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Related Concept Videos

Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Treatment Resistent Cancers02:56

Treatment Resistent Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...

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Updated: May 20, 2026

Competing-Risk Nomogram for Predicting Cancer-Specific Survival in Multiple Primary Colorectal Cancer Patients after Surgery
06:46

Competing-Risk Nomogram for Predicting Cancer-Specific Survival in Multiple Primary Colorectal Cancer Patients after Surgery

Published on: September 27, 2024

Asymptomatic synchronous quintuple primary cancers.

Shinichi Komiyama1, Eiji Nishio, Ryoko Ichikawa

  • 1Department of Obstetrics and Gynecology, Fujita Health University School of Medicine, Toyoake, Japan. shinkomiyama@gmail.com

Gynecologic and Obstetric Investigation
|July 11, 2012
PubMed
Summary

A 46-year-old woman was diagnosed with five synchronous primary cancers, including ovarian, endometrial, colon, rectal, and lung adenocarcinomas. The absence of MSH2 and MLH1 protein expression suggests a DNA mismatch repair defect contributed to her multiple cancers.

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Oncogenic Gene Fusion Detection Using Anchored Multiplex Polymerase Chain Reaction Followed by Next Generation Sequencing
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Oncogenic Gene Fusion Detection Using Anchored Multiplex Polymerase Chain Reaction Followed by Next Generation Sequencing

Published on: July 5, 2019

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Last Updated: May 20, 2026

Competing-Risk Nomogram for Predicting Cancer-Specific Survival in Multiple Primary Colorectal Cancer Patients after Surgery
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Competing-Risk Nomogram for Predicting Cancer-Specific Survival in Multiple Primary Colorectal Cancer Patients after Surgery

Published on: September 27, 2024

Oncogenic Gene Fusion Detection Using Anchored Multiplex Polymerase Chain Reaction Followed by Next Generation Sequencing
09:49

Oncogenic Gene Fusion Detection Using Anchored Multiplex Polymerase Chain Reaction Followed by Next Generation Sequencing

Published on: July 5, 2019

Area of Science:

  • Oncology
  • Genetics
  • Pathology

Background:

  • Synchronous multiple primary cancers are rare and pose diagnostic and therapeutic challenges.
  • Early detection and understanding the underlying genetic mechanisms are crucial for patient management.

Observation:

  • A 46-year-old asymptomatic woman was incidentally diagnosed with five distinct primary cancers during gynecological screening.
  • The identified cancers included clear cell ovarian adenocarcinoma, endometrioid endometrial adenocarcinoma, ascending colon adenocarcinoma, rectal adenocarcinoma, and papillary lung adenocarcinoma.

Findings:

  • Fluorodeoxyglucose-positron emission tomography (FDG-PET) and other imaging modalities were vital for diagnosing these synchronous primary malignancies.
  • Immunohistochemical analysis revealed absent MSH2 protein expression in tumors of the ovary, endometrium, ascending colon, and rectum.
  • Additionally, the rectal cancer showed a lack of MLH1 protein expression.

Implications:

  • The concurrent absence of MSH2 and MLH1 protein expression strongly suggests a defect in DNA mismatch repair (MMR) as the underlying cause of carcinogenesis.
  • This case highlights the importance of comprehensive molecular profiling in patients with multiple primary cancers to guide treatment and genetic counseling.
  • Further investigation into MMR gene abnormalities may reveal new therapeutic targets for managing patients with multiple synchronous cancers.