Intricate Interplay of Entwined Metabolic and Inflammatory Life-threatening Processes in Tumor Lysis Syndrome Complicating Prostate Cancer: A Systematic Review with a Single Institution Experience

Findakly, Dawood; Wang, Jue

doi:10.7759/cureus.7395

Cited by 5 publications

(10 citation statements)

References 31 publications

(15 reference statements)

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“…Similarly, LDHA expression and LDH level were increased in prostate cancer samples and were prognostic indicators for prostate cancer patients with metastasis. [28][29][30] Furthermore, downregulation of LDHA also suppresses prostate cancer cell proliferation, migration, and invasion, increases cell apoptosis and reprograms glucose metabolism. 28 LDHA protein abundance and total LDH activity are suppressed by the presence of FAM46B.…”

Section: Discussionmentioning

confidence: 99%

<p>FAM46B Promotes Apoptosis and Inhibits Glycolysis of Prostate Cancer Through Inhibition of the MYC-LDHA Axis</p>

Tao

Yan

et al. 2020

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Increased dependence on glycolysis is a known element of cancer. This study was designed to examine critical glycolysis components including transcription factor MYC and its downstream target lactate dehydrogenase A (LDHA), potential upstream regulators of glycolysis such as family with sequence similarity 46 member B (FAM46B), and the impact of the abundance of these proteins on apoptosis and glycolysis in prostate cancer. Materials and Methods: A total of 70 primary prostate cancer patient samples were compared to normal tissues for FAM46B and LDHA expression and the corresponding patients' survival was monitored for 60 months. Prostate cancer cell lines were employed for protein expression manipulation, glucose uptake and LDH assays, and apoptosis measurements. A xenograft mouse model was used to quantify the role of FAM46B and LDHA on tumor growth in vivo. Results: FAM46B expression was reduced in prostate tumor tissue compared to normal tissue and prostate cancer patients who expressed low amounts of FAM46B had shortened average lifespans compared to those who expressed higher amounts of FAM46B (p=0.008). FAM46B overexpression reduced glucose uptake, decreased LDH activity, and induced apoptosis in prostate cancer cell lines while FAM46B shRNA increased MYC levels in a non-malignant prostate cell line (P69). Conversely, forced expression of LDHA in LNCaP cells produced an increase in glycolysis markers with a corresponding decrease in apoptosis. FAM46B-overexpressing xenografts had starkly blunted growth which was restored with cooverexpression of LDHA. Conclusion: FAM46B plays a central role in regulating glycolysis and apoptosis in prostate cancer and operates through the regulation of LDHA via MYC. FAM46B's keystone status in prostate cancer makes it a potential, robust biomarker for prostate cancer prognosis and a promising therapeutic target.

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Section: Discussionmentioning

confidence: 99%

<p>FAM46B Promotes Apoptosis and Inhibits Glycolysis of Prostate Cancer Through Inhibition of the MYC-LDHA Axis</p>

Tao

Yan

et al. 2020

OTT

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“…Systemic tumor lysis syndrome b [1,2, Spontaneous (idiopathic) c [1,2,[6][7][8][10][11][12][13][14][15][16][17][18][19][20][21][22][23] Hematologic malignancies [1,6,10,[12][13][14][15] Solid tumors [2,7,8,10,11,[15][16][17][18][19][20][21][22][23] Therapy-associated d [1,2,[9][10][11]15,17,20,21,[23]…”

Section: Subtype References Aunclassified

“…Spontaneous (idiopathic) systemic tumor lysis syndrome is less common than therapy-associated tumor lysis syndrome. However, multiple reports now document its occurrence [1,2,[6][7][8][10][11][12][13][14][15][16][17][18][19][20][21][22][23].…”

Section: Spontaneous (Idiopathic) Systemic Tumor Lysis Syndromementioning

confidence: 99%

“…Similar to individuals with associated hematologic malignancies, spontaneous (idiopathic) systemic tumor lysis syndrome may occur in patients with recently diagnosed, but untreated, visceral cancers, or it may be an initial clinical feature that heralds the diagnosis of an unsuspected solid tumor. Although solid tumor-associated idiopathic systemic tumor lysis syndrome is uncommon, reports of individuals in whom this occurs seem to be increasing [2,7,8,10,11,[15][16][17][18][19][20][21][22][23].…”

Section: Spontaneous (Idiopathic) Systemic Tumor Lysis Syndromementioning

confidence: 99%

“…Solid tumor-associated spontaneous (idiopathic) systemic tumor lysis syndrome has subsequently been observed in patients with various cancers. These include adenocarcinoma of unknown primary, breast carcinoma, colorectal carcinoma, endometrial carcinoma, gastric carcinoma, germ cell tumors, hepatocellular carcinoma, lung cancer (non-small cell and small cell), melanoma, prostate carcinoma, renal cell carcinoma, and rhabdomyosarcoma (embryonal and parietal) [2,7,8,10,11,[15][16][17][18][19][20][21][22][23].…”

Section: Spontaneous (Idiopathic) Systemic Tumor Lysis Syndromementioning

confidence: 99%

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Tumor Lysis Syndrome: Introduction of a Cutaneous Variant and a New Classification System

Cohen¹,

Prieto

Kurzrock

2021

Cureus

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Tumor lysis syndrome, an oncological emergency, is characterized by laboratory parameters such as hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia, as well as renal injury with an elevated creatinine. Tumor lysis syndrome is seen in patients with aggressive malignancies and high tumor burden. More frequently, it occurs in individuals with hematologic malignancies such as high-grade lymphomas (such as Burkitt lymphoma) and leukemia (such as acute lymphocytic leukemia). It also, albeit less commonly, can be seen in patients with widespread solid tumors that are rapidly proliferating and are markedly sensitivity to antineoplastic therapy. Tumor lysis syndrome is usually preceded by cancer-directed therapy; however, the syndrome can present spontaneously prior to the individual receiving malignancydirected treatment. We reported a man with metastatic salivary duct carcinoma who had cutaneous metastases that presented as carcinoma hemorrhagiectoides. Microscopic examination demonstrated that the metastatic tumor cells had infiltrated and replaced the entire dermis. After the patient received his first dose of antineoplastic therapy, he had an excellent response and the cutaneous metastases developed into ulcers; we hypothesize that most of the dermis, which had been replaced by tumor cells, disappeared as a result of the therapeutic response, and the overlying epidermis became necrotic and shed, leaving an ulcer. His dramatic response to treatment prompted us to propose a new classification of tumor lysis syndrome, which should include the systemic form of the condition as well as the new variant: cutaneous tumor lysis syndrome. We anticipate that, with improvement in targeted therapies, there may be an increase in therapyassociated cutaneous tumor lysis syndrome.

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Tumor Lysis Syndrome in Breast Cancer

Sengupta

Daw

2021

American Journal of Therapeutics

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Intricate Interplay of Entwined Metabolic and Inflammatory Life-threatening Processes in Tumor Lysis Syndrome Complicating Prostate Cancer: A Systematic Review with a Single Institution Experience

Cited by 5 publications

References 31 publications

<p>FAM46B Promotes Apoptosis and Inhibits Glycolysis of Prostate Cancer Through Inhibition of the MYC-LDHA Axis</p>

<p>FAM46B Promotes Apoptosis and Inhibits Glycolysis of Prostate Cancer Through Inhibition of the MYC-LDHA Axis</p>

Tumor Lysis Syndrome: Introduction of a Cutaneous Variant and a New Classification System

Tumor Lysis Syndrome in Breast Cancer

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