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PubMed1994

[In vitro and in vivo targeting therapy of immunoliposomes against human gastric cancer].

Nine kinds of antineoplastic agents and 2 boron-10 compounds were encapsulated respectively into the immunoliposomes targeted with monoclonal antibody, MGb2, against human gastric cancer. The immunoliposomes were characterized in vitro and in vivo with different nude mouse xenograft models and different routes of administration. The immunore activity was well preserved. The diameter was 100nm for reverse-phase evaporation vesicles and 35nm for small unilamellar vesicles. 1,000-10,000 molecules of antitumor agent were entrapped and 30-80 molecules of MGb2 incorporated per one liposome. They showed selective cytotoxicity to human gastric cancer cell SGC-7901 but very low toxicity to human normal embryonic lung cell SL7. Biodistribution studies indicated that both were better than non-specific liposomes and free drugs. Boronated immunoliposomes could carry boron-10 specifically to SGC-7901 and showed targeted boron neutron capture therapy effects after thermal neutron irradiation. The results confirmed the specific antitumor effects of immunoliposomes in vitro and in vivo and demonstrated the potentiality of the immunoliposomes in the targeting therapy of human gastric cancer.

Animals↗
PubMed2000

Recent advances in antigen-targeted therapy in non-Hodgkin's lymphoma.

Substantial advances in antigen-targeted lymphoma therapy have been achieved in recent years that make the use of monoclonal antibodies a highly attractive concept and promise further improvements in the clinical management of malignant lymphoma. The development of the chimeric anti-CD20 antibody IDEC-C2B8 (Rituximab) proved the concept of an effective therapy with a single unconjugated monoclonal antibody in lymphoma patients. Radioimmunoconjugates with myeloablative activity induced response rates of 80-100% in heavily pretreated patients. Progress in the genetic engineering of immunotoxins has improved the efficacy of these constructs. Ongoing prospective clinical trials will define the optimal use of these innovative therapeutic agents in patients with malignant lymphoma, and may establish therapeutic strategies with a high anti-lymphoma specificity and a low unspecific toxicity.

Antibodies, Bispecific↗
PubMed2006

Antiviral therapy targeting viral polymerase.

Viral DNA and RNA polymerases are enzymes, which are responsible for copying the genetic materials of viruses and are therefore central components in the life cycles of viruses. The polymerases are essentially required for the replication of viruses. The reverse transcriptase (RT) of the retroviruses and the hepadnaviruses is the sole viral enzyme required for the synthesis of DNA from viral RNA. Viral polymerases are therefore an extremely favorable target for the development of antiviral therapy. The success of anti-HIV-1 therapy using inhibitors specifically targeting HIV RT suggests that other viral polymerases can be the valid molecular targets for the design of antiviral drugs. Intensive structural and functional studies of viral polymerases have been conducted and have opened new avenues for the development of more effective antiviral therapy. This review summarizes the insights gained from recent structural and functional studies of antiviral agents, which target viral polymerases. The primary focus will be on hepatitis C virus (HCV), herpesviruses, HIV, hepatitis B virus (HBV) and influenza virus.

Antiviral Agents↗
PubMed2006

Targeted therapy by disabling crossroad signaling networks: the survivin paradigm.

Embedded in the concept of targeted cancer therapy is the expectation that disabling a single oncogenic pathway will eliminate the tumor cells and leave the normal tissues unscathed. Although validated by clinical responses in certain malignancies, challenges exist to generalize this approach to most tumors, as multiple genetic lesions, chromosomal instability, insensitivity of the cancer stem cell compartment, and emergence of drug resistance complicate the identification and therapeutic exploitation of a single, driving oncogenic pathway. Instead, broader therapeutic prospects may be offered by targeting crossroad signaling networks that are selectively exploited in cancer and oversee multiple aspects of tumor cell maintenance. One such pathway is centered on survivin, a cancer gene that intersects cell proliferation, cell survival, and the cellular stress response. Several clinical trials targeting survivin with a collection of approaches from immunotherapy to small-molecule antagonists are currently under way. By simultaneously disabling multiple signaling circuitries, targeting survivin may provide a novel perspective in rational cancer therapy selective for specific cancer mechanisms but broadly applicable to disparate tumors regardless of their genetic makeup.

Genetic Therapy↗
PubMed2006

The role of targeted therapy in the treatment of colorectal cancer.

Recent years have brought significant advances in the treatment of metastatic colorectal cancer. Combination regimens with standard chemotherapeutic agents have extended survival to nearly 2 years, and recent studies suggest that chemotherapy-free intervals may be feasible in some patients without compromising survival outcomes. The most significant recent progress has centered on the use of targeted biologic therapies. The first targeted agent to show a significant benefit in metastatic colorectal cancer was bevacizumab. This monoclonal antibody is directed against vascular endothelial growth factor, a molecule known to be involved in the angiogenic process that is central to cancer growth and metastasis. In clinical trials, bevacizumab has improved survival when added to multiple chemotherapy regimens. The second targeted agent to be approved for colorectal cancer is the monoclonal antibody cetuximab, which is directed against the epidermal growth factor receptor, another key mediator of cancer growth. Cetuximab has been shown to increases the efficacy of irinotecan in irinotecan-refractory patients, indicating that cetuximab may make tumors more sensitive to chemotherapeutic agents. Bevacizumab and cetuximab continue to be evaluated alone as maintenance therapy and in combination in different settings to determine their optimal use in colorectal cancer. Additional targeted agents are also being developed and are showing promise in clinical trials.

Antibodies, Monoclonal↗
PubMed1999

Hexokinase type II: a novel tumor-specific promoter for gene-targeted therapy differentially expressed and regulated in human cancer cells.

The use of tissue- or tumor-selective promoters in targeted gene therapy for cancer depends on strong and selective activity. Hexokinase type II (HK II) catalyzes the first committed step of glycolysis and is overexpressed in tumors, where it is no longer responsive to normal physiological inhibitors, e.g., glucagon. We show, in a reporter gene assay, activation of HK II in non-small cell lung carcinomas NCI-H661 and NCI-H460 at 61 and 40%, respectively, relative to the activation observed with a constitutive promoter, while it was only 0.9% in different preparations of primary normal human bronchial epithelial cells (NHBECs). Similar results were observed in a variety of normal and tumor cells. Moreover, treatment of the transfectants with glucagon did not inhibit promoter activation in the transformed H661 cells, while endogenous HK II in NHBECs is suppressed by glucagon. H460 and H661 cells infected with a recombinant adenovirus carrying an HK II/LacZ expression cassette, AdHexLacZ, demonstrated beta-galactosidase activity that correlated with the level of HK II promoter activation in these cells. Under similar conditions, no enzyme activity was observed in NHBECs. Cells were then infected with AdHexTk and treated with GCV. Our results demonstrate selectivity in toxicity, with a 10- to 100-fold increase in IC50 between lung cancer cell lines H661 and H460, respectively, and NHBECs. There was also a 100-fold increase in IC50 in NHMECs relative to breast carcinoma cell line MCF-7. In HepG2 cells, an IC50 of 1 microg/ml was observed, comparable to that of other tumor cell lines. This represents a novel use of the hexokinase type II as a selective promoter in cancer gene therapy.

Adenoviridae↗
PubMed2006

Clinical efforts to combine endocrine agents with targeted therapies against epidermal growth factor receptor/human epidermal growth factor receptor 2 and mammalian target of rapamycin in breast cancer.

Enhancing the benefit of endocrine therapy by overcoming de novo or acquired resistance remains an important goal in systemic breast cancer therapy. Progress continues to be made in elucidating the molecular pathways by which estrogen receptor-positive breast cancer cells escape from endocrine therapy. The increasing recognition of the roles of epidermal growth factor receptor (EGFR) and human EGFR2 in cross-talk activation of estrogen receptor signaling has led to studies aimed at identifying whether small-molecule tyrosine kinase inhibitors targeted against these receptors give additive or synergistic effects when combined with endocrine agents. Activation of the phosphatidylinositol-3-OH kinase/Akt pathway has also been associated with resistance to either tamoxifen or estrogen deprivation, and preclinical studies have shown that the mammalian target of rapamycin antagonist temsirolimus can restore endocrine sensitivity in breast cancer cells. Randomized phase II trials of aromatase inhibitors combined with EGFR/human EGFR2 tyrosine kinase inhibitors or mammalian target of rapamycin antagonists have been completed in both the neoadjuvant and advanced breast cancer settings. Larger phase III trials with both approaches are now in progress and have been powered to detect whether either strategy can significantly prolong time to disease progression compared with endocrine therapy alone. The correlation of molecular and clinical results from these ongoing studies will be important to establish appropriate biological variables for selecting those patients who may benefit most from this combined approach.

Antineoplastic Agents, Hormonal↗
PubMed2005

Novel targeted therapies in the treatment of gastric and esophageal cancer.

Esophageal cancer (EC) and gastric cancer (GC) constitute a major cause of cancer deaths worldwide. Recent improvements in both surgical techniques and adjuvant/neoadjuvant radiotherapy and chemotherapy approaches have increased the survival of patients with loco-regional disease. However, most of the patients with GC or EC have advanced disease either at diagnosis or at follow-up. Despite recent advances in the treatment of advanced disease, these patients still do poorly. An emerging understanding of the molecular pathways that characterize cell growth, cell cycle, apoptosis, angiogenesis and invasion has provided novel targets in cancer therapy. In this review we describe the current status of targeted therapies in the treatment of EC and GC. These therapeutic strategies include EGFR inhibitors, antiangiogenic agents, cell cycle inhibitors, apoptosis promoters and matrix metalloproteinases inhibitors. The emerging data from the clinical development of these compounds has provided novel opportunities in the treatment of EC and GC that will probably translate into efficacy advantage in the treatment of these common malignancies.

Antineoplastic Agents↗
PubMed2005

Targeted therapy comes of age in scleroderma.

Systemic sclerosis (SSc, also known as scleroderma) has the highest case-specific mortality among the rheumatic diseases; however, advances in understanding of pathogenesis and an appreciation of the clinical heterogeneity of this disease, together with therapeutic advances in other areas, have raised the possibility of substantial improvements in its management. Key areas of advance include the development of clinical and laboratory methods for early detection of complications and the integration of vascular, immunomodulatory and antifibrotic therapies. Disease models have facilitated the identification of key mediators or processes that could be targeted therapeutically and have provided a platform for preclinical testing of novel candidate therapies. This review will consider current clinical aspects of SSc and the emergence of targeted therapy that is linked to key pathogenic processes or that targets pivotal mediators.

Age Factors↗
PubMed2001

Bone-targeted therapy for advanced androgen-independent carcinoma of the prostate: a randomised phase II trial.

BACKGROUND: Prostate carcinoma is linked to osteoblastic metastasis. We therefore investigated the value of bone-targeted consolidation therapy in selected patients with advanced androgen-independent carcinoma of the prostate. METHODS: 103 patients received induction chemotherapy, consisting of ketoconazole and doxorubicin alternating with estramustine and vinblastine. After two or three cycles of induction chemotherapy, we randomly assigned 72 patients who were clinically stable or responders to receive doxorubicin with or without strontium-89 (Sr-89) every week for 6 weeks. FINDINGS: Overall 62 of the 103 (60%, 95% CI 50-70) patients had a 50% or greater reduction in serum prostate-specific antigen concentration that was maintained for at least 8 weeks, and 43 (42%, 32-52) had an 80% or greater reduction. 49 (52%) patients with bone pain at registration had complete resolution of pain. After follow-up of 67 patients until death, the estimated median survival for all 103 patients was 17.5 months (range 0.5-37.7). For the 36 patients randomly assigned to receive Sr-89 and doxorubicin, the median survival time was 27.7 months (4.9-37.7), and for the 36 who received doxorubicin alone it was 16.8 months (4.4-34.2) (p=0.0014). The hazard ratio was 2.76 (95% CI 1.44-5.29). INTERPRETATION: Bone-targeted consolidation therapy consisting of one dose of Sr-89 plus doxorubicin once a week for 6 weeks, when given to patients with stable or responding advanced androgen-independent carcinoma of the prostate after induction chemotherapy, improved overall survival.

Adult↗
PubMed1995

Combination anti-gene therapy targeting c-myc and p53 in ovarian cancer cell lines.

Gene therapy clinical trials targeting p53 and other genes are underway in nongynecologic cancer systems. To explore the potential for antigene therapy in gynecologic oncology, we examined the in vitro effects of oligonucleotides targeting c-myc and p53 in the ovarian cancer cell lines CAOV-3, SKOV-3, and BG-1. The ATP cell viability assay was used to measure growth effects after 6-day treatments with 27-mer antisense phosphorothioate oligodeoxyribonucleotides (oligos) targeting the Puf/nm23 binding region of c-myc and promoter/ATG region of p53. A random sequence of the p53 27-mer was used as a control, and an untransformed fibroblast cell line was used for comparison. IC50 was defined as the oligo concentration required for 50% growth reduction compared to untreated controls. Synergistic vs antagonistic effects of oligo combinations were quantitated by combination indexes (CI) as calculated from median effect parameters by the methods of Chou and Talalay. Mean +/- SE IC50's of c-myc and p53 antisense oligos in CAOV-3 and SKOV-3 ranged from 1.0 +/- 0.2 to 9.7 +/- 1.3 microM. The IC50's of c-myc oligos were consistently lower than corresponding p53 oligos in all cell lines (P < 0.034, t test). The fibroblast cell line was sensitive to anti-c-myc and combination anti-c-myc/p53 oligos (IC50 = 1.5 +/- 0.6 and 1.4 +/- 0.2 microM, respectively), but not to anti-p53 oligos alone (IC50 > 16 microM). Nonspecific toxicity was observed at concentrations of 16 microM for all cell lines except in BG-1, where maximal growth stimulation occurred at this concentration with anti-p53 oligos. Growth stimulation was also observed in BG-1 with anti-c-myc and anti-c-myc/p53 combinations at intermediate doses, with inhibition at higher doses. While c-myc/p53 combinations in CAOV-3 were synergistic (CI < 0.8), they were antagonistic in SKOV-3 (CI > 3.2). Phosphorothioate oligos directed against c-myc and p53 in different cell lines were shown to have both antiproliferative and stimulatory activity, as single agents and in combination, at concentrations that are achievable in vivo. Because of the complex patterns of effects, further in vitro studies are warranted before considering clinical trials with these agents in gynecologic cancers.

Base Sequence↗
PubMed2006

On our way to targeted therapy for cachexia in cancer?

PURPOSE OF REVIEW: Cachexia, the occurrence of involuntary weight loss due to loss of adipose tissue and skeletal muscle mass, is among the most common and devastating symptoms in patients with advanced cancer. It is a significant factor contributing to the poor performance status and high mortality rate of these patients, and is a distressing problem for both patients and their families. Despite extensive research in an attempt to better understand the mechanisms involved, progress in the management of cancer cachexia has been slow. RECENT FINDINGS: The pathogenic mechanisms of cachexia and anorexia are multifactorial, but cytokines and tumour-derived factors are known to play a significant role, thereby representing suitable therapeutic targets. Moreover, recent advances in the field of molecular biology have shed light on other mediators involved in the mechanisms leading to muscle wasting, thus increasing potential targets for new therapies. SUMMARY: This review will focus on recent findings in relation to the molecular pathways leading to muscle wasting that have improved our current understanding of cachexia and will direct the future management of cachexia in cancer towards targeted therapies.

Antineoplastic Agents↗
PubMed2004

New cytotoxic and molecular-targeted therapies of head and neck tumors.

PURPOSE OF REVIEW: The purpose of this review is to provide an update on novel medical treatments for head and neck cancer. RECENT FINDINGS: Despite the continuing introduction of new cytotoxic agents, such as antimetabolites (capecitabine, pemetrexed), and topoisomerase I inhibitors, the management of advanced head and neck cancer remains challenging. Epidermal growth factor receptor is an appealing target for novel therapies in head and neck cancer. Several rational approaches have been designed to abrogate epidermal growth factor receptor function, among which the development of small molecules, such as gefitinib or erlotinib, that inhibit tyrosine kinase activity, therefore abrogating the receptor's catalytic activity, autophosphorylation, and its engagement with signal transducers. The development of monoclonal antibodies, such as cetuximab, directed against the receptor's extracellular domain and competing for the binding of receptor ligands is another antireceptor strategy, because it induces epidermal growth factor receptor downregulation from the tumor cell surface. Gefitinib has been evaluated in a phase II study in head and neck cancer, at a dose of 500 mg/day. In this study, a 53% disease control rate was achieved, with a low toxicity. Currently, a phase II study at a dose of 250 mg/day is ongoing. A phase II study of erlotinib in advanced head and neck cancer has provided similar results to those of gefitinib, with a 46% control rate and an acceptable toxicity. Phase I studies of cetuximab have been carried out in advanced head and neck cancer, mainly combining the drug with chemotherapy or radiotherapy. Three phase II studies have evaluated the combination of cetuximab with platinum-based chemotherapy in pretreated patients with recurrent/metastatic head and neck cancer, with a control rate ranging from 29 to 66%. A phase III placebo-controlled trial has shown that the addition of cetuximab to cisplatin does not significantly improve median progression-free survival, despite a difference in the response rate between the two arms. Other molecular-targeted approaches in head and neck cancer include farnesyl transferase inhibitors, cell cycle regulators, and gene therapy. SUMMARY: Novel targeted therapies are highly appealing in advanced head and neck cancer, and the most clever way to use them is a matter of intense investigation.

Alkyl and Aryl Transferases↗
PubMed2004

Vascular-targeting therapies for treatment of malignant disease.

BACKGROUND: Tumor endothelium represents a valuable target for cancer therapy. The vasculature plays a critical role in the survival and continued growth of solid tumor masses; in addition, the inherent differences between tumor blood vessels and blood vessels associated with normal tissue make the tumor vasculature a unique target on which to base the design of novel therapeutics, which may allow highly selective treatment of malignant disease. Therapeutic strategies that target and disrupt the already formed vessel networks of growing tumors are actively being pursued. The goal of these approaches is to induce a rapid and catastrophic shutdown of the vascular function of the tumor so that blood flow is arrested and tumor cell death due to the resulting oxygen and nutrient deprivation and buildup of waste products occurs. METHODS: Biologic approaches and small-molecule drugs that can be used to damage tumor vasculature have been identified. Physiologic, histologic/morphologic, and immunohistochemical assessments have demonstrated that profound disruption of the tumor vessel network can be observed minutes to hours after treatment. The small-molecule agents that have made the greatest advances in the clinical setting (5,6-dimethylxanthenone-4-acetic acid [DMXAA], combretastatin A4 disodium phosphate [CA4DP], and ZD6126) are the focus of the current review. RESULTS: Loss of patent blood vessels, decreased tumor blood flow, extensive necrosis, and secondary ischemia-induced tumor cell death have been well documented in a variety of preclinical tumor models treated with agents such as DMXAA, CA4DP, and ZD6126. The use of such agents in conjunction with irradiation and other chemotherapeutic agents has led to improved treatment outcomes. CONCLUSIONS: The targeting of tumors' supportive blood vessel networks could lead to improvements in cancer cure rates. It is likely that this approach will prove to be most efficacious when used in concert with conventional treatment strategies.

Angiogenesis Inhibitors↗
PubMed1996

Microdosimetry and radiocurability: modelling targeted therapy with beta-emitters.

Tumour control probability (TCP) is a more relevant quantity than the dose distribution in the target volume for estimating the likely efficacy of any type of radiation therapy, be it external beam or targeted using radionuclides. This paper concentrates on a TCP modelling study, for tumour spheres of different radii assuming a uniform uptake of six different beta emitters (ranging from 67Cu to 90Y or 0.58 to 2.3 MeV in endpoint energy). The dose at varying radii, expressed as a fraction of the equilibrium dose, D beta (R)/Deq, was computed by numerical integration of the point-dose kernel over the sphere volume, and shows clearly the effect of electron disequilibrium for small radii and also at the edges of the spheres. These D beta(R)/Deq were converted into volume-dose distribution V(D) and thence into clonogenic cell numbers, n(D), from which the TCPs for spheres of different radii were computed, for different cumulated activities per unit mass, in megabecquerel hours per gram assuming a clonogenic cell density of 10(8) cm-3 and a tumour-cell radiosensitivity alpha of 1.0 Gy-1. Using V(D) rather than simply the mean dose decreases the TCP at both large and small tumour radii for a given number of megabecquerel hour per gram. Curves of iso-TCP go through a shallow minimum in megabecquerel hour per gram at a tumour radius approximately equal to the maximum beta-particle range. The fall in dose at small radii outweighs the reduction in cell number, making it improbable that micrometastases can be eliminated solely by beta-emitters targeted to the tumour cells. An explicit comparison with external-beam therapy for a fixed number of tumour cells divided into different numbers of spheres further emphasizes the difficulties caused by small tumours in beta-particle targeted therapy. Alternative strategies to overcome these limitations are briefly discussed.

Beta Particles↗
PubMed2026

SOD1 Variants in Patients With Amyotrophic Lateral Sclerosis in Central Eastern Europe: From Genetic Testing to SOD1 Targeted Therapy.

BACKGROUND: Amyotrophic lateral sclerosis (ALS) is one of the most devastating fatal motor neuron diseases, characterized by progressive degeneration of motor neurons in the brain and spinal cord. A significant advance in ALS therapy was achieved with the recent European Medicines Agency approval of Tofersen, the first antisense oligonucleotide (ASO) specifically targeting SOD1 mRNA, a key genetic determinant of the disease. Yet, despite its clinical relevance, data on SOD1-ALS in Central Eastern Europe remain scarce. METHODS: Here, we present a multicentric study across six countries-Austria, Czechia, Poland, Hungary, Slovakia, and Slovenia-representing approximately 16% of the European Union's population. We report all pathogenic, likely pathogenic, and uncertain SOD1 variants, along with the phenotypic features, including heritability, age, site of onset, and survival. We also assessed the availability of genetic testing, counseling, and access to Tofersen therapy across the region. RESULTS: Out of 1200 patients with confirmed ALS, we identified 24 distinct pathogenic SOD1 variants in a total of 67 patients (median age at onset 47 [40-55] years), of whom 65.7% had familial ALS (fALS) and 34.3% had sporadic ALS (sALS). We characterized the associated phenotypes and reported that 42 patients are currently receiving Tofersen therapy. CONCLUSION: This study provides the first comprehensive overview of SOD1-ALS in Central Eastern Europe. Our findings underscore the importance of genetic testing and counseling, as well as equitable access to targeted therapies such as Tofersen to advance patient-specific care in this region.

Humans↗
PubMed2001

Heat-inducible TNF-alpha gene therapy combined with hyperthermia using magnetic nanoparticles as a novel tumor-targeted therapy.

Heat-induced therapeutic gene expression is highly desired for gene therapy to minimize side effects. Furthermore, if the gene expression is triggered by heat stress, combined therapeutic effects of hyperthermia and gene therapy may be possible. We combined TNF-alpha gene therapy driven by the stress-inducible promoter, gadd 153, with hyperthermia using magnetite cationic liposomes (MCLs). In nude mice, MCLs induced cell death throughout much of the tumor area on heating under an alternating magnetic field. This heat stress also resulted in a 3-fold increase in TNF-alpha gene expression driven by the gadd 153 promoter as compared with that of nonheated tumor. TNF-alpha gene expression was also observed in the peripheral area where the hyperthermic effect was not enough to cause cell death. The combined treatment strongly arrested tumor growth in nude mice over a 30-day period, suggesting potential for cancer treatment.

Animals↗
PubMed1996

Use of Epstein-Barr virus nuclear antigen-1 in targeted therapy of EBV-associated neoplasia.

To target expression of toxic genes to Epstein-Barr virus (EBV)-associated tumor cells, we have developed an EBV-driven enzyme prodrug system (EDEPS) that takes advantage of the trans-activating properties of EBNA1, a latent protein expressed in all EBV-containing cells, to direct expression of cytosine deaminase (CD) at high levels in those cells only. Plasmids were constructed in which the CD gene or a luciferase reporter gene were cloned downstream of the herpes simplex virus thymidine kinase (tk) promoter and the family of repeats (FR) sequence from the oriP region of EBV. Analysis of luciferase activity after transient transfection into a panel of EBV-negative or -positive human cell lines showed that the presence of the FR element enhanced transcription from the tk promoter in all EBV-positive cell lines, whereas transcription from tk was repressed in all EBV-negative cell lines, including B, T, and fibroblast cell lines. In clonogenicity assays following transfection with the CD vector, the presence of 5-fluorocytosine (5-FC) in the culture medium completely abolished cell growth in EBV-positive cell lines, but did not affect the growth of EBV-negative cell lines. This vector system should have wide applicability in that it allows targeted expression of any gene of interest to tumors that carry EBV, irrespective of the role EBV plays in their pathogenesis.

Antigens, Viral↗