Catalina Garcia CRP Protein

Validated biomarkers are needed to assess disease activity and response to interventions in patients with NASH. Creative Biolabs can offer the customized biomarker development services aided by our advanced technique platforms and the most professional proposal for NASH non-invasive diagnosis. Learn more: NASH biomarker

In infectious disease research, the development of interfering nucleic acid drugs is progressing rapidly. These drugs show great potential for treating various infectious diseases, including viral and bacterial diseases, by specifically targeting pathogen genes or modulating the host's immune response. Learn more: Interfering Nucleic Acid Discovery Services for Infectious Disease Research

Microorganisms are tiny organisms found everywhere, including surfaces, air, soil, water, and even within our bodies. They encompass bacteria, fungi, and protists, and play both beneficial and harmful roles.

Beneficially, they produce antibiotics, aid in health (probiotics), and contribute to food production (Corynebacterium glutamicum). However, they can also pose threats, causing diseases (Yersinia pestis, Mycobacterium tuberculosis) and food contamination (Aspergillus flavus).

Check more details: microbiology research

Since its inception, Creative Biolabs has concentrated on improving the quality of our products and services and thus gained a good reputation in the scientific research area. We are committed to offering high-quality peripheral blood mononuclear cells isolated from multiple species for global researchers' projects. All these cells will be quality tested according to a multi-step standard operating procedure (SOP) and can help improve your experimental success rate to a great degree. Check more details: Peripheral Blood Mononuclear Cell (PBMC) Products

Immunotherapy has become a revolution in the area of cancer treatment. Compared to the traditional methods, such as invasive surgeries, radiation and chemotherapy, immunotherapy is more specific and less toxic to patients. Chimeric antigen receptor (CAR)-engineered T cell therapy is the most promising approach, which has shown remarkable ability to eliminate various kinds of tumors, especially for B cell malignancies, with up to 95% response rates and durable complete remission.
For more information: car t cell production

Creative Biolabs offers a battery of rodent models including chemically- and surgically- induced OA models for studies of disease mechanisms as well as the testing of therapeutic candidates. We have talented experts and scientists who are willing to help to set up a detailed research plan based on your specific needs. Herein, you can find the most comprehensive services with the most reasonable prices.
For more information: mia model

Although many types of disease models such as immortalized cell systems have been developed, it is challenging to design disease models that involve multiple genes and mimic in vivo human disease state during disease research. iPSCs (induced pluripotent stem cells) that can differentiate into any cell type have emerged as an effective platform for the construction of disease models.
For more information: iPSC for Disease Model Construction

Monoclonal antibody-based immunotherapies against cancer and other infectious diseases are highly advantageous comparing to conventional therapeutic approaches due to their high specificity and affinity towards well-defined targets. Antibody-drug conjugates (ADCs) inherit such superiorities and more remarkably, expand the therapeutic window of the conjugated drugs (payloads), which are usually highly toxic and diverse in their biochemical nature. For more information: abc laboratories

Cancer immunotherapy has shown great promise in cancer treatment over the last decade. Several cancer immunotherapies, such as immune checkpoint blockade therapies, cancer vaccines, and CAR-T therapies, have been extensively researched and have yielded promising results.

Cancer vaccines, which elicit tumor-specific immune stimulation, are one of the most important immunotherapeutic strategies and have great potential in cancer treatment. Patients have responded favorably to cancer vaccines based on neoantigens and messenger RNA (mRNA).

Despite enormous efforts in the development of cancer vaccines, which are still in the cancer prevention phase, eliciting a large number of immune responses in cancer patients remains a significant challenge, owing to the cancer vaccines' low immunogenicity, the immunosuppressive tumor microenvironment, and the ground correlation between antigens in cancer vaccines and specific patient tumors.

Autologous tumors have been used to produce cancer vaccines in vitro or in vivo, so-called personalized cancer vaccines, to improve the therapeutic efficacy of cancer vaccines. Autologous tumor cell-based cancer vaccines benefit from tumor-specific tumor-associated antigens (TAA) and induce a stronger immune response than conventional cancer vaccines.

However, in vitro preparation of autologous tumor cell cancer vaccines suffers from complex processes, low yields, and suboptimal efficacy, which limit the clinical application of autologous tumor vaccines. In contrast, large-scale in situ generation of autologous tumor cell cancer vaccines in vivo avoids the complex in vitro vaccine preparation process and is ideal for the production of cancer vaccines.

On November 1, 2022, Fu-Gen Wu's team from Southeast University's School of Bioscience and Medical Engineering published a research paper in Nature Communications titled: In situ generation of micrometer-sized tumor cell-derived vesicles as autologous cancer vaccines for boosting systemic immune responses. HDDT nanoparticles were created using dendritic polymers loaded with adriamycin (DOX), tyrosine kinase inhibitor (TKI), and hyaluronic acid (HA) encapsulated nanoparticles. HDDT nanoparticles have the ability to convert 100% of cancer cells into micron-sized vesicles (HMVs).

Experiments in tumor mouse models revealed that HDDT nanoparticles could inhibit tumor growth, induce strong immunogenic cell death, and convert primary tumors into antigenic reservoirs by producing HMVs in situ as personalized cancer vaccines for cancer immunotherapy. Furthermore, after HDDT nanoparticle treatment, tumor model mice showed strong immune memory effects, which could prevent tumor recurrence in the long run.

In this study, the research team fabricated a series of nanobombs (NBs), including dendritic polymers (Dendritic Polymers) loaded with adriamycin (DOX, an anti-cancer drug) and tyrosine kinase inhibitors (TKI, an anti-cancer drug) and hyaluronic acid (HA, used for tumor targeting) encapsulation, called HDDT NBs.

The team found that after treatment of cancer cells with HDDT NBs, almost all cells (10-30 microns in diameter) were transformed into uniform micron-sized vesicles (1.6-3.2 microns), and cell-to-vesicle conversion efficiency was as high as 100%, meaning that all cancer cells could be efficiently converted into HDDT-induced micron-sized vesicles (HMVs).

Further studies revealed that HDDT NBs, after systemic administration, could accumulate in tumor areas, inhibit tumor growth under different tumor models, induce immunogenic cell death on a large scale, and produce HMVs in situ, transforming tumor tissues into antigenic reservoirs. Immune checkpoint blockade therapy, alone or in combination, could induce intra-tumor and systemic immune responses, establish a strong immune memory effect, cure mouse tumors, and effectively protect against recurrence.

Overall, the HDDT-induced micron-sized vesicles (HMVs) developed in this study provide a simple and promising nanotechnology-based strategy for the in situ production of autologous tumor cell vaccines and may provide clues for the development of personalized cancer vaccines.
 

In cancer immunotherapy, the spotlight has fallen on STING as a pivotal target of recent interest. Biopharmaceutical companies worldwide are vigorously developing innovative therapies targeting STING with the goal of activating immune pathways to combat cancer cells.

While these STING agonists have demonstrated promise in preclinical studies, a perplexing phenomenon has emerged in certain clinical trials. Contrary to expectations, drugs designed to activate the STING pathway have not consistently yielded the desired benefits for advanced cancer patients. For instance, a Phase 1 clinical trial assessing STING agonists reported only one out of 47 patients with advanced or metastatic cancer displaying a definitive partial response. In another Phase 1 clinical trial involving a STING agonist co-administered with a PD-1 inhibitor, the overall remission rate for advanced cancer patients hovered around 10%.

So, what accounts for the unexpected outcomes of STING agonists in the fight against cancer? In their quest for answers, researchers at the Memorial Sloan Kettering Cancer Center, in collaboration with Weill Cornell Medicine, have uncovered a counterintuitive possibility—drugs inhibiting STING activation may prove more beneficial to patients with advanced cancer than STING activators.

This revelation hinges on the nature of the STING signaling pathway itself. Within the human body, the presence of double-stranded DNA molecules in the cytoplasmic matrix serves as an early warning signal, indicating the intrusion of pathogens, the existence of cancer cells, or cell rupture. Once intracellular sensors detect cytoplasmic DNA, they activate the STING protein, which, in turn, triggers the expression of inflammation-associated genes, igniting an innate immune response that shields the body from foreign invaders and abnormal cells—a pivotal process in anti-tumor immunity.

However, the new study suggests that cancer cells disrupt the STING signaling pathway, creating an immunosuppressive tumor microenvironment. Particularly in advanced cancer stages, where cancer cells exhibit high chromosomal instability, the STING pathway remains persistently active, leading to "desensitization." This, in turn, rewires the downstream signaling pathway, inducing endoplasmic reticulum stress—a favorable environment for cancer cell metastasis.

Dr. Samuel Bakhoum, co-corresponding author of the study, analogizes this phenomenon, "think of STING signaling as a car alarm. If it rarely sounds, the loud noise will grab your attention. But if it keeps going off, you become accustomed to it and tune it out."

To understand the interactions between cancer cells and immune cells in the tumor microenvironment, another co-corresponding author, Dr. Ashley Laughney, led the team in developing a specialized computational tool named "Contact Tracing". This tool predicts cell-cell interactions and assesses how ligand-receptor interactions influence signal-receiving cells based on single-cell sequencing data.

Dr. Laughney highlights a significant discovery, "one of our most crucial findings is that altering the degree of chromosomal instability or activating STING significantly changes the response within the tumor and its surroundings."

The researchers confirmed the link between chromosomal instability-driven cancer cell metastasis and STING signaling in mouse models implanted with various tumor cells, as well as in human healthy cells and tumor samples. These findings also open the door to innovative therapeutic concepts—for advanced cancer patients with chromosomal instability, activating STING may prove ineffective due to cellular desensitization". In such cases, inhibiting STING could be a promising alternative.

In experimental settings, the researchers administered STING inhibitors to mouse models of melanoma, breast cancer, and colorectal cancer, effectively reducing metastasis driven by chromosomal instability.

Additionally, these insights suggest that by identifying tumors still capable of robust responses to STING activation, clinicians can select patients who would genuinely benefit from STING agonist therapy.