Transcoelomic spread and ovarian seeding during ovulation: A possible pathogenesis of Krukenberg tumor

Shah, Bikash; Tang, Wen-hao; Karn, Shammi

doi:10.4103/0973-1482.206234

Cited by 6 publications

(6 citation statements)

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“…Disease spread and recurrence follow the reattachment and establishment of metastatic tumor colonies. 14,56,6,7,12 Thus anoikis resistant cells and aggregates in ascites and in circulation (circulating tumor cells, CTC) have both been associated with poor clinical outcomes, specifically with relapse and chemoresistance. 57,58,2,[59][60][61][62] CTCs are thought to remain in circulation for several hours as the larger size of tumor cells compared to the small diameter of capillary vessels can lead to their arrest inside the small vessels of organs.…”

Section: Discussionmentioning

confidence: 99%

“…OV90 LUC GFP cells derived from P0 (Parental), and P7 (7 cycles of detachment) were expanded in TC treated plates. Subsequently, 5 × 10 6 were injected intraperitoneally. Tumor progression and disease burden was tracked every 10 days by IVIS Lumina III In vivo Imaging System (Caliper Life Sciences, MA) at UAB’s Small Animal Imaging Facility.…”

Section: Methodsmentioning

confidence: 99%

“…Ovarian cancer is the most devastating of gynecological cancers (fifth in cancer deaths among women) and an archetypal example of a cancer that leverages the metastatic hallmark of anoikis resistance for both trancoelomic/intraperitoneal and distant metastasis . [4][5][6][7][8] Accumulation of malignant ascites in the peritoneal cavity occurs as disease progresses, and this process necessitates suspension survival and/or bypass of cell death mechanisms in tumor cells. [9][10][11][12] The precise mechanisms by which cells acquire such anoikis resistance and adapt for apoptosis avoidance as a result of detachment stress remains a subject of intense investigation.…”

Section: Introductionmentioning

confidence: 99%

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Development of adaptive anoikis resistance promotes metastasis that can be overcome by CDK8/19 Mediator kinase inhibition

Monavarian,

Page,

Rajkarnikar

et al. 2023

Preprint

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Anoikis resistance or evasion of cell death triggered by cell detachment into suspension is a hallmark of cancer that is concurrent with cell survival and metastasis. The effects of frequent matrix detachment encounters on the development of anoikis resistance in cancer remains poorly defined. Here we show using a panel of ovarian cancer models, that repeated exposure to suspension stress in vitro followed by attached recovery growth leads to the development of anoikis resistance paralleling in vivo development of anoikis resistance in ovarian cancer ascites. This resistance is concurrent with enhanced invasion, chemoresistance and the ability of anoikis adapted cells to metastasize to distant sites. Adapted anoikis resistant cells show a heightened dependency on oxidative phosphorylation and can also evade immune surveillance. We find that such acquired anoikis resistance is not genetic, as acquired resistance persists for a finite duration in the absence of suspension stress. Transcriptional reprogramming is however essential to this process, as acquisition of adaptive anoikis resistance in vitro and in vivo is exquisitely sensitive to inhibition of CDK8/19 Mediator kinase, a pleiotropic regulator of transcriptional reprogramming. Our data demonstrate that growth after recovery from repeated exposure to suspension stress is a direct contributor to metastasis and that inhibition of CDK8/19 Mediator kinase during such adaptation provides a therapeutic opportunity to prevent both local and distant metastasis in cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Development of adaptive anoikis resistance promotes metastasis that can be overcome by CDK8/19 Mediator kinase inhibition

Monavarian,

Page,

Rajkarnikar

et al. 2023

Preprint

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show abstract

“…At presentation, patients are often asymptomatic, present in the fourth decade of their life, and predominantly have bilateral disease [11][12][13][14]. The most frequent site of primary malignancy is the stomach, often referred to as Krukenberg tumors, named after Friedrich Ernst Krukenberg who first described them [11,15].…”

Section: Introductionmentioning

confidence: 99%

“…While the biologic mechanisms for spread remain fundamentally unknown, various pathways have been proposed including transcoelomic, lymphatic, and hematogenous pathways [10]. At presentation, patients are often asymptomatic, present in the fourth decade of their life, and predominantly have bilateral disease [11–14]. The most frequent site of primary malignancy is the stomach, often referred to as Krukenberg tumors, named after Friedrich Ernst Krukenberg who first described them [11, 15].…”

Section: Introductionmentioning

confidence: 99%

Ovarian Metastasis from Pancreatic Ductal Adenocarcinoma

et al. 2021

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Background Pancreatic ductal adenocarcinoma (PDAC) has a high propensity for systemic dissemination. Ovarian metastases are rare and poorly described. Methods We identified PDAC cases with ovarian metastasis from a prospectively maintained registry. We reported on the association between outcomes and clinicopathologic factors. Recurrence‐free (RFS) and overall survival (OS) were calculated using Kaplan–Meier analysis. Results Twelve patients with PDAC and synchronous or metachronous ovarian metastases were identified. Nine patients (75%) underwent pancreatectomy for localized PDAC and developed metachronous ovarian recurrence. The median OS for all patients was 25.4 (IQR:15.4–82.9) months. For the nine patients with metachronous ovarian metastasis, the median RFS and OS were 14.2 (IQR:7.2–58.3) and 44.6 (IQR:18.6–82.9) months, respectively. Nodal disease, poor grade, vascular invasion in the pancreatic primary, and bilateral ovarian disease tended to confer worse outcomes. Conclusion Patients with resected PDAC and ovarian recurrence tend to have a comparable disease course to more common patterns of recurrence. Primaries with nodal disease, poorer grade, vascular invasion, and bilateral ovarian disease were indicative of more aggressive disease biology. The ideal management remains largely unknown, and future collaborative efforts should optimize therapeutic strategies.

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Colorectal Peritoneal Metastases: Correlating Histopathological Findings and Disease Biology

Bhatt

Gléhen

2020

Pathology of Peritoneal Metastases

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Transcoelomic spread and ovarian seeding during ovulation: A possible pathogenesis of Krukenberg tumor

Cited by 6 publications

References 0 publications

Development of adaptive anoikis resistance promotes metastasis that can be overcome by CDK8/19 Mediator kinase inhibition

Development of adaptive anoikis resistance promotes metastasis that can be overcome by CDK8/19 Mediator kinase inhibition

Ovarian Metastasis from Pancreatic Ductal Adenocarcinoma

Colorectal Peritoneal Metastases: Correlating Histopathological Findings and Disease Biology

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