Welcome to TCABS-E Intramural Research-Core!

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Leukemia: Previously it has been shown that the JAK (Janus kinase) - STAT (Signal transducer and activator of transcription factors) pathway plays a role in hematologic malignancies. We hypothesize that it is possible to therapeutically intervene with this pathway in the context of ALL (Acute lymphoblastic leukemia) for a possible chemotherapy in the future. Details...

 

Project leader: Ms. Ramani, T. (B.Sc., final year)

Diabetes (type-2):

Insulin resistance-OGT: The O-GlcNAc transferase (OGT) enzyme has been reported to play a role in insulin signaling cascade particularly in insulin-resistance. We hypothesize that small molecule modulation of OGT could have therapeutic benefits for patients with type-2 Diabetes. Details...

Project leader: Ms. Krishna Priya, Y. (B.Sc., final year)

Insulin resistance-HMGA1: The HMGA1 (High mobility group A1) protein is an epigenetic regulator that plays a critical role in the transcription of many genes including insulin, insulin receptor, insulin-like growth factor receptor, to name a few. We hypothesize that small molecule modulation of HMGA1 protein may therapeutically benefit patients with type-2 Diabetes, especially those experiencing insulin-resistance. Details...

Project leader: Ms. Joycee, T. (B.Sc., II year)

Cervical Cancer: Human K-Ras (Kristen RAt Sarcoma) has been implicated in Cervical Cancer through its mutational burden. Multiple such mutations (amino acid substitutions) have been reported from clinical samples to date. We hypothesize that by targeting the mutant K-Ras along with HPV (Human papillomavirus) infection might yield a synergistic therapeutic outcome. Details...

Project leader: Ms. Himashaila, Ch. (B.Sc., II year)

Breast Cancer:

BRCA1-BARD1 interactions: It has been previously shown that the interactions between the BRCA1 the BARD1 proteins is essential to retain the Ubiquitin Ligase activity during DNA damage repair. However mutations in this interface that disrupt the BRCA1-BARD1 interactions have been reported in Breast Cancer. We hypothesize that by using small molecules, one can restore the BRCA1-BARD1 interaction to overcome such mutations. Details...

Project leaders: Ms. Divya, G. (B.Sc., II year) and Ms. Ramysri, P. (B.Sc., II year)

Triple Negative Breast Cancer (TNBC): It has been shown previously that the Sphingosine kinase 1 (Sphk1)  is up-regulated in TNBC cell lines and that the inhibition of Sphk1 inhibits cellular metastatic ability. We hypothesize that by selective degradation of Sphk1 in TNBC cell lines may give us novel therapeutic approaches to control the metastatic ability of highly aggressive Breast Cancer cells. Details...

Project leader: Ms. Sony, H. (B.Sc., final year)

Melanoma (Skin Cancer): The protein, PTEN (Phosphatase and TENsin homolog) with its inactivating mutations and deletions has been reported in many Cancers. We hypothesize that by targeting the mutant PTEN or up-regulating the wild type PTEN one can achieve therapeutic benefits in Melanoma patients. Details...

Project leader: Ms. Subha Sirisha, K. (B.Sc., II year)

Polycystic Ovarian Syndrome (PCOS):

Targeting the SHBG: The expression levels of SHBG (Sex harmone-binding globulin) in liver have consequences on the circulating blood hormones and has implications in PCOS. We hypothesize that by therapeutically intervening with the liver SHBG expression levels, one can treat PCOS with hopefully lesser side effects compared to the present therapies. Details...

Project leader: Ms. Likhitanjali, U. (B.Sc., final year)

Targeting the androgen synthesis: Increased blood androgen levels is one of the characteristics of PCOS. We hypothesize that by selective modulation of enzymes involved in androgen synthesis, one can decrease the blood androgen levels thus helping the patients with PCOS. Details...

Project leader: Ms. Ganga Bhavani, P. (B.Sc., II year)

Thyroid disorders:

Hypothyroidism: The autoimmune antibodies attack critical Thyroid proteins such as the thyroglobulin and TPO (Thyroid peroxidase) resulting in Thyroid abnormalities. We hypothesize that by inhibiting these antibodies, one can achieve normal Thyroxine (T4) levels in the blood and thereby a new safer therapeutic approach to treat patients with hypothyroidism. Details...

Project leader: Ms. Sonanjali, U. (B.Sc., final year)

Thyroglobulin regulation: Thyroglobulin protein plays a critical role in the synthesis of Thyroxine (T4). We hypothesize that by controlling the expression levels of Thyroglobulin, one can treat thyroid abnormalities. Details...

Project leader: Ms. Navya Sree, S. (B.Sc., II year)

Hyperthyroidism: Graves' disease (Hyperthyroidism) is a condition where the blood levels of Thyroxine (T4) are elevated. We hypothesize that by therapeutically intervening with the process of T4 release, one can control the T4 levels in blood. Details...

Project leader: Ms. Swarnalatha, G. (B.Sc., II year)

Glioblastoma (Brain Cancer): The mutational burden on p53 has direct consequences in many Cancers including neuroblastoma. We hypothesize that by selectively targeting the mutant forms of p53 through therapeutic interventions, one can achieve a safer treatment for Glioblastoma. Details...

Project leader: Ms. Keerthi, G. (B.Sc., final year)

Spinal disc damage repair: Damage to the intervetebral discs requires surgery and pain management with long recovery times. We hypothesize that by precisely delivering genetically engineered stem cells to the site of disc damage, one can not only repair the disc but also significantly cut down on the recovery time. Details...

Project leader: Ms. Devi Lakshmi, K. (B.Sc., final year)

HIV/AIDS

Antibody engineering: Drug-resistance is the most common reason in HIV-1/AIDS treatment failure due to rapid viral replication and mutational burden. We hypothesize that by designing multivalent antibodies one can neutralize the virus in patient blood to inhibit further viral replication within and lower infectivity. Details...

Project leader: Mr. Chiranjeevi, G. (B.Sc., II year)

Selective cytotoxicity: Drugs used in anti-retroiral therapy for HIV/AIDS mainly target viral proteins. However, the viral genome after integrated into the host genome goes into latency which is undetectable but could be reactivated in future. We hypothesize that by causing cytotoxicity selectively in the T-cells that harbor latent HIV-genome one can successfully stop future infections. Details...

Project leader: Ms. Sowjanya, R. (B.Sc., II year)

CRISPR-based approach: Due to the viral latency, the anti-retroviral drugs are unable to target HIV-1 infections. We hypothesize that by using a CRISPR-Cas9 approach, one can reactivate the latent virus or permanently silence the viral gene expression in the infected host T-cells. Details...

Project leader: Ms. Shalini, R. (B.Sc., final year)

Tuberculosis (TB): Unfortunately it has been estimated that India has the burden of a quarter of global TB cases as of 2017. In addition to the variable efficacy of the available vaccines, drug-resistance has become a problem for treatment. We hypothesize that by therapeutically intervening with the host-microbe interactions, one can reduce the infections hopefully in the case of drug-resistant strains as well. Details...

Project leader: Ms. Shakeena, K. (B.Sc., final year)

Liver cirrhosis: Activation of hepatic stellate cells cause liver fibrosis eventually leading to the liver cirrhosis. We hypothesize that by selectively inhibiting the activation of hepatic stellate cells during liver injury, one can inhibit or slow down the process of liver cirrhosis. Details...

Project leader: Ms. Lakshmi Sahitya, B. (B.Sc., II year)