Seven PhD Positions with Fully-funded Scholarships at MUSCBC

Seven PhD Positions with Fully funded Scholarships at MUSCBC

We are hiring seven enthusiastic early career scientists whom we can offer a three/four year fully funded scholarship for conducting PhD research at Department of Biochemistry, Faculty of Science, Mahidol University. These scholarships provide an average monthly stipend of at least 15,000 THB along with tuition fees, health insurance and so on. PhD students will study different aspects of biochemistry, molecular biology, and cell biology under our International Graduate Program in Biochemistry.

We are looking for different profiles that will combine in a multidisciplinary team of scientists, embedded within MUSCBC: 

Project 1: Asst. Prof. Kanlaya Katewongsa

Project 2: Prof. Sarawut Jitrapakdee

Project 3: Assoc. Prof. Sittinan Chanarat

Project 4: Prof. Tavan Janvilisri

Project 5: Assoc. Prof. Thaned Kangsamaksin

Project 6: Assoc. Prof. Ruchanok Tinikul

Project 7: Assoc. Prof. Kornkamon Lertsuwan

Eligibility: For all positions, a person must be aged 40 or under and a Bachelor or Master of Science degree is required; BSc GPAx ≥ 3.25, MSc GPAx ≥ 3.5. Excellent knowledge of the English language is a prerequisite; IELTS ≥ 6, TOEFL-iBT ≥ 79, or MU GRAD Plus ≥ 90. Candidates of all nationalities are eligible.

We welcome applications by 15/6/2023 or until filled. Applications must include a CV and a motivation letter, sent to Informal inquiries are also welcome. 

Project 1: Development of theranostic nanoparticles for cancer cell targeting
Asst. Prof. Kanlaya Katewongsa

This project seeks a student interested in designing theranostic nanoparticles (NPs) with both diagnostic and therapeutic properties. The NPs will be optimized to deliver large doses of anti-cancer drugs or genes to diseased cells, minimizing side effects from standard chemotherapies, enhancing permeability and retention in cancer tissues, and improving drug stability. Additionally, The NPs surface will be modified with biomolecules like peptides, antibodies, or nucleic acids to enable precise delivery to specific cancer cells such as breast or colorectal cancer. The student will also study the relevant cellular mechanisms and evaluate the efficacy of these NPs in in vitro system.

Please contact Asst. Prof. Kanlaya Katewongsa,, for more information.

Project 2
Prof. Sarawut Jitrapakdee

Cancer is a disease caused by the deregulation of cell growth, resulting in rapid proliferation. Cancer cells can invade the surrounding and distant tissues to establish growth at the secondary location known as metastasis. While staying in the neoplastic state, the cancer cell maintains its highly malignant status by sustaining the proliferative signal, invasion and metastasis, and angiogenesis while resisting growth inhibition, programmed cell death, and altered energy metabolism. Cellular metabolism is a central biochemical pathway that enables cells to produce energy and biomolecules as cellular components. Depletion of energy level and cellular building blocks can affect the bioenergetic status, causing cancer cell death. Targeting cancer metabolism has paved the way for developing novel metabolism-targeted therapeutic approaches. Our laboratory is emphasized cancer metabolism using a multidisciplinary approach including genetic modification, cell imaging, metabolism, organic chemistry, and nanotechnology, aiming at:

  1. Identifying novel drugs targeted cancer metabolism
  2. Determining cellular & molecular mechanisms underlying drug actions

Please contact Prof. Sarawut Jitrapakdee,, for more information.

Project 3
Assoc. Prof. Sittinan Chanarat

A) Image-based cell phenotyping with deep learning for studying lipodystrophic Type 2 diabetes: This research project aims to investigate the relationship between lipodystrophic Type 2 diabetes and lipid metabolism using image-based cell phenotyping with deep learning techniques. By analyzing cellular images, we will be able to identify various cellular components such as lipid droplets and mitochondria, and relate them to the cellular phenotypes of interest. The use of deep learning algorithms will enable the creation of accurate and efficient models for predicting the phenotypic responses of cells to various stimuli, providing valuable insights into the mechanisms underlying lipodystrophic Type 2 diabetes.

B) Molecular mechanisms underlying Cryptococcus pleomorphism: C. neoformans is able to exhibit pleomorphism, an ability to exist in different forms or shapes during its life cycle. It has been shown that its pleomorphism is associated with virulence. Particularly, hypervirulent strains of C. neoformans exhibit a larger size of capsule, higher variation in cell size, and an increase in shed capsules and microcells. The mechanism of the pleomorphism, however, is largely unknown. This project will use multidisciplinary approaches to better understand the mechanism and hopefully discover a clue towards developing a cure for the disease.

Please contact Assoc. Prof. Sittinan Chanarat,, for more information.

Project 4
Prof. Tavan Janvilisri

(Please visit TJ lab’s website for more information.)

Project 5
Assoc. Prof. Thaned Kangsamaksin

Project Title: Dissecting the role of hypovascularity and vasculogenic mimicry in pancreatic cancer
Principal investigator: Assoc. Prof. Thaned Kangsamaksin, Ph.D.
Lab: Laboratory of Vascular and Cancer Biology, Department of Biochemistry, Faculty of Science, Mahidol University, Bangkok, Thailand

About our lab

Our lab seeks a student who has a solid background in biology, biochemistry, and molecular biology and is passionate about doing basic and translational research. We are interested in cell and molecular biology of cancer and blood and lymphatic vessels, focusing the elucidation of the molecular mechanisms of blood and lymphatic vessel formation and their functions in cancer progression and cancer therapy.

About the project

The growth of solid tumors requires a continuous supply of oxygen and nutrients. One of the most important factors and characteristic hallmarks for cancer is the formation of new blood vessels from pre-existing vessels, or angiogenesis. Bevacizumab (Avastin) has been approved by the US-FDA and used to treat patients with various types of cancer by blocking the vascular endothelial growth factor (VEGF) pathway. However, increasing evidence indicates tumor resistance to the VEGF inhibitor, and therefore, confirms that the benefits of anti-VEGF therapy are at best transitory and followed by a restoration of tumor growth and progression. There are several proposed mechanisms of how a tumor can invade angiogenesis inhibition, including upregulation of alternative pro-angiogenic signaling pathways, increased protection of tumor vasculature from anti-angiogenic drugs, and changes in tumor cell behavior and characteristics to mimic blood vessels, also known as vasculogenic mimicry.

Vasculogenic mimicry (VM) describes the ability of aggressive cancer cells to express endothelium-associated genes and form extracellular matrix (ECM)-rich vessel-like networks, which recapitulate embryonic vasculogenesis. This process has been associated with aggressive behaviors of cancer. Recent evidence has demonstrated the presence of VM first in melanoma and, subsequently, in many other cancer types. However, the signaling cascades that regulate the VM process still remain elusive. Therefore, the aims of this project are:

  • To understand the mechanisms underlying the hypovascularized nature of PDAC
  • To investigate the presence of VM in pancreatic cancer in vitro and in PDAC patients and elucidate signaling pathways that are important in different steps of this process.

Please contact Assoc. Prof. Thaned Kangsamaksin,, for more information.

Project 6
Assoc. Prof. Ruchanok Tinikul

Chemo-electroenzymatic cascade for CO2 conversion

Our research focuses on the mechanistic study of enzymes and their application in biocatalysis and biodetection areas. The main strategies employed are protein/enzyme engineering, metabolic pathway engineering, and enzymatic cascade design.  This project is seeking students who are interested in studying and characterization of dehydrogenase /reductase enzymes and chemo/electroenzymatic cascade design for CO2 conversion. Enzyme engineering and immobilization approaches will also be employed to optimize the conversion system. The established enzymatic conversion of CO2 will provide a sustainable and eco-friendly approach to mitigating CO2 emissions.

Please contact Assoc. Prof. Ruchanok Tinikul, for more information.

Project 7
Assoc. Prof. Kornkamon Lertsuwan

Investigation and therapeutic development of iron overload and sugar-induced osteoporosis.

Imbalanced bone metabolism, i.e. abnormal activity of bone forming cells VS bone degrading cells, contributed to osteoporosis in many pathological conditions. Unfortunately, current therapeutics are not specific to each cell types in bone microenvironment. Accordingly, our lab aims to develop adeno-associated virus (AAV) that can specifically target each type of bone cells for precise genetic engineering. In addition, two osteoporosis induction conditions are studied including iron overload and high sugar conditions.

Bone marrow mesenchymal stromal cells are stem cells that can differentiate into either adipocyte or bone forming cells. For the first project, iron overload was shown cause abnormal mesenchymal stem cell differentiation to differentiate to adipogenic linages (fat cells) more than osteogenic (bone cells). Accordingly, both chemicals and AAV-mediated metabolic reprograming will be used to bring the correct differentiation potential of these stem cells back to normal.

High blood sugar level in type 2 diabetes patients and animal models have been shown to correlate to osteoporosis. Glucose was also shown to cause osteoblast (bone forming cell) death. However, the comparative effects of different types of monosaccharides and disaccharides in this condition is not known. The second project aims to compare effects of different types of sugars on bone metabolism as well as to use chemicals and AAV-mediated genetic modification to investigate their mechanism behind osteoporosis induction and to develop potential therapeutic agent for sugar-induced osteoporosis.

Please contact Assoc. Prof. Kornkamon Lertsuwan, for more information