Bulk chemotherapy and drug release strategies for cancer treatment have been associated with lack of specificity and high drug concentrations that often result in toxic side effects. This work presents the results of an experimental study of cancer drugs (prodigiosin or paclitaxel) conjugated to Luteinizing Hormone-Releasing Hormone (LHRH) for the specific targeting and treatment of triple negative breast cancer (TNBC). Injections of LHRH-conjugated drugs (LHRH-prodigiosin or LHRH-paclitaxel) into groups of 4-week-old athymic female nude mice (induced with subcutaneous triple negative xenograft breast tumors) were found to specifically target, eliminate or shrink tumors at early, mid and late stages without any apparent cytotoxicity, as revealed by in vivo toxicity and ex vivo histopathological tests. Our results show that overexpressed LHRH receptors serve as binding sites on the breast cancer cells/ tumor and the LHRH-conjugated drugs inhibited the growth of breast cells/tumor in in vitro and in vivo experiments. The inhibitions are attributed to the respective adhesive interactions between LHRH molecular recognition units on the prodigiosin (PGS) and paclitaxel (PTX) drugs and overexpressed LHRH receptors on the breast cancer cells and tumors. The implications of the results are discussed for the development of ligand-conjugated drugs for the specific targeting and treatment of TNBC. Breast cancer is the most commonly diagnosed cancer and the second most frequent cause of death in women 1. In general, breast tumors are intrinsically heterogeneous in nature, making them difficult to detect and treat 2. Approximately, 75-80% of breast cancers are hormone receptor-positive 2,3. Also, these overexpressed receptors are usually estrogen and/or progesterone receptors 2,3. However, Triple Negative Breast Cancer (TNBC) (which represents approximately 10-17% of all breast cancers) does not express estrogen receptors (ER), or progesterone receptors (PR), or the human epidermal growth factor receptor 2 gene (HER2) 4-8. In addition, TNBCs also exhibit distinctive clinical features 7,8 and are more common in younger patients 6 and African American/African women 9. TNBC is an aggressive and immunopathology subtype of breast cancer that usually does not respond to drugs that target ER, PR and HER2 6. Furthermore, since the most common and conventional breast cancer diagnosis and treatment techniques tend to focus and target ER, PR and HER2, it is often difficult to detect 10 and treat 11 TNBCs with conventional targeted hormonal therapy and chemotherapy. The challenges associated with TNBCs

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This article presents the correlation of creep and viscoelastic properties to the cytoskeletal structure of both tumorigenic and non‐tumorigenic cells. Unique shear assay and strain mapping techniques were used to study the creep and viscoelastic properties of single non‐tumorigenic and tumorigenic cells. At least 20 individual cells, three locations per cell, were studied. From the results, lower densities in the volume of actin, and keratin 18 structures were observed with the progression of cancer and were correlated to the increased creep rates and reduced mechanical properties (Young's moduli and viscosities) of tumorigenic (MDA‐MB‐231) cells. The study reveals significant differences between the creep and viscoelastic properties of non‐tumorigenic breast cells versus tumorigenic cells. The variations in the creep strain rates are shown to be well characterized by lognormal distributions, while the statistical variations in the viscoelastic properties are well‐described by normal distributions. The implications of the results are discussed for the study of discrete cell behaviors, strain and viscoelastic responses of the cell, and the role of cell cytoskeleton in the onset and progression of cancers.

This article presents silica nanoparticles for the sustained release of AMACR antibody-conjugated and free doxorubicin (DOX) for the inhibition of prostate cancer cell growth. Inorganic MCM-41 silica nanoparticles were synthesized, functionalized with phenylboronic acid groups (MCM-B), and capped with dextran (MCM-B-D). The nanoparticles were then characterized using Fourier-transform infrared spectroscopy, scanning electron microscopy, transmission electron microscopy, zeta potential analysis, nitrogen sorption, X-ray diffraction, and thermogravimetric analysis, before exploring their potential for drug loading and controlled drug release. This was done using a model prostate cancer drug, DOX, and a targeted prostate cancer drug, α-Methyl Acyl-CoA racemase (AMACR) antibody-conjugated DOX, which attaches specifically to AMACR proteins that are overexpressed on the surfaces of prostate cancer cells. The kinetics of sustained drug release over 30 days was then studied using zeroth order, first order, second order, Higuchi, and the Korsmeyer-Peppas models, while the thermodynamics of drug release was elucidated by determining the entropy and enthalpy changes. The flux of the released DOX was also simulated using the COMSOL Multiphysics software package. Generally, the AMACR antibodyconjugated DOX drug-loaded nanoparticles were more effective than the free DOX drug-loaded formulations in inhibiting the growth of prostate cancer cells in vitro over a 96 h period. The implications of the results are then discussed for the development of drug-eluting structures for the localized and targeted treatment of prostate cancer.