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PubMed1998

[Anticancer drug intraperitoneal chemotherapy using T-type reservoir sheet for unresectable gastric cancer].

T-type reservoir sheets (anti-adhesion sheets developed to prevent adhesions + reservoir) were intraperitoneally implanted in 16 patients with unresectable gastric cancer and postoperatively used to suction off ascitic fluid, to prevent cancerous adhesions of the intestines, and to intraperitoneally infuse anticancer drugs with a view to improving QOL and prolonging survival time. The results showed that whereas all of the patients had been class V according to intraoperative cytodiagnosis, postoperatively they were all class I-II and their ascites had either completely or temporarily resolved. Performance status (PS) improved in 14 patients (87.5%), and 14 patients (87.5%) were discharged. According to the Cancer Body Cavity Efficacy Rating Criteria (Japan Society for Cancer Therapy), CR was achieved in 10 cases, PR in 3 cases, NR in 3 cases, and the mean home care rate was 45.4%. Mean survival time to date, February 1997, is 7.8 months, two patients are alive, and the longest survival time has been 22 months. This method facilitates suctioning of ascitic fluid. It prevents irregular adhesions of the intestine, and protects against the development of ileus. It enables repeated intraperitoneal administration of high concentrations of anticancer drugs, uniformly, extensively, safely and easily. It facilitates intraperitoneal cytodiagnosis, ascitic fluid sampling, and monitoring of the efficacy of anticancer agents. The special features of this method are the high percentage of patients residing at home and the ability to administer intraperitoneal infusions of anticancer agents continually and repeatedly on an outpatient basis.

Adult↗

PubMed1995

Inhibitors of carbohydrate processing: A new class of anticancer agents.

There is a need for anticancer agents with novel mechanisms of action. Recently identified molecular targets for new anticancer agents include inducers of cell differentiation, cell cycle arrest, and apoptosis, as well as signaling pathways for growth factors and cytokines. Another unexplored opportunity is presented by the ubiquitous intracellular glycoprotein glycosylation pathway. This complex process, concerned with the addition of sugars onto newly synthesized proteins, occurs in the lumen of the rough endoplasmic reticulum and in the Golgi. There are estimates of over 200 glycosyltransferase enzymes in this pathway, which results in considerable structural diversity of carbohydrates found on secreted and transmembrane glycoproteins. The specificity of glycosyltransferases for acceptors and sugar-nucleotide donors dictates linkage positions between sugars, anomeric configuration of linkages, and monosaccharide composition. Specific carbohydrate structures participate in cell-cell and cell-substratum interactions affecting processes such as lymphocyte trafficking, immune cell stimulation, embryogenesis, and cancer metastasis. Of the carbohydrate-processing inhibitors presently available, the alkaloid swainsonine, a Golgi alpha-mannosidase II inhibitor, is the first to have been selected for clinical testing based on its anticancer activity, p.o. availability, and low toxicity in mice. Herein, we review the rationale for targeting Golgi carbohydrate processing pathways in the treatment of cancer, and summarize the preclinical and clinical results with swainsonine. Prospects for the development of second generation inhibitors with improved specificity for Golgi-processing enzymes are discussed. Potential clinical applications of this new class of anticancer agents are emphasized.

Animals↗

PubMed1999

Apoptotic response to camptothecin and 7-hydroxystaurosporine (UCN-01) in the 8 human breast cancer cell lines of the NCI Anticancer Drug Screen: multifactorial relationships with topoisomerase I, protein kinase C, Bcl-2, p53, MDM-2 and caspase pathways.

Derivatives of camptothecins, topoisomerase I inhibitors and 7-hydroxystaurosporine (UCN-01), a protein kinase C (PKC) inhibitor and cell cycle checkpoint abrogator, are promising anticancer drugs. We characterized the apoptotic response to camptothecin and UCN-01 for the 8 human breast carcinoma cell lines (MCF-7, MCF-7/ADR, T47D, HS578T, BT549, MDA-N, MDA MB231, MDA435) from the National Cancer Institute (NCI) Anticancer Drug Screen. MCF-7 and T47D cells exhibited marked resistance to apoptosis, whereas MCF-7/ADR (NCI/ADR-RES) and HS578T cells exhibited the most pronounced apoptotic response. Apoptotic response was not correlated with growth inhibition measured by sulforhodamine B (SRB) assay, indicating that apoptosis is not the only mechanism of drug-induced cell death. Measurements of topoisomerase I levels and cleavage complexes and of PKC isoforms demonstrated that primary target inhibition was not correlated with apoptotic response. Several key apoptotic pathways were evaluated. Only MCF-7 cells had wild-type p53, indicating that p53 is not required for drug-induced apoptosis. MCF-7 cells also showed the highest MDM-2 expression (along with T47D cells, which were also resistant to apoptosis). Bcl-2, Mcl-1 and caspases 2 and 3 protein levels varied widely, whereas Bax expression was comparable among cell lines. Interestingly, Bcl-2, Mcl-1 and Bcl-X(L) cumulative expressions were inversely correlated with apoptotic response. Our results provide a comparative molecular characterization for the breast cancer cell lines of the NCI Anticancer Drug Screen and demonstrate the diversity of cellular responses to drugs (apoptosis vs. cell cycle arrest) and the importance of multifactorial analyses for modulating/predicting the apoptotic response to chemotherapy.

Alkaloids↗

PubMed1984

In vitro and in vivo studies on potentiation of cytotoxic effects of anticancer drugs or cobalt 60 gamma ray by interferon on human neoplastic cells.

A possibility that interferon may potentiate the cytotoxic effects of anticancer drugs or 60Co gamma ray on human neoplastic cells was studied by in vitro and in vivo experimental procedures. The human neoplastic cells used were HeLa (uterine cervical cancer) and WI-38 CT-1 (embryonic lung fibroblasts transformed in culture by 60Co gamma ray) cells. As normal human cells, WI-38 cells were used. Interferon was a preparation of beta-type produced by human fibroblasts. The cytotoxicity was determined by colony formation for in vitro experiments and by tumor growth for animal experiments. Of 17 anticancer drugs, the cytotoxic effects of six drugs, namely, peplomycin, bleomycin, aclacinomycin, cisplatin, 5-fluorouracil (5-FU), and Adriamycin (doxorubicin) were potentiated by concomitant application of interferon. The cytolethal effects of 60Co gamma ray were also enhanced by interferon. The growth of tumor induced by transplantation of HeLa cells into a nude mouse was remarkably reduced by combination therapy of interferon and 5-FU. The current results indicate a possibility that combined therapy of certain types of anticancer drugs or 60Co gamma ray with interferon may be effective in treatment of cancer patients.

Animals↗

PubMed2000

The antibiotic and anticancer active aurein peptides from the Australian Bell Frogs Litoria aurea and Litoria raniformis. Part 2. Sequence determination using electrospray mass spectrometry.

Sixteen aurein peptides are present in the host defence secretion from the granular dorsal glands of the Green and Golden Bell Frog Litoria aureus and seventeen from those of the related Southern Bell Frog Litoria raniformis. All peptides have been sequenced using a combination of electrospray mass spectrometry and Lys-C digestion, with each sequence confirmed by automated Edman sequencing. The peptides are named in five groups, viz. aureins 1-5. Ten of these peptides are common to both species of frog. Thirteen of the aurein peptides show wide-spectrum antibiotic and anticancer activity. Amongst the more active peptides are aurein 1.2 (GLFDIIKKIAESF-NH2), the smallest peptide from an anuran reported to have both antibiotic and anticancer activity; aurein 2.2 (GLLDIVKKVIGAFGSL-NH2) and aurein 3.1 (GLFDIVKKIAGHIAGSI-NH2). The aurein 4 and 5 peptides, e.g. aurein 4.1 (GLIQTIKEKLKELAGGLVTGIQS-OH) and aurein 5.1 (GLLDIVTGLLGNLIVDVLKPKTPAS-OH), show neither antibacterial nor anticancer activity.

Amino Acid Sequence↗

PubMed2005

New synthetic thiocolchicine derivatives as lowtoxic anticancer agents.

New thiocolchicine derivatives (1-8) were designed as less toxic anticancer agents possessing the power full anticancer activity of colchicine. The synthesis and biological evaluation of these compounds were described. As a preliminary result of biological in vitro investigation, compounds 1, 6, and 7 showed lower toxicities than that of colchicine in combination with potent anticancer activities.

Animals↗

PubMed2002

Antimetabolite incorporation into DNA: structural and thermodynamic basis for anticancer activity.

Antimetabolites are a class of effective anticancer drugs that structurally resemble naturally occurring biochemicals and interfere in essential biochemical processes. In this review, the recent literature describing investigations of the structural and thermodynamic basis for the anticancer activity of three antipyrimidines [1-beta-D-arabinofuranosyl cytidine (AraC). 2',2'-difluoro deoxycytidine (dFdC), and 5-fluoro-2'-deoxyuridine (FdUrd)] is summarized. Our laboratory, and others, have shown that misincorporation of any of these three antipyrimidines into DNA perturbs the structure and decreases the stability of duplex DNA. These data are useful for rationalizing the effects of antipyrimidine misincorporation on the activities of proteins required for DNA replication and repair such as DNA topoisomerase 1 and DNA polymerases. The studies completed to date and summarized in this review demonstrate the utility of investigations into the structure-function relationships between antipyrimidine-substituted DNA complexed with DNA-modifying proteins for the purpose of understanding the basis for effective antipyrimidine cancer chemotherapy and the future design of novel anticancer drugs.

Antimetabolites, Antineoplastic↗

PubMed2005

Potential anticancer activity of tanshinone IIA against human breast cancer.

Tanshinone IIA is a derivative of phenanthrene-quinone isolated from Danshen, a widely used Chinese herbal medicine. It has antioxidant properties and cytotoxic activity against multiple human cancer cell lines, inducing apoptosis and differentiation of some human cancer cell lines. Our purpose was to confirm its anticancer activity on human breast cancer in vitro and in vivo and to elucidate the mechanism of its activity. Human breast cancer cells were tested in vitro for cytotoxicity, colony formation inhibition, BrdU incorporation and gene expression profiling after treatment with tanshinone IIA. Seven nude mice bearing human breast infiltrating duct carcinoma orthotopically were tested for anticancer activity and expression of caspase-3 in vivo by s.c. injection of tanshinone IIA at a dose of 30 mg/kg 3 times/week for 10 weeks. Tanshinone IIA demonstrated a dose- and time-dependent inhibitory effect on cell growth (IC50 = 0.25 microg/ml), and it significantly inhibited colony formation and BrdU incorporation of human breast cancer cells. Oligonucleotide microarray analysis identified 41 upregulated (1.22%) and 24 downregulated (0.71%) genes after tanshinone IIA treatment. Upregulated genes were involved predominantly in cycle regulation, cell proliferation, apoptosis, signal transduction and transcriptional regulation; and downregulated genes were associated mainly with apoptosis and extracellular matrix/adhesion molecules. A 44.91% tumor mass volume reduction and significant increase of casepase-3 protein expression were observed in vivo. Our findings suggest that tanshinone IIA might have potential anticancer activity on both ER-positive and -negative breast cancers, which could be attributed in part to its inhibition of proliferation and apoptosis induction of cancer cells through upregulation and downregulation of multiple genes involved in cell cycle regulation, cell proliferation, apoptosis, signal transduction, transcriptional regulation, angiogenesis, invasive potential and metastatic potential of cancer cells. ADPRTL1 might be the main target at which tanshinone IIA acted.

Abietanes↗

PubMed2005

TX-1877, a bifunctional hypoxic cell radiosensitizer, enhances anticancer host response: immune cell migration and nitric oxide production.

We investigated in the current study the effect of TX-1877, a bifunctional hypoxic cell radiosensitizer, in augmenting anticancer host response. In the syngeneic squamous cell carcinoma-bearing mouse model, a single administration of TX-1877 significantly inhibited the primary tumor growth as well as lung metastasis. TX-1877 administration resulted in a significant infiltration of immune cells, such as CD4+T, CD8+T cells, macrophages and dendritic cells (DCs), and an increased expression of chemokines for cytotoxic T lymphocytes (CTLs), helper T-cell 1 (Th1) cells, monocytes/macrophages and DCs, in tumor tissues. Nitric oxide (NO) production and the expression of inducible NO synthase (iNOS) and interferon-gamma, a major Th1 cytokine that plays a major role in anticancer immunity, were also enhanced. Furthermore, neutralization of NO by N-monomethyl-L-arginine acetate resulted in a marked inhibition of the antitumor effect of TX-1877. In tumor-draining lymph nodes, MHC class I-restricted CD8+ memory CTLs specific for inoculated cancer cells were induced by TX-1877. In in vitro experiments, TX-1877 induced chemokines and iNOS/NO in several types of culture cells. These findings strongly suggested that TX-1877 induces migration of CD8+CTLs, CD4+Th1 cells, macrophage/monocytes and dendritic cells into the tumor site, and that this migration is mediated by chemokine induction. In addition, it was suggested that NO produced by several types of cells stimulated by TX-1877 in the tumor sites plays a major role in the anticancer effect of TX-1877. TX-1877 was thus shown to be an effective immunopotentiator as well as a hypoxic cell radiosensitizer.

Animals↗

PubMed2006

Dramatic synergistic anticancer effect of clinically achievable doses of lovastatin and troglitazone.

Lovastatin (an HMG-CoA reductase inhibitor) and troglitazone (a PPAR-gamma agonist) have been intensively studied prospectively for their application in cancer treatment. However, clinical trials of lovastatin or troglitazone in cancer treatment resulted in only limited responses. To improve their efficacy, lovastatin and troglitazone have, respectively, been tried to combine with other anticancer agents with varied outcomes. In our study, we found a dramatic synergism between lovastatin and troglitazone in anticancer at clinically achievable concentrations. This synergism was found in far majority of cell lines tested including DBTRG 05 MG (glioblastoma) and CL1-0 (lung). This amazing synergism was accompanied by synergistic modulation of E2F-1 and p27(Kip1), which were reported to mediate the anticancer activities of lovastatin and troglitazone, respectively, and other cell cycle regulating proteins such as CDK2, cyclin A and RB phosphorylation status. With this dramatic combination effect of lovastatin and troglitazone, a promising regimen of cancer therapy may be materialized in the future.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1977

Synthesis and anticancer activity of novel cyclic N-hydroxyureas.

To overcome the disadvantages of hydroxyurea in anticancer therapy such as fast biotransformation and low potency, five cyclic N-hydroxyureas were synthesized. A new reaction was developed to prepare the desired products from the appropriate alkyl omega-haloalkylcarbamates with hydroxylamine. This reaction probably involves a two-step mechanism: nucleophilic substitution and intramolecular cyclization. The anticancer screening tests of these compounds were done both in vitro using tissue culture and in vivo. One compound, 1-hydroxy-1,3-diazacylohexan-2-one, had anticancer activity comparable to hydroxyurea both in vivo and in vitro.

Animals↗

PubMedDate not supplied

Liquid chromatography-mass spectrometry for the quantitative bioanalysis of anticancer drugs.

The monitoring of anticancer drugs in biological fluids and tissues is important during both pre-clinical and clinical development and often in routine clinical use. Traditionally, liquid chromatography (LC) in combination with ultraviolet (UV), fluorescence, or electrochemical detection is employed for this purpose. The successful hyphenation of LC and mass spectrometry (MS), however, has dramatically changed this. MS detection provides better sensitivity and selectivity than UV detection and, in addition, is applicable to a significantly larger group of compounds than fluorescence or electrochemical detection. Therefore, LC-MS has now become the method of first choice for the quantitative bioanalysis of many anticancer agents. There are still, however, a lot of new developments to be expected in this area, such as the introduction of more sensitive and robust mass spectrometers, high-throughput analyses, and further optimization of the coupled LC systems. Many articles have appeared in this field in recent years and are reviewed here. We conclude that LC-MS is an extremely powerful tool for the quantitative analysis of anticancer drugs in biological samples.

Animals↗

PubMed2006

Vitamin E analogues as anticancer agents: lessons from studies with alpha-tocopheryl succinate.

The new millennium has witnessed considerable decrease in a number of previously fatal pathologies, largely due to the advancement in molecular medicine and modern approaches to treatment. In spite of this success, neoplastic disease remains a serious problem due to several reasons. These include an exceedingly high variability of cancer cells even within the same type of tumour. Cancer cells, albeit of clonal origin, mutate so that they escape established treatments, resulting in the fatal outcome of current therapies. Moreover, there are types of cancer, such as mesotheliomas, that cannot be treated at present. A novel group of clinically interesting anticancer drugs has been a recent focus in the literature that hold substantial promise as selective anticancer drugs. These compounds, epitomised by alpha-tocopheryl succinate, comprise redox-silent analogues of vitamin E that have been shown to suppress several types of cancer in animal models, including breast, colon and lung cancer as well as mesotheliomas and melanomas, while being nontoxic to normal cells and tissues. It is now proven that the strong anticancer effect of vitamin E analogues stems from their propensity to induce selective apoptosis in malignant cells. The results point to the novel group of vitamin E analogues as promising agents applicable to different types of tumours.

Animals↗

PubMed1994

Highlight on the studies of anticancer drugs derived from plants in China.

Recent progress on the study of anticancer drugs originating from plants in China is reviewed in this paper. Guided by the experience of traditional Chinese medicine, several new drugs have been found. Indirubin from Indigofera tinctoria is useful for the treatment of chronic myelocytic leukemia. Irisquinone from Iris latea pallasii and 10-hydroxy camptothecin from Camptotheca accuminata have exhibited definite activity on rodent tumors. Recent studies indicate that ginsenoside Rh2 is an inducer of cell differentiation in melanoma B-16 cells in vitro. Pharmacological studies have demonstrated that curcumin from Curcuma longa is an antimutagen as well as an antipromotor for cancer. Daidzein and acetyl boswellic acid have been shown to be effective inducers of cell differentiation in HL-60 cells. Guided by the chemotaxonomic principle of plants, harringtonine and homoharringtonine isolated from Cephalotaxus hainanesis have exhibited significant antileukemia activity and are widely used in clinics in China. Taxol from Taxus chinensis has been shown to be an important new anticancer drug with unique chemical structure and mechanism of action. The continuous search for new anticancer drugs from plants will be a fruitful frontier in cancer treatment and chemoprevention.

Antineoplastic Agents, Phytogenic↗

PubMed1999

The N-terminal half of NPM dissociates from nucleoli of HeLa cells after anticancer drug treatments.

NPM (nucleophosmin/B23) is a nucleolar phosphoprotein abundant in tumor cells. It dissociates from nucleoli of cells after treatments with various anticancer drugs. To determine the domain of NPM responsible for nucleolar binding, the N- and C-terminal halves of NPM were fused to GFP (green fluorescent protein) and introduced into HeLa cells. The N-terminal half (aa 1-150) of NPM (GFP-NPM(N)) was found localized in the nucleoli. A stable transformant of GFP-NPM(N) in HeLa cells was prepared and tested for association to nucleoli after anticancer drug treatments. GFP-NPM(N) dissociates from nucleoli after treatments with daunomycin, actinomycin D, camptothecin, and toyocamycin. The dissociation is time- and dose-dependent, and correlates with the cytotoxicity induced by the drugs. These results indicate that a stable transformant of GFP-NPM(N) in HeLa cells may be useful for the screening of anticancer drugs.

Antineoplastic Agents↗

PubMed2000

A genome-wide screening in Saccharomyces cerevisiae for genes that confer resistance to the anticancer agent cisplatin.

Cisplatin is a potent DNA-damaging agent that has demonstrated anticancer activities against several tumors. However, manifestation of cellular resistance is a major obstacle in anticancer therapy that severely limits the curative potential of cisplatin. Therefore, understanding the molecular basis of cisplatin resistance could significantly improve the clinical efficacy of this anticancer agent. Here, we employed Saccharomyces cerevisiae as a model organism to study cisplatin resistance mechanisms and describe a one-step cisplatin selection to identify and characterize novel cisplatin resistance genes. Screening a multicopy yeast genomic library enabled us to isolate several yeast clones for which we could confirm that the cisplatin resistance phenotype was linked to the introduced fragment. In a first attempt, a number of open reading frames could be identified. Among these genes, PDE2 and ZDS2 were repeatedly identified as genes whose overexpression confers cellular resistance to cisplatin. PDE2, encoding cAMP-phosphodiesterase 2, is of particular interest because the overexpression of this yeast gene is known to induce cisplatin resistance in mammalian cells as well, providing proof of the principle of our experimental approach. In addition, the identification of PDE2 shows that our yeast screening system can directly be informative for drug resistance in mammalian cells.

Chromosome Mapping↗

PubMed2002

Electrochemical monitoring of anticancer compounds on the human ovarian carcinoma cell line A2780 and its adriamycin- and Cisplatin-resistant variants.

A novel electrochemical technique which detects and monitors real-time changes in cell behavior in vitro has been used to examine the effects of recognized anticancer drugs on the human ovarian carcinoma cell line A2780 and its adriamycin (A2780adr)- and cisplatin (A2780cispt)-resistant variants. These cells, adherent to gold electrodes or sensors, modify the extracellular microenvironment at the cell:sensor interface, producing an electrochemical potential that is different from that of the bulk culture medium. Confluent, adherent A2780 cells produced an electrochemical signal, measured as an open circuit potential (OCP), of approximately -100 mV compared to a cell-free value of approximately -15 mV. Exposure of A2780 cells to cisplatin (range 10(-4) to 10(-6) M), adriamycin (range 10(-5) to 10(-7) M), and vinblastine (10(-6) M) all produced positive shifts in the OCP signal relative to untreated control cells during 24 h of culture, but Taxotere (range 10(-5) to 10(-7) M) had no effect. These positive shifts in OCP signal were evident well before observations of reduced cellular adhesion and viability after 24 h, as judged in parallel cultures with a plastic substratum and by scanning electron microscopy. By contrast, the same treatments applied to the A2780adr and A2780cispt variants showed that each demonstrated different sensitivities to the same drugs applied to the parental A2780 cells. The effects of the same four anticancer drugs on ovarian carcinoma (A2780) and breast carcinoma (8701-BC) cell lines showed that the former was far more responsive to adriamycin and cisplatin. Such differences in drug sensitivities between the two cell lines were subsequently confirmed using the conventional MTT assay over 5 days. Although this electrochemical technology readily detects changes in cell adhesion and viability, the modified OCP signals recorded within a few hours of anticancer drug treatments are evident well before microscopic morphological changes become apparent. It is proposed that these early changes in OCP signals, relative to control untreated cells, reflect modifications of physiological/behavioral processes manifested at the cell surface.

Antineoplastic Agents↗

PubMed2000

Use of a surrogate marker (human secreted alkaline phosphatase) to monitor in vivo tumor growth and anticancer drug efficacy in ovarian cancer xenografts.

OBJECTIVES: A limitation to preclinical evaluation of possible anticancer therapy is the objective assessment of efficacy, especially in the presence of small tumor burden or inaccessible disease. This study is designed to test whether human secreted alkaline phosphatase (SEAP) could be used as a soluble marker for in vivo tumor burden. METHODS: A SEAP expression construct under control of the CMV promoter was created. The SEAP activity in the conditioned medium was evaluated at 24 h and 48 h after the A2780 cell line was transiently transfected with the SEAP vector using Superfect reagent. Stable transfection of A2780 was accomplished by selection of transfectants in G418. SEAP activity of the stable transfectant was determined in conditioned medium and its relationship to tumor cell number was examined. A highly expressing stable transfectant was implanted into immunocompromised mice (2 x 10(6) subcutaneously and 5 x 10(6) intraperitoneally) and peripheral blood was obtained by orbital puncture every 5 days. The relationship between blood SEAP activity and tumor burden was studied. The usefulness of this marker in preclinical assessment of anticancer drug efficacy was evaluated by studying the plasma SEAP activity in xenografted mice treated or not treated with paclitaxel. RESULTS: After transient transfection of the A2780 cell line (5 x 10(5)) with the plasmid, SEAP activity was found in the medium at 24 h (482.0 +/- 2.0 ng/ml) and 48 h (1296.0 +/- 1.0 ng/ml). The in vitro study using a stable transfectant demonstrated that SEAP activity was linearly related to cell numbers (r = 0.99). The in vivo study demonstrated that SEAP was detectable in plasma one day postinjection, long before measurable tumor or detectable intraperitoneal tumor was present. Once detectable SC tumor was present, the SEAP activity correlated well with tumor volume (r = 0. 94-0.97). The plasma SEAP level was reduced after xenografted mice were treated with paclitaxel (20 mg/kg, weekly x5) compared with untreated mice in both SC and IP tumor models (P = 0.05, P = 0.025, respectively). CONCLUSION: These data suggest that the plasma SEAP activity can be used as an alternative to survival or tumor measurement in evaluating anticancer agents for efficacy, especially in the case of minimal or inaccessible disease.

Alkaline Phosphatase↗