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PubMed2004

Effects of toremifene (TOR) and tamoxifen (TAM) on serum lipids in postmenopausal patients with breast cancer.

This study clarified the difference in the effects on serum lipids between toremifene (TOR) and tamoxifen (TAM). To remove influencing factors, we investigated adjuvant therapy for hormone receptor-positive patients with breast cancer without lymph node metastasis. The subjects were 65 patients who were enrolled in a multicenter randomized comparative study between April 1997 and March 2001. As adjuvant therapy, 20 mg of TAM or 40 mg of TOR was administered for 1 year. The levels of triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein A-1 (Apo A-1), apolipoprotein A(Apo B), and lipoprotein a (Lp(a)) were measured prior to administration and 3, 6, and 12 months after the start of administration. TC, LDL-C, Lp(a) and Apo B significantly decreased from the third month of administration compared with values before the start of administration in both the TOR and TAM groups. HDL-C significantly increased from the third month only in the TOR group. TG significantly increased in the TAM group but significantly decreased in the TOR group in the 12th month of administration. When these two groups were compared, HDL-C was significantly higher (p < 0.01) and TG was significantly lower (p < 0.01) in the TOR group in the 12th month. Improvement of abnormal values of TG, HDL-C and LDL-C was better in the TOR group than in the TAM group after administration for 12 months. The effect on lipid metabolism showed different profiles between the two selective estrogen receptor modulators (SERMs), and TOR gave better results than TAM.

Adult↗
PubMedDate not supplied

Keratinocyte growth factor (KGF) induces tamoxifen (Tam) resistance in human breast cancer MCF-7 cells.

BACKGROUND: Both estrogen receptor-alpha (ER-alpha) and progesterone receptor (PR) are good prognostic factors and indicators of benefit from endocrine therapy in breast cancer patients. The relationship of the ER-alpha and PR status and the difference in clinical benefit from endocrine therapy in breast cancer is currently unclear. It has been suggested that keratinocyte growth factors (KGFs) are important regulatory factors in breast cancer. Our laboratory has demonstrated that KGF can act as an estromedin for the stimulation of breast cancer cell growth. Also, KGF stimulates aromatase activity in primary cultured human breast cells. This enzyme is a key to the conversion of androgens to estrogens. In the present study, ER-alpha, two estrogen-regulated genes, PR and PTPgamma, KGF and their relationship with endocrine resistance in human breast cancer cells were investigated. MATERIALS AND METHODS: MCF-7 cells were treated with KGF (1, 5, 10, 20 ng/ml), KGF-13 (0.1, 1, 10 microM) or vehicles as control for 24 hours. KGF-13 is a potential receptor-binding pentapeptide constructed using the KGF peptide residues 101-105 (RTVAV) as a template, located within the beta 4--beta 5 loop. Total RNA were isolated and real-time PCR was employed to identify ER-alpha, PR and PTPgamma gene expressions in response to KGF and KGF-13. Western blot analysis was used to verify the levels of ER-alpha and PR protein, whereas immunohistochemical staining was used to detect PTPgamma expression in MCF-7 cells. To determine the response of MCF-7 cells to endocrine therapy, MCF-7 was treated with either 20 ng/ml KGF or 10 microM KGF-13 combined with 1, 3 and 5 microM of 4-hydroxytamoxifen (4OH-Tam). A non-radioactive cell proliferation assay was applied to determine the growth rate of MCF-7 cells. The results of real-time PCR and the cell proliferation assay were analyzed by Student's t-test and p-values of less than 0.05 were considered statistically significant. RESULTS: Our data showed that KGF significantly suppressed ER-alpha, PR and PTPgamma expression in MCF-7 cells. KGF suppressed ER-alpha, PR and PTPgamma mRNA to a maximal inhibition at 20 ng/ml by 88%, 57% and 61%, respectively. Western blot analysis and immunohistochemical staining confirmed the down-regulation of ER-alpha, PR and PTPgamma by KGF in protein levels. Ten microM KGF-13 also decreased ER-alpha expression. Ten microM KGF-13 significantly decreased ER-alpha, PR and PTPgamma mRNA expressions by 51%, 57% and 67%, respectively. These KGF-13-mediated mRNA down-regulations were also observed in protein levels. In a cell proliferation assay, 4OH-Tam (3, 5 microM) induced MCF-7 cell death. KGF and KGF-13 alone did not stimulate MCF-7 cell growth. KGF significantly disrupted 4OH-Tam cell killing effects by 1.2- and 1.3-fold at 4OH-Tam concentrations of 3 microM and 5 microM, respectively. KGF-13 significantly disrupted 4OH-Tam cell killing effects by 1.2- and 1.7-fold at 4OH-Tam concentrations of 3 microM and 5 microM, respectively. CONCLUSION: Our results suggested that not only ER-alpha and PR but also PTPgamma could be potential bio-makers for growth factor-induced endocrine resistant in breast cancer. KGF might increase the endocrine resistance via decreasing ER-alpha, PR and PTPgamma as well. Moreover, the functional analysis of KGF-13 implied possible applications of using short receptor-binding peptides derived from intact KGF as breast cancer therapeutic agents. Thus, our experimental data provided evidence of KGF-induced anti-hormone resistance in human breast cancer and suggested novel strategies for breast cancer via interference with KGF signaling.

Antineoplastic Agents, Hormonal↗
PubMed2004

Truncated thioredoxin (Trx80) induces differentiation of human CD14+ monocytes into a novel cell type (TAMs) via activation of the MAP kinases p38, ERK, and JNK.

Thioredoxin truncated at its carboxy terminal (Trx80) acts as a cytokine that stimulates monocytes and eosinophils. In the present study, Trx80 was shown to induce differentiation of human CD14(+) monocytes into a cell type not described previously, which we designate as Trx80-activated monocytes (TAMs). TAMs resemble immature dendritic cells (iDCs) generated in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin 4 (IL-4) in that both these cell populations exhibit increased proportions of CD1a(+) and mannose receptor (MR)(+) cells. However, in contrast to iDCs, TAMs express high proportion of CD14 and lower proportion of CD83 and HLA-DR. Functional assays revealed that, in comparison to iDCs, TAMs 1) exhibit a higher pinocytic capacity; 2) release significantly higher amounts of the proinflammatory cytokines tumor necrosis factor-alpha (TNF alpha), IL-1 beta, and IL-6 and of the anti-inflammatory cytokine IL-10; and 3) induce a significantly lower proliferative response in allogeneic peripheral blood mononuclear cells (PBMCs). Indeed, Trx80 appears to be the first endogenous substance shown to have the capacity on its own to induce IL-10 production by monocytes. Analysis of the mitogen-activated protein (MAP) kinase signaling pathway revealed that Trx80 induces phosphorylation of p38, extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK). We propose that Trx80 is an early signal in response to danger, and that TAMs may play a major role in triggering innate immune responses.

Cell Differentiation↗
PubMed2002

Establishment of immortalized ameloblastoma cell line TAM-1.

OBJECTIVE: To establish an immortalized ameloblastoma cell line. METHODS: The primary cultured ameloblastoma cells were transfected with pRSV-Tag using Transfect AMINE kit. Tansfected cells were passaged to pass through crisis period and immortalize. RESULTS: Cultured ameloblastoma cells were composed predominantly of closely packed small polygonal cells with epithelial morphology. They had limited life-span of 51 days in vitro. The small polygonal cells were eventually replaced by large flattened cells and subsequently became senescent and dead. On the other side, those tumor cells transfected with SV40Tag could live for a longer time. The majority of them died in crisis period while the survived cells from crisis period gained the ability to proliferate. There was no morphological change in TAM-1 compared with original cultured cells. A cell clone was harvested which was alive and keeping on proliferating after having been subcultured for 25 times. It was named TAM-1. The epithelial origin of TAM-1 was confirmed by strong immunoreactivity for cytokeratin in contrast to negative vimentin expression. It was detected that SV40Tag had been transfected into TAM-1 genesome and expressed continuously by PCR and RT-PCR. CONCLUSIONS: TAM-1 is immortalized ameloblastoma cell line in vitro.

Ameloblastoma↗
PubMedDate not supplied

K65R, TAMs and tenofovir.

The management of drug resistance has become part of the management of HIV disease in the treated individual. As two or more nucleoside reverse transcriptase inhibitors (NRTIs) are generally part of each antiretroviral regimen, there is a need to fully understand resistance and cross-resistance within this class of drugs. Broad cross-resistance to NRTIs caused by the group of HIV RT mutations associated with zidovudine and stavudine therapy (thymidine analogue mutations or TAMs) has been well established. The response to tenofovir disoproxil fumarate (TDF) therapy is also limited by certain patterns of TAMs (> or = 3 TAMs with M41L or L210W). The K65R mutation can result from tenofovir DF, abacavir, stavudine, zalcitabine or didanosine therapy. From in vitro phenotypic analysis, the K65R mutation shows no cross-resistance to zidovudine, but low-level resistance to tenofovir and the other NRTIs. Based on clinical cut-offs established for the individual NRTIs, the phenotypic results with K65R suggest full-to-partial drug activity for multiple NRTIs, including tenofovir, against the K65R mutant. Similar to the M184V mutation, the K65R mutation is also associated with reduced in vitro viral replication capacity, hallmarks of which can be demonstrated at the enzymatic level. From cross-sectional genotypic analyses, the K65R mutation and TAMs appear to represent separate patterns of NRTI resistance. Among treatment-naive patients who developed the K65R mutation in clinical trials, successful second line regimens were established. Thus, the K65R mutation appears manageable for the sequencing of treatment regimens in the case of its development.

Adenine↗
PubMed2005

[Prognostic value of serum markers for liver fibrosis in transient abnormal myelopoiesis (TAM)].

Transient abnormal myelopoiesis (TAM) is usually a self-limiting myeloproliferative disorder observed in approximately 10% of newborn infants with Down syndrome. However, progressive liver fibrosis may occur in patients with TAM and is often lethal. We investigated the utility of the serum levels of hyaluronic acid (HA) and N-terminal peptide of III procollagen (P-III-P) as markers of liver fibrosis and indication for chemotherapy. We reviewed 4 cases of TAM retrospectively. HA levels were more than one hundred times as high as the upper limit of the normal range in 2 patients, one of whom died from gastrointestinal bleeding. His HA and P-III-P had increased up to 18,800 U/ml and 26.2 ng/ml, respectively, just before he died. Another patient's serum HA and P-III-P increased to 6,100 U/ml and 12.8 ng/ml, respectively, however his liver fibrosis resolved with low-dose cytosine arabinoside treatment after exchange transfusion during his clinical course. We suggest that serum HA is useful as a marker of liver fibrosis and a prognostic indicator for chemotherapy in patients with TAM. Early treatment including both exchange transfusion and chemotherapy should be considered for patients presenting with extremely high or an elevating tendency of their HA serum levels.

Biomarkers↗
PubMed2006

Tamoxifen (TAM): the dispute goes on.

Tamoxifen (TAM) has been used since early '70s as antitumor agent in the adjuvant therapy of breast carcinoma. The aim was (and is) to reduce the incidence of contralateral breast cancer in primary breast cancer bearing patients. Its efficacy was about 30% when estrogen and progesterone receptors were present in the malignant breast tumor and its use in antitumor therapy is, at the present time, rather correct. Viceversa, the employment of TAM in chemoprevention of breast tumor in healthy and/or at-risk women by more than a decade has been contrasting by many scientists and supporting by others. Indeed, TAM produces not only beneficial effects but also detrimental effects (mainly induction of endometrial cancer). According to the Author of this manuscript, TAM would not be used for primary or secondary mammary tumor chemoprevention. For such purposes the right way is to wait for conclusion of ongoing clinical trials on other pure antiestrogenic agents. Indeed, good candidates to act as an antiestrogen both in breast and in endometrial tissue are under validation. In the meanwhile, the scientific dispute goes on.

Animals↗
PubMed1979

TAM selection of Drosophila somatic cell hybrids.

The selection of MDR3, an adenine-salvage-deficient variant of the Kc line, is described. It is resistant to methylpurine and to diaminopurine and is TAM (thymidine, adenine, methotrexate) sensitive. Two wild-type (TAM-resistant) cell lines, Schneider's line 3 (S3) and Dübendorfer's line 1 (D1), due to their different nutritional requirements, are unable to proliferate in medium ZH1% used for line MDR3. This allowed the selection of hybrids between MDR3 and either D1 or S3 in TAM cloning medium after treatment with polyethyleneglycol. Hybrids were identified by the isoenzyme pattern of NADP-dependent isocitrate dehydrogenase.

Adenine↗
PubMed2026

Pan-cancer analysis identifies APOC1 as a TAM-derived modulator of adaptive immune resistance and predictor of therapeutic response.

BACKGROUND: Apolipoprotein C1 (APOC1) has been implicated in several malignancies, yet its expression patterns, clinical significance, and immunomodulatory roles across cancer types remain poorly characterized. METHODS: We performed a comprehensive multi-omic analysis of APOC1 across 33 cancer types integrating transcriptomic, proteomic, genomic, epigenomic, and pharmacogenomic data from TCGA, GTEx, CPTAC, and multiple independent external cohorts. Immune infiltration was assessed using seven complementary algorithms. Spatial transcriptomics and single-cell RNA sequencing were employed to determine the cellular source of APOC1 expression. RESULTS: APOC1 upregulation in most cancers was associated with cancer type-specific prognosis. After adjustment for clinical covariates and macrophage infiltration, high APOC1 remained an independent adverse factor in KIRC, LGG, and STAD. APOC1 expression positively correlated with genomic instability hallmarks, including homologous recombination deficiency and aneuploidy, with these associations largely independent of immune infiltration; in contrast, associations with tumor mutational burden were substantially confounded by macrophage abundance. Immune infiltration analysis revealed a pattern consistent with adaptive immune resistance: APOC1 correlated positively with immune-activating signatures (STAT1, MHC-II, TCR signaling) and immunosuppressive M2 macrophages and Tregs, yet negatively with anti-tumor effectors (activated NK cells, dendritic cells). Spatial transcriptomics and single-cell RNA sequencing identified tumor-associated macrophages (TAMs) as the primary cellular source of APOC1, with transcripts co-localizing with CD68 in tissue sections. APOC1 expression correlated with multiple immune checkpoint molecules and was elevated in responders to immune checkpoint blockade, consistent with an inflamed yet regulated tumor microenvironment. Pharmacogenomic analyses revealed that APOC1-high tumors display distinct drug response profiles, characterized by resistance to MAPK pathway inhibitors and potential sensitivity to the HDAC inhibitor Entinostat. CONCLUSION: This pan-cancer analysis establishes APOC1 as a context-dependent biomarker and a TAM-derived modulator of adaptive immune resistance, with prognostic and therapeutic implications across malignancies. APOC1-expressing TAMs represent a potential target for combination immunotherapy strategies.

APOC1↗
PubMed2006

TAM receptor function in the retinal pigment epithelium.

The TAM receptor tyrosine kinase Mer is expressed by cells of the retinal pigment epithelium (RPE), and genetic studies have demonstrated that Mer is essential for RPE function. RPE cells that lack Mer exhibit a severely compromised ability to phagocytose the distal ends of photoreceptor (PR) outer segments, which leads to the complete postnatal degeneration of photoreceptors and to blindness. Although in vitro experiments have implicated Gas6 as the critical TAM ligand for this process, we find that Gas6 mutant mice have a histologically intact retina with no photoreceptor degeneration. We further find that, in addition to Mer, RPE cells also express another TAM receptor--Tyro 3--and that both of these receptors are instead activated independently by the Gas6-related ligand Protein S. This protein is also expressed by RPE cells. Finally, we demonstrate that loss of Mer function is accompanied by a substantial down-regulation in Tyro 3 as well. These observations indicate that both Mer and Tyro 3 act in mouse RPE cells and suggest that their biologically relevant ligand in these cells is Protein S.

Animals↗
PubMed1995

F2(Pmp)2-TAM zeta 3, a novel competitive inhibitor of the binding of ZAP-70 to the T cell antigen receptor, blocks early T cell signaling.

Signaling by the T cell antigen receptor (TCR) is mediated by 17-residue tyrosine-based activation motifs (TAM) present in the cytoplasmic tails of the TCR zeta and CD3 chains. TAMs become tyrosine-phosphorylated upon TCR stimulation, creating a high affinity binding site for the tandem SH2 domains of ZAP-70. In permeabilized T cells, the association of TCR and ZAP-70 was inhibited by a protein tyrosine phosphatase (PTPase)-resistant TAM peptide analog, in which difluorophosphonomethyl phenylalanyl (F2Pmp) residues replaced phosphotyrosine. Inhibition of this association prevented TCR-stimulated tyrosine phosphorylation of ZAP-70 and reduced ZAP-70 kinase activity to basal levels. The reduction in ZAP-70 activity coincided with reduced tyrosine phosphorylation of a number of substrates. Such PTPase-resistant peptides, capable of disrupting SH2 domain-mediated protein-protein interactions, should prove useful in further dissection of multiple signaling pathways and may serve as models for rationally designed chemotherapeutic agents for the treatment of autoimmune and neoplastic disorders.

Amino Acid Sequence↗
PubMed2000

Qui tam claims: threat to voluntary compliance programs in health care organizations.

The Department of Justice (DOJ) reports that after violent crime, health care fraud is the department's top priority. The number of health care fraud investigations pending at the DOJ increased from 270 cases in 1992 to more than 4,000 in 1997. The DOJ's primary weapon in prosecuting health care fraud is the federal False Claims Act (FCA) of 1863 (31 U.S.C. secs. 3729-3733). Almost unique among federal antifraud provisions, the FCA may also be used by "private prosecutors" to file lawsuits on behalf of the federal government charging organizations with submitting false claims to the government. The FCA rewards such whistle-blowers with a share of any resulting recoveries as a bounty and protects them from discharge for filing false claims lawsuits against their employers. It also requires defendants to pay the costs and attorneys fees of successful claimants. Although the private "bounty hunter" features of the FCA data back to the Civil War, these so-called qui tam claims were nearly dormant until 1986, when Congress amended the FCA to revive their use. Following the 1986 amendments, and paralleling the rapid increase in federal reimbursements for health care costs, private qui tam claims have far expanded beyond their traditional purview of defense contracts into the field of health care. By 1997, health care providers were the targets of 54 percent of the 530 private qui tam lawsuits field that year.

Fraud↗
PubMed1995

Against a role for attentional disengagement in the gap effect: a friendly amendment to Tam and Stelmach (1993).

Saccadic reaction time (RT) is reduced when the fixation point is removed shortly before target onset. Although Tam and Stelmach (1993) argued that this gap effect could not be explained solely by the idea that fixation offset disengaged visual attention and preferred an explanation based on disengagement of the oculomotor system, they felt that they could not rule out a hybrid model in which both oculomotor and attentional disengagement contribute to the gap effect. Our analysis of the dual response experiment (Experiment 4), upon which this hybrid model was based, shows that manual and saccadic responses were likely compromised by a grouping or delay strategy and that subjects may not have been attending as instructed. On these grounds, we argue that Tam and Stelmach (1993), like Kingstone and Klein (1990; 1993a) provide no evidence that attentional disengagement contributes to the gap effect. An alternative proposal (Klein & Kingstone, 1993), that motor preparation and oculomotor disengagement combine additively to produce the gap effect, is consistent with the data from Tam and Stelmach's Experiments 1-3, is similar to the explanation that they prefer, and has been strongly supported when directly tested (Kingstone, Klein, & Taylor, 1994).

Fixation, Ocular↗
PubMed1999

Et Tu, Counselor: may an in-house attorney file a qui tam action against the attorney's employer?

Most corporations probably do not consider their in-house counsel to be potential qui tam threats. That may be a naive assumption. Case law provides an illustrative view of the legal ramifications involved when an attorney brings a qui tam suit. In general, there is no prohibition on attorneys who wish to bring these actions. Nevertheless, a corporation can take preventive steps to eliminate the likelihood of attorney qui tam actions. In addition, the corporation can take advantage of state professional ethics laws to mount a defensive action against the attorney who files any such action.

Confidentiality↗
PubMed2000

Microarthropod community structures (Oribatei and Collembola) in Tam Dao National Park, Vietnam.

A study on the microarthropod community with special reference to species diversity of Oribatid and Collembola communities (Microarthropoda: Oribatei and Collembola) in Tam Dao National Park of Vietnam, a subtropical evergreen broad leaf alpine forest, was undertaken with the aim to explain how they are related to forest decline, and whether they can be used as bioindicators of forest plant succession. The results have shown that microarthropod community structures, particularly species diversity of oribatid and collembolan communities, are related to forest decline. Therefore they can be used as bioindicators of forest plant succession. In Tam Dao National Park, there was an inverse relation between species diversity of the oribatid and Collembola communities. The species diversity of the oribatid community gradually decreased with forest decline whereas the species diversity of the Collembola community gradually increased.

Animals↗
PubMed2007

Polychlorinated biphenyls in sediments of the Tam Giang-Cau Hai Lagoon, Central Vietnam.

The Tam Giang-Cau Hai Lagoon, the largest in south east Asia, suffers from a great anthropogenic pressure and appears subject to a process of progressive environmental deterioration. To establish causes, history and trends of lagoon contamination, sediment samples representing three major parts of the systems were sampled and analysed for porosity, organic carbon, total nitrogen, delta(13)C, grain size, radiotracers and PCBs. PCB surficial concentrations range from 10.2 to 24.5 microg kg(-1), and maximum values are close to NOAA ERL guidelines. The downcore distribution of PCBs shows two well defined peaks in the core from Tam Giang (25.5 and 16.2 microg kg(-1)), whereas the sediment from Cau Hai is characterised by a maximum at the surface. Therefore, present trends indicate that contamination is still increasing or slightly decreasing. The prevailing congeners are 3-CB and 4-CB, hence recent PCBs appear to be mostly originated by Aroclor 1016- and 1242-like mixtures, with some samples influenced also by Aroclor 1248. Present sources seem to be similar everywhere and probably they are widespread all over the territory of the Thua Thien-Hue province.

Cities↗
PubMed2026

Next-generation macrophage engineering in cancer therapy: From TAM reprogramming to CAR-macrophages.

Macrophages are central regulators of the tumor microenvironment (TME), shaping immune suppression, angiogenesis, metabolism, and therapeutic resistance in solid cancers. While early strategies sought to deplete tumor-associated macrophages (TAMs) or block monocyte recruitment, limited efficacy and compensatory mechanisms revealed the need for functional reprogramming rather than elimination. Recent advances in viral vectors, CRISPR-Cas genome editing, and RNA-based delivery platforms have enabled precise genetic modification of macrophages, giving rise to chimeric antigen receptor macrophages (CAR-Ms) and related engineered products. Beyond antigen targeting, effective macrophage engineering requires stabilization of pro-inflammatory identity, resistance to tumor-induced repolarization, metabolic reinforcement, and integration of checkpoint modulation pathways. This review synthesizes current strategies across DNA, mRNA, and siRNA-based platforms, highlighting convergent design principles that connect TAM reprogramming with CAR-M development. We discuss reshaping phagocytosis checkpoints, metabolic and transcriptional stabilization, cytokine augmentation, and synthetic receptor architecture, emphasizing combinatorial and context-aware engineering, while proposing new candidate gene targets. Engineered macrophages are thus evolving from simple effector cells into programmable immune coordinators capable of converting immunologically "cold" tumors into inflamed, therapy-responsive niches.

CAR-M↗
PubMed2005

Influence of three resistance sources in winter wheat derived from TAM 107 on yield response to Russian wheat aphid.

A study to determine yield response to the Russian wheat aphid, Diuraphis noxia (Mordvilko), was conducted during the 1997-1998 and 1998-1999 growing seasons at three eastern Colorado locations, Akron, Fort Collins, and Lamar, with three wheat lines containing either Russian wheat aphid-resistant Dn4 gene, Dn6 gene, or resistance derived from PI 222668, and TAM 107 as the susceptible control. Russian wheat aphids per tiller were greater on TAM 107 than the resistant wheat lines at the 10x infestation level at Fort Collins and Akron in 1999. Yield, seed weight, and number of seeds per spike for each wheat line were somewhat affected by Russian wheat aphid per tiller mainly at Fort Collins. The infested resistant wheat lines harbored fewer Russian wheat aphids and yielded more than the infested susceptible wheat lines. Wheat lines containing the Dn4, Dn6, and PI 222668 genes contain different levels of antibiosis or antixenosis and tolerance. Although differences existed among sites and resistance, there is a benefit to planting resistant wheat when there is a potential for Russian wheat aphid infestations.

Animals↗