PTEN Deficient Metastatic Hormone Sensitive Prostate Cancer | Primary Research (KOL's Insight) | Market Intelligence | Epidemiology & Market Forecast-2035

Phosphatase and Tensin Homology Deleted on Chromosome 10 (PTEN) is an established tumor suppressor with dual phosphatase-dependent and phosphatase-independent functions. It was identified as phosphatase for the first time in 1997 and is mutated or lost in a number of cancers. The tumor suppressor phosphatase and tensin homologue deleted on chromosome 10 (PTEN) negatively regulates the PI3K-AKT-mTOR pathway, and loss of PTEN is strongly associated with advanced prostate cancer progression and poor clinical outcome. The tumor suppressor phosphatase and tensin homologue deleted on chromosome 10 (PTEN), which is strongly associated with advanced prostate cancer progression and a poor clinical outcome, negatively regulates the PI3K-AKT-mTOR pathway.

Description

Phosphatase and Tensin Homology Deleted on Chromosome 10 (PTEN) is an established tumor suppressor with dual phosphatase-dependent and phosphatase-independent functions. It was identified for the first time in 1997 as a phosphatase that is lost or mutated in a number of cancers. A link between PTEN loss and the poor prognosis of patients with castration-resistant prostate cancer (CRPC) has also been found. It is well known that lesions in the PTEN gene, which is located on chromosome 10q23, occur at a significant rate in the majority of human tumor subtypes, and that this locus is thought to have the highest preference for loss in people. PTEN plays the tumor-suppressive role that has been most thoroughly researched as a lipid phosphatase that blocks phosphatidylinositol 3-kinase (PI3K) signaling. PI3K serves as a crucial node in a crucial signaling pathway that regulates the growth, survival, and metabolism of cancer cells. When PI3K is turned on, it phosphorylates the inositol ring's 3' (D3) position on phosphatidylinositol (4,5)-bisphosphate (PIP2) to produce phosphatidylinositol (3,4,5)-trisphosphate (PIP3), which is present on the inner leaflet of the plasma membrane. PIP3, a second messenger, can be contacted by proteins with pleckstrin homology (PH) domains. AKT and other PH domain-containing proteins are drawn to the plasma membrane, where they become activated and start subsequent signaling cascades. Cytoplasmic PTEN negatively controls this pathway by dephosphorylating PIP3 at its D3 position, which prevents downstream kinase activation and inhibits cancer cell growth and survival. According to two recent studies, translational PTEN variants can be secreted from cells and can interact with neighboring cells. Similar to cytoplasmic PTEN, secreted PTEN has lipid phosphatase activity and blocks PI3K signaling in target cells.

PTEN Deficient Metastatic Hormone Sensitive Prostate Cancer (Epidemiology)

One in seven men in North America are expected to develop prostate cancer (PCa) at some point in their lives. Up to 70% of castrate-resistant and metastatic PCa as well as roughly 25% of the initial PCa at radical prostatectomy are affected when the PTEN gene is inactivated by deletion or mutation. PTEN loss is linked to invasive clinical traits and an early biochemical recurrence after initial therapies in PCa malignancies. Recent studies suggest that PTEN may play additional lipid phosphatase-independent roles outside of the PI3K/AKT pathway, such as those that influence tumor progression by modifying the immune system and the tumour microenvironment (TME). Prostate cancer incidence varies more than 50 times across the globe, with the highest rates found in North America, Australia, Northern and Central Europe, and the lowest in Southeast Asia, Central and South Asia, and North Africa. The most typical non-skin cancer in American men is prostate cancer. Prostate cancer is more likely to develop with age, with an estimated lifetime incidence of one in six white men and one in five Black men receiving a diagnosis. In 2022, there will likely be 268.490 new cases of prostate cancer, according to the American Cancer Society. Men under the age of 40 and men under the age of 50 both have a low incidence of prostate cancer diagnosis. Between 1989 and 1992, there was a sharp rise in prostate cancer incidence in the United States. This increase may have been brought on by the increased use of PSA blood tests, which allowed for earlier diagnosis of asymptomatic men with prostate cancer.

PTEN Deficient Metastatic Hormone Sensitive Prostate Cancer -Current Market Size & Forecast Trends

The market for PTEN-deficient metastatic hormone-sensitive prostate cancer (mHSPC) is currently part of the broader prostate cancer treatment landscape, which is projected to grow significantly. The overall prostate cancer treatment market is expected to reach approximately USD 12.03 billion by 2033, reflecting a compound annual growth rate (CAGR) of 3.9%. Specifically, recent developments indicate that treatments targeting PTEN-deficient mHSPC, such as the combination of capivasertib (an AKT inhibitor) with abiraterone and androgen deprivation therapy (ADT), have shown promising results in improving radiographic progression-free survival (rPFS) in clinical trials. As these targeted therapies advance and gain approval, the market for PTEN-deficient mHSPC is anticipated to expand significantly through 2035, driven by ongoing research, increased awareness, and the urgent need for effective treatment options for this aggressive cancer subtype.

The tumor suppressor phosphatase and tensin homologue deleted on chromosome 10 (PTEN) negatively regulates the PI3K-AKT-mTOR pathway, and loss of PTEN is strongly associated with advanced prostate cancer progression and poor clinical outcome. Therefore, a number of therapeutic approaches are being researched to treat PTEN-deficient tumors. The PI3K-AKT-mTOR signaling network can be inhibited using conventional methods as well as cutting-edge methods that either target PTEN regulation of chromosome stability, DNA damage repair, and the tumor microenvironment or restore PTEN function. Although it is still challenging to treat PTEN-deficient prostate cancer, recent advances in precision medicine indicate that PTEN loss can be used as a useful biomarker to stratify prostate cancer patients for treatment, potentially improving overall outcomes. For metastatic hormone-sensitive prostate cancer, there have been many more treatment options recently. The conventional treatment for these patients, androgen-deprivation therapy alone, is now thought to be ineffective. Using docetaxel, abiraterone acetate, enzalutamide, and apalutamide in addition to traditional androgen deprivation therapy (ADT) has been shown to increase survival, according to data. Docetaxel, abiraterone acetate, enzalutamide, apalutamide, and/or radiotherapy to the primary tumor have all been shown to have significant clinical benefits, including noticeably better overall survival and quality of life. These methods are now included in treatment recommendations and are considered standard of care.

Report Highlights

PTEN Deficient Metastatic Hormone Sensitive Prostate Cancer - Current Market Trends

PTEN Deficient Metastatic Hormone Sensitive Prostate Cancer - Current & Forecasted Cases across the G8 Countries

PTEN Deficient Metastatic Hormone Sensitive Prostate Cancer - Market Opportunities and Sales Potential for Agents

PTEN Deficient Metastatic Hormone Sensitive Prostate Cancer - Patient-based Market Forecast to 2035

PTEN Deficient Metastatic Hormone Sensitive Prostate Cancer - Untapped Business Opportunities

PTEN Deficient Metastatic Hormone Sensitive Prostate Cancer - Product Positioning Vis-a-vis Competitors' Products

PTEN Deficient Metastatic Hormone Sensitive Prostate Cancer - KOLs Insight