel regimen showed the efficacy was well maintained but risk of neutropenia was reduced. This study was conducted to evaluate the efficacy, including response rate and median survival time, and toxicities of weekly administration of gemcitabine combined with docetaxel in Chinese patients with advanced NSCLC. Methods: Patients with histological confirmed stage IIIB/IV NSCLC, presented measurable and evaluable diseases were eligible for this study. Gemcitabine was given 800-1200mg/m2 by intravenous infusion on day 1, 8, 15 of a 28-day cycle. Docetaxel was 35mg/m2 i.v. the same day following with gemcitabine. No prophylactic use of G-CSF was allowed. CTC criteria were used to grade toxicities and WHO response criteria was used to assess response rate in this study. Results: From January 2000 to May 2001, 26 patients were enrolled (11 chemo-naive, 15 patients pre-treated at least one platinum-based chemotherapy regimen). Average 3 cycles per patient were administrated. 1 patient achieved a complete response (CR, 3.8%), and 6 patients were partial response (PR, 23.1%), overall response rate was 26.9%, but in chemo-naïve NSCLC patients 45% overall response rate was achieved. Median survival was 9.5 months and 1-year survival rate was 38%. The main toxicities were hematological toxicties, includes Grade 4 neutropenia in one patient (3.8%), Grade III/IV thrombocytopenia in 5 patients (19%). 1 patient died from allergic shock. Non-hematological toxicities were mild and manageable. Conclusions: Gemcitabine combined docetaxel is an active and well-tolerated regimen for patients with advanced NSCLC. . No significant financial relationships to disclose.
An early origin of plastids within the cyanobacterial divergence is suggested by evolutionary trees based on complete 16S rRNA sequences.
Authors: B Nelissen, Y Van de Peer, A Wilmotte, R De Wachter
Journal: Molecular Biology and Evolution (1995)

It is generally accepted that the plastids arose from a cyanobacterial ancestor, but the exact phylogenetic relationships between cyanobacteria and plastids are still controversial. Most studies based on partial 16S rRNA sequences suggested a relatively late origin of plastids within the cyanobacterial divergence. In order to clarify the exact relationship and divergence order of cyanobacteria and plastids, we studied their phylogeny on the basis of nearly complete 16S rRNA gene sequences. The data set comprised 15 strains of cyanobacteria from different morphological groups, 1 prochlorophyte, and plastids belonging to 8 species of plants and 12 species of diverse algae. This set included three cyanobacterial sequences determined in this study. This is the most comprehensive set of complete cyanobacterial and plastidial 16S rRNA sequences used so far. Phylogenetic trees were constructed using neighbor joining and maximum parsimony, and the reliability of the tree topologies was tested by different methods. Our results suggest an early origin of plastids within the cyanobacterial divergence, preceded only by the divergence of two cyanobacterial genera, Gloeobacter and Pseudanabaena.
Evaluation of soluble B7x as a serum marker in patients with clear cell renal cell carcinoma
Authors: R. H. Thompson, X. Zang, C. M. Lohse, B. C. Leibovich, S. F. Slovin, V. E. Reuter, M. L. Blute, P. Russo, E. D. Kwon, J. P. Allison
Journal: Journal of Clinical Oncology (2008)

5052 Background: Discovered in 2003, B7x is the newest member of the B7-CD28 family and is thought to dampen immune responses via negative costimulation. Tumor expression of B7x was recently described in renal cell carcinoma (RCC) and was associated with poor outcome. We developed an assay to detect serum soluble B7x (sB7x) and investigated patients with RCC. Methods: We identified 101 patients who underwent nephrectomy for clear cell RCC between 2003 and 2007 and had preoperative serum available. Enzyme- linked immunosorbent assay for sB7x was then performed with a minimum detection level of 0.1ng/ml. We also obtained serum from 101 sex- matched blood donors within the same age range who served as controls. Results: Detectable levels of sB7x were present in 53 RCC patients compared with 18 controls (p<0.001) with median (range) concentrations of 14.4ng/ml (0.1–56.9) and 2.7ng/ml (0.2–37.1), respectively. Among the RCC patients, no significant clinical, laboratory, or pathologic associations were observed between patients positive versus negative for sB7x. However, among RCC patients with detectable sB7x, median levels were significantly higher for patients with a tumor thrombus (19.2 vs 6.6ng/ml; p=0.007), positive lymph nodes (41.3 vs 10.3ng/ml; p=0.018), and distant metastases at nephrectomy (43.3 vs 8.5ng/ml; p=0.002). Additionally, median sB7x levels for TNM stage I-IV RCC were 6.6, 10.3, 14.5, and 43.3ng/ml, respectively (p=0.012). Conclusions: In this first evaluation of sB7x in RCC, we demonstrate that RCC patients are more likely to have detectable sB7x compared with controls and higher sB7x levels are associated with advanced tumor stage. These early results warrant further investigation of this serum marker for potential diagnostic and prognostic purposes. No significant financial relationships to disclose.
Are trends in recruitment of older patients in clinical trials (CT) changing?
Authors: M. Garcia, X. Perez, J. Saldaña, F. Cardenal, J. R. Germà
Journal: Journal of Clinical Oncology (2006)

16007 Background: It has been widely reported that older patients are underrepresented in CT. This barrier has been extensively studied and some efforts have been made to increase older patient participation. This study was performed to characterize and evaluate the enrolment of elderly patients in CT in a cancer centre (Barcelona, Spain). Methods: A database-based analysis of patients entered in CT of any cancer type in a single institution between 1998 and 2005 was performed. (1) During the first 6-month period in 2005 we selected opened age-unspecified trials (AUT). Rates of patients of 74 Y entered in those trials (between 2001–2005) were analysed and compared with the corresponding rates on target population (new patients seen in Oncology Department in the first 6-month period in 2005). (2) Averages of age of CT patients in two periods of time: 1998–1999 and 2004–2005 were compared. Chi-squared and T-student analyses were used. Results: 2029 patients were entered in CT between 1998–2005. There were 1006 FTSP patients during the first 6-month period of 2005. The number of patients entered in AUT (19 trials among 71 opened [27%]) between 2001–2005 was 277. Table 1 summarizes the data by age groups. Statistically significant differences were found only between &gt;74 y patients in CT and FTSP populations. Average age was 57.4 during 1998–1999, and 60.5 during 2004–2005 (p: 0.004). Conclusions: The number of patients &gt;74 Y accrued in CT in a single cancer centre has clearly increased over time, maybe due to the rise of life expectancy, better patient care and the efforts in improving recruitment rates. In spite of the increase, this patient population remains underrepresented in general cancer CT. [Table: see text] No significant financial relationships to disclose.
Immunophenotyping of solid tumors, a new approach for molecular profiling solid tumors
Authors: R. Nunez, J. Magenau, S. Zamorano, A. Lostumbo, D. Mehta
Journal: Journal of Clinical Oncology (2006)

10057 Methods of determining prognosis in breast, ovary, and colon cancer includes detection of molecular markers such as the estrogen receptor (ER), progesterone receptor (PR), and HER-2/neu. These markers are routinely assessed via immunohistochemistry (IHC) and Fluorescent In-situ hybridization (FISH). Flow cytometry (FC) has not yet been established for routine detection of these markers in tumors. We performed FC on cells from fourteen ovary, five breast, and four colon cancer tumors. FC was used to detect the presence of ER, PR, HER-2/neu, Epidermal Growth Factor Receptor (EGFR), E-cadherin, RAS, ERK and TUJ1. Cells obtained directly from tumoral tissue were simultaneous analysized by cell cycle stage (G0, G2M, and &gt; G2M) and presence of antigenic markers. In ovarian tumors, 7 of 14 samples demonstrated &gt;50% of cells with her-2/neu expression in aneuploid fractions (&gt;G2M), 9 of 14 in G2M phase, and only 2 of 14 in G0 phase. With respect to ER, 7 of 14 ovarian tumors exhibited &gt;19% of cells in G2M and &gt;G2M fractions, while only 1 of 14 samples had &gt;19% at G0. The PR receptor was expressed in &gt;19% of cells in 8 of 14 (&gt;G2M), 7 of 14 (G2M), and 2 of 14 (G0). In breast tumors, 4 of 5 tumors demonstrated &gt;50% expression of HER-2/neu in G2M and &gt;G2M cell phases, and only 2 of 5 demonstrated &gt;50% her2neu expression in G0. Three of five tumors had &gt;19% cellular expression of ER in the &gt;G2M and G2M phases, while only one had &gt;19% in G0. With PR, 3 of 5 breast tumors had &gt;19% cellular expression in G0, G2M, and &gt;G2M phases. In colon tumors, 2 of 4 had &gt;50% cellular expression of her2neu in &gt;G2M fractions, 4 of 4 in G2M, and only 1 of 4 in G0. Interestingly, cell fractions containing G2M and &gt; G2M DNA had &gt; 50% cellular expression for RAS and ERK in 2 of 4 colon tumors. No colon tumors expressed RAS and ERK significantly in G0 cells. We found that ER, PR, and HER-2/neu marker expression were consistent with established expression patterns. Additionally, these data point to specific expression patterns that are associated with the cell cycle stage. In particular, we note high expression levels of Her-2/nue, ER, and PR in aneuploid (&gt;G2M) cell populations. These results suggest that patterns of differential expression can be readily assessed in tumor tissues using flow cytometry, and has the potential for broad application to the study of solid tumors. No significant financial relationships to disclose.